Condition Afflicts Millions: Do you have “YBS”?

After one of the harshest winters, spring has finally arrived.  The welcomed warmer temperatures and longer daylight hours infuse us with a sense of renewal and new beginnings.   Low and behold we begin to come out of hibernation and start the mad dash to engage in positive lifestyle changes such as eating better, exercising, proper sleep and taking appropriate nutritional supplements.  But invariably, life happens.  

Yep, just when you were about to get started, it happens.  YBS sets in.   I see this “condition” all too often with clients attempting to enter or re-enter into any number of behavior changes.  I will go so far as to say we all have been afflicted at one point or another in our lives.  I call this condition Yeah But Syndrome, or “YBS”.    It is often paralyzing and prevents those afflicted from moving into action, instead remaining in a state of inertia.  

There are many symptoms of YBS but the following are some of the most common.  

Yeah I planned to go to the gym today BUT, the kids needed a ride to practice.  
Yeah I really want to eat better BUT I don’t have the time.   
Yeah I didn’t plan to eat the cake BUT my husband wanted too, so I did also.   
Yeah I really meant to go to the grocery shopping BUT I was too tired, so I hit the drive- thru.  
Or this is a good one. Yeah I meant to start today BUT, I’ll start tomorrow.  

But tomorrow never comes.  You get the drift.  We can all come up with a million yeah buts, in other words, excuses.    The good news is the treatment for YBS is simple--just do it!  Take action.  The reality of today’s 24-7 planet is there will always be something.  The kids, work commitments, family obligations and various projects that need your attention will perpetually be present in some shape or form.  The difference to make the difference is to learn to dance in the rain, not wait for the rain to pass.  When will all the stars align so that your world will be “just right” to start?  If not NOW, WHEN will you begin?  

The key word here is begin.   Far too frequently, I coach clients that shoot themselves in the foot before they start.   Instead of consuming yourself with all the barriers to entry, select reasonable, low-hanging fruit that is “doable.”    The art of lifestyle change is to avoid all-or-nothing thinking and begin to appreciate what you CAN do, versus focusing energy on what you can’t do.  What is one action you can do TODAY to move toward your wellness goal(s)?  Start to focus on what you can do in the mist of your existing life demands. This mantra is a friendly reminder: BE-DO-HAVE.  Be committed.  Do what it takes.  And you will have results.  

Lastly, if you think removing cereal from your morning routine it is too difficult and you can’t do it. Guess what-- you’re likely right.   What you think is what you get!   But what if you think instead, “I can do this.  There are many truly healthy options for breakfast to replace cereal such as eggs and veggies that will help me look and feel my best.”  Then guess what--you will!  This simple change in mind-set can start a tidal wave of change and prevent you from abandoning ship when life tosses you into rough waters.  Ongoing support is hugely important to sustain lifestyle changes.  Join the conversations in the Cureality Forum to engage the support of health coaches and Cureality Members to stay on track. 

We Need More.....Kettlebell

You either love them or you hate them.

When you are in love with kettlebells, like I am, you enjoy the multi-muscle group movements.  Kettlebell workouts are fluid, like a dance, putting together a chain of movements that leave your heart pounding and sweat pouring.  Yes, there’s some sneaky cardio component to a kettlebell workout.   A great blend of aerobic and anaerobic conditioning.

If you hate kettlebells it’s because kettlebell exercises keep you honest with proper exercise execution.  Form is imperative to moves like the kettlebell swing or the kettlebell snatch.  Do it incorrectly and you’ll be either sore or have bruised wrists the next day.  But this is no reason to shy away from the kettlebell.  You have way too much to gain from this odd looking piece of exercise equipment.  

You will get a mega -caloric burn.  The American council on Exercise states that the average kettlebell workout burns 20 calories per minute.  That’s 1200 calories in just one hour.   Kettlebell workouts utilize many muscle groups to give you an efficient, total body conditioning workout.  

If you’re looking for a toned back side get a kettlebell.  The classic kettlebell swing works all the posterior muscles like your glutes, hamstrings, and lower back.  But only if you use correct form.  Otherwise you'll find yourself with nagging back pain, instead of a better butt.  

