Thoughts on this report please....
Cohort Population Lipids
Total Cholesterol = 281 mg/dl LDL Cholesterol: 5.62 mmol/L = 219.18 mg/dL HDL Cholesterol: 1.25 mmol/L = 48.75 mg/dL Triglerides: .73 mmol/L = 64.97 mg/dL Topics for discussion: - TG/HDL 65mg/dl / 49 mg/dl ratio = 1.32 Generally LDL Phenotype A, LgLDL prevails in cohort. - apoB / apoA-1 ratio 165 / 128 = 1.29 in the study population. Is this a warning value ratio for TYP members. Very long living Ashkenazi Jewish people and Han chinese have apoB/apoA-1 of appx .65 TYP members with plaque regression or stability (Wherehouse list) tend to have apoB/apoA-1 of < .4 - Low HDL 49 mg/dl in the presence of 219 LDL-C mg/dl. Why would there be CVD, CAD if LgLDL was not atherogenic in the study population. - Presence of Lp(a) in LgLDL atherogenicity - TYP members with FH conferring protection to their children Figure 1 LDL cutoff of 135 mg/dl 4.35% likely not FH FOR CHILDREN Treat children early based on the cutoff threashold - Figure 2 and Figure 3 event free level separation based on LDL-C and HDL-C 243mg/dl 39mg/dl The more soft plaque or calcified plaque you leave in the artery, not cholesterol reverse transported by HDL, the more significantly worse the event-free of the adult parents. - Statin reduces apoB which changes the course of the disease. Which infers reduction in LgLDL which allows low HDL to handle better reverse cholesterol transport. - LgLDL is atherogenic in the format of existing Lp(a). Discuss the consideration of LgLDL without the Lp(a), the consideration of LgLDL atherogenicity in the presense of sufficient HDL-C for reverse transport. Interpretation of atherogenicity of LgLDLs. - Significance of the atherogenicity of the title post population lipids versus Paleo lifestyle lipids. Many Paleos have considerably higher LDL-C, TC. - What about Jimmy Moore. He is like a supersized FH. Like the population in the study Jimmy has high Lp(a) by any measure. He has "not to ignore amounts of smLDLs" but basically LDL phenotype A like the study population above. Jimmy Moore's lipids: Total Cholesterol 351 LDL-C 278 HDL-C 57 Triglycerides 79 LDL Particle Number 2130 Small LDL-P 535 LDL Part. Size 22.0 Large HDL-P 10.9 Large VLDL-P 0.4 Jimmy had a VAP Lp(a) of 16 range < 10. - Dr. Davis, Dr jgoldstrich How would you treat the study population in the study with medication. What kinds of RX? What is your stragety with regards to lipids. What would you do different with normal people without the 50% LDL receptor problem as in these FHs, but having similar lipid values Dr Davis, Dr. jgoldstrich from your own patient population of FH (1:500) what is in common(lipids or otherwise) with those patients without severe CAC score or having only minor or no CVD, CAD. - Of note in Figure 2 and 3, CVD free survival for the children's parents really takes a drop after age 40. Must be that same old story____soft plaque becomes calcified plaque as the person aged. Isn't Jimmy Moore now 38 years old. (This TYP Forum Thread is a good heads-up for Jimmy.) - others discussions for this thread as TYP forum members bring forth. |
Well, the tendency is for people to think that at this moment in time we know everything there is to know about the topic. Perhaps there are some other factors that contribute to heart disease we know nothing about? Maybe there's something about those genotypes that protects them? We don't know diddly squat about what 99.95% of the genes in the body do. Oh sure, we've figured out how a few predispose us to certain diseases but it's going to be a looong time before we figure out all of them. And having a gene or not is just the first step, then you have to figure out what happens in the body if you have a certain gene. Maybe that gene produces a protein that binds to something... it's a very complicated thing.
Then once that gets figured out (in the next few hundred years, providing we're still going strong then) they can start working out own the epigenome works... :lol: I wouldn't call an HDL of 49 low. It isn't high but it sure isn't low. |
I am trying not to get bogged down over there. Nancy, can I help you join?? I'll do it right now!!! I wish I had you to respond. He likes talking to me the most. I am getting more and more confused too!!
------------------------------------------------------- CADHEART Master Contributor Posted: 2/16/2010 12:32:28 AM -------------------------------------------------------------------------------- LDL1 Pattern A 29.0 LDL2 Pattern A 4.1 LDL3 Pattern B 72.6 13- 15 lower is better LDL4 Pattern B 40 You hubby has 72.6 + 40 = 112.6 mg/dl small very dangerous LDLs You hubby has 29 + 4.1 = 33.1 mg/dl fluffy LDLs, also dangerous especially if apob is very high like 144. 112.6 / 112.6+ 33.1 is 77% small dangerous small sized LDL. This your husband have. CADHEART Master Contributor Posted: 2/16/2010 12:48:15 AM -------------------------------------------------------------------------------- Hubby TG / HDL = 191 / 33 = 5.79 On the male graph 5.79 means 9% chance of being LDL pheno type A or large LDL dominate 42% chance of being LDL phenotype B small LDLs or 49% chance of being either way. As it came out on VAP "LDL Density pattern B" How you get rid of this crappy LDL see TG/ HDL. Make the HDL go up higher. Make the TG go down lower. Niacin is really powerful for this. Fish oil can lower TG. If you are the right ApoE. Loose weight helps a lot. |
You're succumbing to a snow-job. That's where you overwhelm someone with details they don't understand, and you can't or won't explain adequately, so they'll accept you as an expert.
You need to stop being afraid of asking questions. If I'm curious about something I ask questions. If I don't understand something I either take a pass on the info or try to understand it. But I never assume that someone talking over my head knows what the hell they're talking about. And if they can't explain it in terms you can understand then chances are they don't understand it either. |
I agree with you, Nancy. Majoring on minutia, then they don't explain is a sure sign that something is amiss.
100 years ago, nobody knew their cholesterol levels and heart disease was not common. When did heart disease become common? After the introduction of hydrogenated oils/trans-fats, convenience/processed foods, artificial sweeteners, then high fructose corn syrup, and low-fat foods into the diet. Eating real foods matters more than numbers, imo. |
This is what he wrote back - when asking about ALT and AST regarding Niacin and I also asked him what her did for a living....
He has a bunny eating a carrot as his avatar. CADHEART Master Contributor Posted: 2/17/2010 2:15:03 AM -------------------------------------------------------------------------------- RK AST ALT are liver enzymes. From the chart in the link above on slo-niacin you see the alt ast goe up with higher dosage. Doctors follow that every 3 months or so when you do niacin to see if everything is ok. If one of those are too high thedoc will also test another different liver indicator to see if damage to liver has begun. My background is Computers, Physics and Science. I data crunch a lot. Information that is. That was before. Now my only computer is a Sony Laptop and HP Laptop with not much data on the hard drive. I seem to have extensive knowledge in some Cancers and CAD, CVD. Its the Bunny. I do not know how long my time here will be. The Bunny knows where I should be or go. It brought me here from another place that vitally needed Health Information. Very, very extensive information. I don't question the Bunny. |
From what I understand, your main concern are the triglycerides. They need to be under 100. That changes the texture of the LDL cholesterol transporters which gives cholesterol a fluffy consistancy and is a healthier form of LDL . Jimmy Moore has had other tests done which proved that he had no arterial plaque or heart disease. He's not worried.
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He sounds pretty nutty.
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