(1) Small Dense LDL, particularly the 'death band' LDL-IVb produced by dietary deficiencies of saturated fatty acid and/or ketones and/or excessive dietary carb loads
(2) Low HDL-2 (ditto)
No individual at TYP with subclinical or post-CAD event fails to demonstrate the above two characteristics. Without a doubt, these 2 metabolic parameters describes all atherosclerotic processes that lead to obstructive disease, clinical events, morbidity and mortality. Some individuals with 2-4 stents or bypasses, exhibit zero HDL-2 at the start of our program and 100% sd-LDL.
Of course it immediately changes on the TrackYourPlaque program (faster when it is STATIN-LESS).
Krauss and Pattern 'A'
Of all the literature I have reviewed on Pattern A, Krauss has performed nearly all the seminal, landmark research. He has explored a variety of manners to shift to Pattern 'A' (sans statins, sans niacin).
Lots of Fat. 46% minimum.
Saturated Fat. 18% saturated minimum.
Carb restriction. See first diagram, at top.
Can we obtain zero% Pattern B:100% Pattern A in individuals? Minimal and near-zero 'death bands' of LDL-IVb? It sure would be nice.
When the line breaks 'zero' fat intake is ~ 65% and carb intake 20%. Is 20% still too high for some inviduals? I believe so.
I consume about 20-50 grams daily when I am insulin resistant (around my mense when my body thinks I'm getting ready for a baby; during the year of synthetic hormone h*ll). How do I know when carbs are excessive for me (eg, eating a whole dark chocolate candy carb = 30-40grams)? I ck my blood glucose on a meter 10-20min afterwards (because I peak fast on high GI foods) and it may be > 110-120 g/dl. After rice/sushi, the BG may peak to 180 g/dl for like... 5 min. I can tell the damaging high glucoses are followed by damaging high insulin (and a reduction in adiponectin, the hormone related to body fat loss) because I may have heart palpitations, rapid/racing heart rate, a little anxious (? or is it the I.V. Caffeine), not relaxed, (HUNGER for 24-72hrs afterwards) and basically feel like... CR*P.
I weigh about 125 lbs now and consume about 1-2 g per kilo of protein daily (somedays more with more exercise, somedays less with IF) which is approx 45-56 grams daily (= approx 2 chicken breasts) which makes up about ~15% of energy (or more).
If I estimate I obtain about 1000-1600 cal/day and calculate 20% would be allocated to carbs as an example, then that would be equivalent to ~50-80 grams of carbs daily. WOW. That is a lot more than my current consumption and my experience is that I would gain weight on that dietary intake (esp during insulin resistant periods), even if I consumed 65% fat and 15% protein (or even 50% fat and 30% protein).
Perhaps if carbs were restricted further, more individuals would have achieved Pattern 'A'?
See below, same graph, I've extrapolated into Pattern A territory by extending the Fat%/Carb% x-axis.
In summary, the present study showed that changes in dietary saturated fat are associated with changes in LDL subclasses in healthy men. An increase in saturated fat, and in particular, myristic acid, was associated with increases in larger LDL particles (and decreases in smaller LDL particles). LDL particle diameter and peak flotation rate were also positively associated with saturated fat, indicating shifts in LDL-particle distribution toward larger, cholesterol-enriched LDL. This study also showed that increases in dietary saturated fat were associated with decreases in HL activity. This finding, together with our previous cross-sectional analyses that revealed significant inverse relations of HL activity with LDL peak flotation rate (15), suggests an inverse association of HL activity with concentrations of buoyant LDL particles.
Low fat diet--24% of energy as fat (6% saturated, 12% monounsaturated, and 4% polyunsaturated) --59% as carbohydrate, with equal amounts of simple and complex carbohydrates.
High fat diet--46% of energy as fat (18% saturated, 13% monounsaturated, and 12% polyunsaturated) --39% as carbohydrate. TOO HIGH!!
The main fat as described by the authors was "Palmitic acid (16:0) ... the primary dietary saturated fatty acid in both diets, followed bystearic (18:0) and myristic (14:0) acids, which are representative of the major saturated fatty acids in most human diets (3)." The carbohydrates would be considered high and associated with a higher incidence of Pattern B according to the first Krauss trial described earlier in the post. Nonetheless the results were quite fascinating. Only saturated fatty acids corresponded statistically with improvements in shifting to Pattern A, increased LDL diameter size and to reductions in small dense LDL (both LDL-III and LDL-IV). Please see below stats.
Reduction of LDL-IV by 39% With Increased Saturated Fat
The amount of dietary saturated fat tripled up from 6% to 18% of total energy. This change statistically correlated to reductions in LDL-IV by a total of 39%. The 'death band' which would have corresponded to LDL-IVb was not determined in this trial but definitely some proportion was significantly decreased. Between LDL-IVa and LDL-IVb, we do not know the precise proportional changes.