Kettlebell exercises are functional movements that will allow you to play hard without getting injured.  If you are an athlete, a nature enthusiast, or just want to keep up with the kids then you need to give kettlebells a try.  During a workout, the exercises will target movements that will make getting up and down off the floor easier, as well as bending over to pick something up.

If you are interested in doing kettlebell workouts start with a coach or take class.  You can’t fake form with kettlebell exercises or you could end up hurt.  I’m not trying to scare anyone away because good form is easy to learn.   Your body will memorize the correct movement pattern and you’ll be on your way to a successful kettlebell workout.  

Thyroid and the gut: Hidden health partners

Though I have personally dealt with both auto-immune thyroiditis (Hashomoto’s) and several gut issues (wheat sensitivity, gastritis, etc.), it was not until recently that I discovered how close the thyroid and gut work together to keep you healthy – and how problems with one can affect the other along with your overall health.
 
Most of us understand that the primary function of the gut, that 25 to 30 feet of “tubing” that includes everything from your stomach to your large intestines, is to process the food we eat and allow the “good stuff” (essential nutrients) to pass into our blood stream while keeping the “bad stuff” (harmful proteins) out. However, it may surprise some that the gut also holds as much as 70% of all the immune tissue in the body.
 
Now, imagine all the health havoc that could ensue if, suddenly, the gut stopped doing its job – particularly if it failed to stop toxic proteins from entering the blood stream and then mounted an overzealous immune response against them.  Sometimes, those overzealous immune responses reach beyond their intended targets to attack otherwise healthy tissues and organs – like the thyroid gland.
 
Recent studies indicate that thyroid hormones play a significant role in maintaining gut integrity, preventing leaky gut that can, in some cases, lead to auto-immune attacks against the thyroid.  A properly functioning gut also aids the production of thyroid hormones by converting some of the inactive “T4” thyroid hormone into the functional “T3” hormone.  Failure to simultaneously maintain both a healthy gut and a healthy thyroid can create a vicious cycle leading to chronic health problems and declining vitality.
 
What it all means is that to enjoy optimal health, you must promote good thyroid health to promote good gut health and vice versa.  Unfortunately, traditional medicine tends to focus on one issue to the exclusion of others.  A typical endocrinologist may treat your under active thyroid without spending a moment to address underlying gut issues.  A gastroenterologist will work alleviate a gut problem but will rarely address a potential thyroid problem.
 
This illustrates, once again, how our bodies work as a system and why it is necessary to bridge the “healthcare gaps” in traditional medicine by becoming personally responsible for your health.  I encourage everyone to consult the Cureality Program Guide and online Cureality Diet and Thyroid Health Tracks to learn more about how to optimize both your gut and thyroid health on your journey to realizing complete, whole-body health.

Omega-3 fatty acids likely NOT associated with prostate cancer

A weakly constructed study was reported recently that purportedly associated higher levels of omega-3 fatty acid blood levels and prostate cancer. See this CBS News report, for instance.

Lipid and omega-3 fat expert, Dr. William Harris, posted this concise critique of the study, exposing some fundamental problems:

First, the reported EPA+DHA level in the plasma phospholipids in this study was 3.62% in the no-cancer control group, 3.66% in the total cancer group, 3.67% in the low grade cancer group, and 3.74% in the high-grade group. These differences between cases and controls are very small and would have no meaning clinically as they are within the normal variation. Based on experiments in our lab, the lowest quartile would correspond to an HS-Omega-3 Index of <3.16% and the highest to an Index of >4.77%). These values are obviously low, and virtually none of the subjects was in “danger” of having an HS-Omega-3 Index of >8%. So to conclude that regular consumption of 2 oily fish meals a week or taking fish oil supplements (both of which would result in an Index above the observed range) would increase risk for prostate cancer is extrapolating beyond the data.

This study did not test the question of whether giving fish oil supplements (or eating more oily fish) increased PC risk; it looked only a blood levels of omega-3 which are determined by intake, other dietary factors, metabolism and genetics.


