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Old Wed, Feb-17-10, 23:48
aeroangie's Avatar
aeroangie aeroangie is offline
Senior Member
Posts: 1,087
 
Plan: Dr. Eric Westman's/Atkins
Stats: 150/148/132 Female 5'-4"
BF:
Progress: 11%
Location: NC Southern Outer Banks
Default 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.
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