3X Increase in Saturated Fat Increased HDL-2 by 50%
Recall in the HATS regression trial (NEJM, 2001) where 90% reduction in death and events were observed, the niacin arm was associated with a 70% shift to large buoyant LDL and HDL-2 increase of 60%. With an increase in saturated fats of from 6% to 18% daily, the HDL-2 subfraction increased 50%.
'Death Band': Percent-LDL-IV Changed from 6.0% to Only 3.4%
Examing the relative amount of the 'death band' LDL-IV, Percent of LDL-IV changed from 6.0% in the low-fat group to only 3.4% in the high-fat group. Recall in the previous post Krauss observed that regression (where stenosis is > 30%) was highly associated with quartiles of LDL-IVb less than 2.5%.
Summary of Heart-Healthy Improvements with a High-Saturated Fat (18%) Diet in only Six Weeks (1) Increased total HDL-Cholesterol 18% and the improvements were in vast increases of the regression subspecies HDL-2 of 50%
(2) Reduced Triglyercides by 30%
(3) Increased total LDL-Cholesterol by 13% which is a good indicator that large buoyant LDL are starting to prevail because this change is accompanied by increases in HDL-Cholesterol. An increase in LDL-C is a good thing and associated with regression when the HDL-C is increasing concomitantly. This is not the case in Metabolic Syndrome. Increasing LDL-C in MetSyn are ONLY associated with higher small dense LDL-C which translates to Pattern B (for extremely BBBBAAADD).
(4) Decreased small dense LDL (LDL-III) from 27% on the low fat diet to 18% on high saturated fat. Not bad. The TYP is goal is < 10-30%. For our TYP members who restrict dietary carbohydrates (eg, grains, fruit/berries, etc) and add significant amounts of saturated fat, in 4-6wks they observe basically eradication of small dense LDL to ZERO. These members may have struggled with dense LDL of even 70-80% for years.
(5) Decrease in the deadliest, smallest LDL (LDL-IV) from 6.0% to 3.4% with high saturated fat intakes.
Longevity: Small Dense LDL and HDL-2
We learn so many lessons from the regression trials with niacin, vitamin D (Dr. Davis publication, CKD hemodialysis patients HERE ) and the omega-3 trials. The longevity observations in centenarians fascinate me to no end. I enjoy reading them since they conceptualize the same principal components that Krauss, Superko, Callister, Davis and other forward-thinking, visionary cardiologists and physicians advocate for heart health(a) achieve low small dense LDL (b) bank on high HDL-2
Centenarians Exhibit Pattern 'A+' With sd-LDL << 10%
The Ashkenazi Jewish study compared centenarians, their offspring and population controls (both short-living Ashkenzi Jewish as well as Framingham). Corollaries exist between the long-living (probrand) centenarians and the CAD regression pattern in the trials that we have reviewed here. The long-living typically have resistance against hypertension, diabetes, cancer and coronary artery disease. Uncannily, these centenarians have Pattern A and an extremely low percentage of small dense LDL subparticles, not unlike our Paleo (low carb, high fat) friends and Paleo/ TYP members who achieve all of Dr. Davis TYP goals.
Figure 1. Frequency Distribution of Lipoprotein Properties in Female Probands, Offspring, and Controls. The frequency distribution of plasma high-density lipoprotein (HDL) oncentration levels and particle sizes, and low-density lipoprotein (LDL) particle sizes in female probands, their offspring, and an Ashkenazi control population. [To convert HDL oncentration to mmol/L, multiply by 0.0259. The solid lines represent the mean and the dotted lines represent 1 SD of control.]
What strikes me is that the centenarians (probrands) exhibit generous quantities of large buoyant LDL (60-70+%), only < 10% sd-LDL, Pattern 'A' lipoproteins and an inordinate amount of large-sized HDL-2. Even with modern eating (refined processed foods), their children also similarly exhibit a prevalence of high HDL-2 and high buoyant LDLs. Like good wine, the centenarians' HDL-2 and buoyant LDL appear to have gotten better with age!
Maximize Genetic Expression
Burst your genetic ceilings and boundaries! With the appropriate diet low in carbohydrates, wheat/gluten-free, containing sufficient saturated fatty acids, we can achieve similar longevity-associated lipoproteins. Many are doing it and it's not that hard. Clinical studies support the validity of the benefits of high-saturated fat diets for achieving regression, shifting to Pattern ' A ', controlling small dense LDL, and raising HDL-2.
I personally shifted from pattern B to pattern A by undertaking a high protein, low carbohydrate diet with ample butter and cream. My physician attributes it to the fish oil - Lovaza - which he prescribed. I have also been exercising a great deal more and increased vitamin intake including vitamin D. I, however, think it is diet related.