The authors also failed to present the fuller story taught by the literature. The same team reported in 2010 that the use of fish oil supplements was not associated with any increased risk for prostate cancer. A 2010 meta-analysis of fish consumption and prostate cancer reported a reduction in late stage or fatal cancer among cohort studies, but no overall relationship between prostate cancer and fish intake. Terry et al. in 2001 reported higher fish intake was associated with lower risk for prostate cancer incidence and death, and Leitzmann et al. in 2004 reported similar findings. Higher intakes of canned, preserved fish were reported to be associated with reduced risk for prostate cancer. Epstein et al found that a higher omega-3 fatty acid intake predicted better survival for men who already had prostate cancer, and increased fish intake was associated with a 63% reduction in risk for aggressive prostate cancer in a case-control study by Fradet et al). So there is considerable evidence actually FAVORING an increase in fish intake for prostate cancer risk reduction.

Another piece of the picture is to compare prostate cancer rates in Japan vs the US. Here is a quote from the World Foundation of Urology:


"[Prostate cancer] incidence is really high in North America and Northern Europe (e.g., 63 X 100,000 white men and 102 X 100,000 Afro-Americans in the United States), but very low in Asia (e.g., 10 X 100,000 men in Japan).”

Since the Japanese typically eat about 8x more omega-3 fatty acids than Americans do and their
blood levels are twice as high, you’d think their prostate cancer risk would be much higher...
but the opposite is the case.


Omega-3 fatty acids are physiologically necessary, normalizing multiple metabolic phenomena including augmentation of parasympathetic tone, reductions of postprandial (after-meal) lipoprotein excursions, and endothelial function. It would indeed make no sense that nutrients that are necessary for life and health exert an adverse effect such as prostate cancer at such low blood levels. (Recall that an omega-3 RBC index of 6.0% or greater is associated with reduced potential for sudden cardiac death.)

I personally take 3600 mg per day of EPA + DHA in highly-purified, non-oxidized triglyceride form (Ascenta Nutrasea liquid) that yields an RBC omega-3 index of just over 10%, the level that I believe the overwhelming bulk of data suggest is the ideal level for humans.

Are statins and omega-3s incompatible?

French researcher, Dr. Michel de Lorgeril, has been in the forefront of thinking and research into nutritional issues, including the Mediterranean Diet, the French Paradox, and the role of fat intake in cardiovascular health. In a recent review entitled Recent findings on the health effects of omega-3 fatty acids and statins, and their interactions: do statins inhibit omega-3?, he explores the question of whether statin drugs are, in effect, incompatible with omega-3 fatty acids.

Dr. Lorgeril makes several arguments:

1) Earlier studies, such as GISSI-Prevenzione, demonstrated reduction in cardiovascular events with omega-3 fatty acid supplementation, consistent with the biological and physiological benefits observed in animals, experimental preparations, and epidemiologic observations in free-living populations.

2) More recent studies (and meta-analyses) examining the effects of omega-3 fatty acids have failed to demonstrate cardiovascular benefit showing, at most, non-significant trends towards benefit.

He points out that the more recent studies were conducted post-GISSI and after agencies like the American Heart Association's advised people to consume more fish, which prompted broad increases in omega-3 intake. The populations studied therefore had increased intake of omega-3 fatty acids at the start of the studies, verified by higher levels of omega-3 RBC levels in participants.

In addition, he raises the provocative idea that the benefits of omega-3 fatty acids appear to be confined to those not taking statin agents, as suggested, for instance, in the Alpha Omega Trial. He speculates that the potential for statins to ablate the benefits of omega-3s (and vice versa) might be based on several phenomena:

--Statins increase arachidonic acid content of cell membranes, a potentially inflammatory omega-6 fatty acid that competes with omega-3 fatty acids. (Insulin provocation and greater linoleic acid/omega-6 oils do likewise.)
--Statins induce impaired mitochondrial function, while omega-3s improve mitochondrial function. (Impaired mitochondrial function is evidenced, for instance, by reduced coenzyme Q10 levels, with partial relief from muscle weakness and discomfort by supplementing coenzyme Q10.)
--Statins commonly provoke muscle weakness and discomfort which can, in turn, lead to reduced levels of physical activity and increased resistance to insulin. (Thus the recently reported increases in diabetes with statin drug use.)

Are the physiologic effects of omega-3 fatty acids, present and necessary for health, at odds with the non-physiologic effects of statin drugs?

I fear we don't have sufficient data to come to firm conclusions yet, but my perception is that the case against statins is building. Yes, they have benefits in specific subsets of people (none in others), but the notion that everybody needs a statin drug is, I believe, not only dead wrong, but may have effects that are distinctly negative. And I believe that the arguments in favor of omega-3 fatty acid supplementation, EPA and DHA (and perhaps DPA), make better sense.



DHA: the crucial omega-3

Of the two omega-3 fatty acids that are best explored, EPA and DHA, it is likely DHA that exerts the most blood pressure- and heart rate-reducing effects. Here are the data of Mori et al in which 4000 mg of olive oil, purified EPA only, or purified DHA only were administered over 6 weeks:



□ indicates baseline SBP; ▪, postintervention SBP; ○, baseline DBP; •, postintervention DBP; ⋄, baseline HR; and ♦, postintervention HR.

In this group of 56 overweight men with normal starting blood pressures, only DHA reduced systolic BP by 5.8 mmHg, diastolic by 3.3 mmHg.

While each omega-3 fatty acid has important effects, it may be DHA that has an outsized benefit. So how can you get more DHA? Well, this observation from Schuchardt et al is important:

DHA in the triglyceride and phospholipid forms are 3-fold better absorbed, as compared to the ethyl ester form (compared by area-under-the-curve). In other words, fish oil that has been reconstituted to the naturally-occurring triglyceride form (i.e., the form found in fresh fish) provides 3-fold greater blood levels of DHA than the more common ethyl ester form found in most capsules. (The phospholipid form of DHA found in krill is also well-absorbed, but occurs in such small quantities that it is not a practical means of obtaining omega-3 fatty acids, putting aside the astaxanthin issue.)

So if the superior health effects of DHA are desired in a form that is absorbed, the ideal way to do this is either to eat fish or to supplement fish oil in the triglyceride, not ethyl ester, form. The most common and popular forms of fish oil sold are ethyl esters, including Sam's Club Triple-Strength, Costco, Nature Made, Nature's Bounty, as well as prescription Lovaza. (That's right: prescription fish oil, from this and several other perspectives, is an inferior product.)

What sources of triglyceride fish oil with greater DHA content/absorption are available to us? My favorites are, in this order:

Ascenta NutraSea
CEO and founder, Marc St. Onge, is a friend. Having visited his production facility in Nova Scotia, I was impressed with the meticulous methods of preparation. At every step of the way, every effort was made to limit any potential oxidation, including packaging in a vacuum environment. The Ascenta line of triglyceride fish oils are also richer in DHA content. Their NutraSea High DHA liquid, for instance, contains 500 mg EPA and 1000 mg DHA per teaspoon, a 1:2 EPA:DHA ratio, rather than the more typical 3:2 EPA:DHA ratio of ethyl ester forms.

Pharmax (now Seroyal) also has a fine product with a 1.4:1 EPA:DHA ratio.

Nordic Naturals has a fine liquid triglyceride product, though it is 2:1 EPA:DHA.





Krill oil: Do the math

The manufacturers of krill oil claim that the phospholipid form of omega-3 fatty acids, EPA and DHA, enhance their absorption. There are indeed some data to that effect:


Here are some representative krill oil preparations available on the market:


MegaRed Krill Oil:
EPA 50 mg
DHA 24 mg
Total omega-3s (EPA + DHA + other forms) 90 mg
Price: $28.99 for 60 softgels

Source Naturals (a fine company otherwise, by the way):

EPA 150 mg
DHA 90 mg
Total omega-3 fatty acids 300 mg
Price: $24.99 for 60 softgels

Alright, let's do some simple math:

Average volume of blood in the human body (all components): 5000 cc
Percentage of red blood cells (RBCs) by volume: 45%
Total volume RBCs: 2250 cc
Percentage of total volume RBCs occupied by fatty acids:

What tests are MORE important than cholesterol?

In the conventional practice of early heart disease prevention, cholesterol testing takes center stage. Rarely does it go any further, aside from questions about family history and obvious sources of modifiable risk such as smoking and sedentary lifestyle.

So standard practice is to usually look at your LDL cholesterol, the value that is calculated, not measured, then--almost without fail--prescribe a statin drug. While there are indeed useful values in the standard cholesterol panel--HDL cholesterol and triglycerides--they are typically ignored or prompt no specific action.

But a genuine effort at heart disease prevention should go farther than an assessment of calculated LDL cholesterol, as there are many ways that humans develop coronary atherosclerosis. Among the tests to consider in order to craft a truly effect heart disease prevention program are:

--Lipoprotein testing--Rather than using the amount of cholesterol in the various fractions of blood as a crude surrogate for lipoproteins in the bloodstream, why not measure lipoproteins themselves? These techniques have been around for over 20 years, but are simply not part of standard practice.

Lipoprotein testing especially allows you to understand what proportion of LDL particles are the truly unhealthy small LDL particles (that are oxidation- and glycation-prone). It also identifies whether or not you have lipoprotein(a), the heritable factor that confers superior survival capacity in a wild environment ("The Perfect Carnivore"), but makes the holder of this genetic pattern the least tolerant to the modern diet dominated by grains and sugars, devoid of fat and organ meats.

--25-hydroxy vitamin D--The data documenting the health power of vitamin D restoration continue to grow, with benefits on blood sugar and insulin, blood pressure, bone density, protection from winter "blues" (seasonal affective disorder), decrease in falls and fractures, decrease in cancer, decrease in cardiovascular events. I aim to keep 25-hydroxy vitamin D at a level of 60 to 70 ng/ml. This generally requires 4000-8000 units per day in gelcap form, at least for the first 3 or so years, after which there is a decrease in need. Daily supplementation is better than weekly, monthly, or other less-frequent regimens. The D3 (cholecalciferol) form is superior to the non-human D2 (ergocalciferol) form.

--Hemoglobin A1c (HbA1c)--HbA1c represents glycated hemoglobin, i.e., hemoglobin molecules within red blood cells that are irreversibly modified by glucose, or blood sugar. It therefore provides an index of endogenous glycation of all proteins of the body: proteins in the lenses of the eyes that lead to cataracts; proteins in the cartilage of the knees and hips that lead to brittle cartilage and arthritis; proteins in kidney tissue leading to kidney dysfunction.

HbA1c provides an incredibly clear snapshot of health: It reflects the amount of glycation you have been exposed to over the past 90 or so days. We therefore aim for an ideal level: 5.0% or less, the amount of "ambient" glycation that occurs just with living life. We reject the notion that a HbA1c level of 6.0% is acceptable just because you don't "need" diabetes medication, the thinking that drives conventional medical practice.

--RBC Omega-3 Index--The average American consumes very little omega-3 fatty acids, EPA and DHA, such that a typical omega-3 RBC Index, i.e., the proportion of fatty acids in the red blood cell occupied by omega-3 fatty acids, is around 2-3%, a level associated with increased potential for sudden cardiac death (death!). Levels of 6% or greater are associated with reduced potential for sudden cardiac death; 10% or greater are associated with reduced other cardiovascular events.

Evidence therefore suggests that an RBC Omega-3 Index of 10% or greater is desirable, a level generally achieved by obtaining 3000-3600 mg EPA + DHA per day (more or less, depending on the form consumed, an issue for future discussion).

--Thyroid testing (TSH, free T3, free T4)--Even subtle degrees of thyroid dysfunction can double, triple, even quadruple cardiovascular risk. TSH values, for instance, within the previously presumed "normal" range, pose increased risk for cardiovascular death; a TSH level of 4.0 mIU, for instance, is associated with more than double the relative risk of a level of 1.0.

Sad fact: the endocrinology community, not keeping abreast of the concerning issues coming from the toxicological community regarding perchlorates, polyfluorooctanoic acid and other fluorinated hydrocarbons, polybrominated diphenyl ethers (PDBEs), and other thyroid-toxic compounds, tend to ignore these issues, while the public is increasingly exposed to the increased cardiovascular risk of even modest degrees of thyroid dysfunction. Don't commit the same crime of ignorance: Thyroid dysfunction in this age of endocrine disruption can be crucial to cardiovascular and overall health.


All in all, there are a number of common blood tests that are relevant--no, crucial--for achieving heart health. Last on the list: standard cholesterol testing.

Cranberry Sauce

Happy Thanksgiving 2012, everyone, from all the staff at Track Your Plaque!

Here’s a zesty version of traditional cranberry sauce, minus the sugar. The orange, cinnamon, and other spices, along with the crunch of walnuts, make this one of my favorite holiday side dishes.

There are 31.5 grams total “net” carbohydrates in this entire recipe, or 5.25 grams per serving (serves 6). To further reduce carbs, you can leave out the orange juice and, optionally, use more zest.

1 cup water
12 ounces fresh whole cranberries
Sweetener equivalent to 1 cup sugar (I used 6 tablespoons Truvía)
1 tablespoon orange zest + juice of half an orange
½ cup chopped walnuts
1 teaspoon ground cinnamon
½ teaspoon ground nutmeg
¼ teaspoon ground cloves

In small to medium saucepan, bring water to boil. Turn heat down and add cranberries. Cover and cook at low-heat for 10 minutes or until all cranberries have popped. Stir in sweetener. Remove from heat.

Stir in orange zest and juice, walnuts, cinnamon, nutmeg, and cloves.

Transfer mixture to bowl, cool, and serve.


Apple Cranberry Crumble

Apple, cranberry, and cinnamon: the perfect combination of tastes and scents for winter holidays!

I took a bit of carbohydrate liberties with this recipe. The entire recipe yields a delicious cheesecake-like crumble with 59 “net” grams carbohydrates (total carbs – fiber); divided among 10 slices, that’s 5.9 grams net carbs per serving, a quantity most tolerate just fine. (To reduce carbohydrates, the molasses in the crumble is optional, reducing total carbohydrate by 11 grams.)

Other good choices for sweeteners include liquid stevia, stevia glycerite, powdered stevia (pure or inulin-based, not maltodextrin-based), Truvía, Swerve, and erythritol. And always taste your batter to test sweetness, since sweeteners vary in sweetness from brand to brand and your individual sensitivity to sweetness depends on how long you’ve been wheat-free. (The longer you’ve been wheat-free, the less sweetness you desire.)


Crust and crumble topping
3 cups almond meal
1 stick (8 tablespoons) butter, softened
1 cup xylitol (or other sweetener equivalent to 1 cup sugar)
1½ teaspoons ground cinnamon
1 tablespoon molasses
1½ teaspoons vanilla extract
Dash sea salt

Filling
16 ounces cream cheese, softened
2 large eggs
½ cup xylitol (or other sweetener equivalent to ½ cup sugar)
1 Granny Smith apple (or other variety)
1 teaspoon ground cinnamon
1 cup fresh cranberries

Preheat oven to 350° F.

In large bowl, combine almond meal, butter, sweetener, cinnamon, molasses, vanilla, and salt and mix.

Grease a 9½-inch tart or pie pan. Using approximately 1 cup of the almond meal mixture, form a thin bottom crust with your hands or spoon.

In another bowl, combine cream cheese, eggs, and sweetener and mix with spoon or mixer at low-speed. Pour into tart or pie pan.

Core apple and slice into very thin sections. Arrange in circles around the edge of the cream cheese mixture, working inwards. Distribute cranberries over top, then sprinkle cinnamon over entire mixture.

Gently layer remaining almond meal crumble evenly over top. Bake for 30 minutes or until topping lightly browned.
Why small LDL particles are the #1 cause of heart disease in the US

Why small LDL particles are the #1 cause of heart disease in the US

Ask your doctor: What is the #1 cause of heart disease in the US?

Let's put aside smoking, since it is an eminently modifiable risk and none of those crazies read this blog anyway. What will your doctor say? Most like he or she will respond:

High cholesterol or high LDL cholesterol

Too much saturated fat

Obesity

Pfizer, Merck, AstraZeneca and their kind would be overjoyed to know that they can add your doctor to their eager following.

I'd tell you something different. I would tell you that small LDL particles are, by far and away, the #1 cause for heart disease. I base this claim on several observations:

--Having run over 10,000 lipoprotein panels (mostly NMR) over the past 15 years, it is a rare person who does not have a moderate, if not severe, excess of small LDL particles. 50%, 70%, even 90% or more small LDL particles are not rare. Over the course of a year, the only people who show no small LDL particles are slender, athletic, pre-menopausal females.

--In studies in which lipoproteins have been quantified in people with coronary disease, small LDL particles dominate, just as they do in my office. Here's a 2006 review.

--Small LDL is largely the province of people who consume carbohydrates, such as the American population instructed to "cut fat and eat more healthy whole grains." Conventional diet advice has therefore triggered an expllosion in small LDL particles.

--When fasting triglycerides exceed 60 mg/dl, small LDL particles increase as a proportion of total LDL particles. This includes the majority of the US population. (This ignores postprandial, or after-eating, triglycerides, which also contribute to small LDL formation.)

If you were to read the data, however, you might conclude that small LDL affects a minority of people. This is because in most studies small LDL categorize it as either "pattern B," meaning exceeding some arbitrary threshold of percentage of small LDL particles, versus "pattern A," meaning falling below that same arbitrary threshold.

Problem: There is no consensus on what percentage of small LDL particles should mark the cutoff between pattern A vs. pattern B. In many studies, for instance, people with 50% small LDL particles are called "pattern A."

If, instead, we were to set the bar lower to identify this highly atherogenic (atherosclerotic plaque-causing) particle at, say, 20-30% of total, then the number or percentage of people with "pattern B" small LDL particles would go much higher.

I see this play out in my office and in the online program, Track Your Plaque, every day: At the start eating a low-fat, grain-filled diet with lots of visceral fat ("wheat belly") to start, they add back fat and cut out all wheat and limit carbohydrates. Small LDL particles plummet

Comments (77) -

  • Bill

    9/15/2011 1:13:26 PM |

    But is there any real evidence that small LDL is a *cause* of heart disease? Correlation alone isn't sufficient, of course, and Chris Masterjohn has said that even the correlation largely disappears when traditional "risk factors" such as HDL, LDL, and triglycerides are added to the model.

    I ask in part because I am about to arm wrestle with my primary care doctor about my recent cholesterol panel:

    Total: 382
    HDL: 157
    LDL: 217 (calculated)
    Triglycerides: 39

    He's upset about the LDL, of course, especially since it's progressively risen over time (coinciding with dietary changes pretty compatible with TYP and including quite a bit of sat fat after years as a low-fat vegetarian). Naturally, he wants me to reduce my fat consumption and retest in four months, and I'm sure a statin drug recommendation will follow just as the sunset inevitably follows the sunrise.

    I am thinking of asking for a full lipoprotein panel, with the expectation that it will calm him down by showing 1) much lower real, measured LDL with my rock bottom triglycerides and 2) strong Pattern A LDL with my sky high HDL and low triglycerides.

    But I'm not certain if I can really make a convincing empirical case to him that Pattern A is benign with a high LDL. (I'm also hesitating after hearing Chris Masterjohn say that LDL particle size measurements are hugely dependent on the type of assay used and that as a result it's not clear what, biologically, any given result means until these methodological discrepancies are sorted out.)

  • Peter Silverman

    9/15/2011 2:41:59 PM |

    The article you cite says the number of LDL particles may be more important than the size.  Is that your experience?

  • Howard

    9/15/2011 3:02:31 PM |

    @Bill : Chris Masterjohn also mentioned in a recent podcast that the current measurement technology for LDL particle size is just not sufficiently accurate to be useful.

  • chuck

    9/15/2011 3:48:18 PM |

    what is your feeling on oxidized ldl?

  • chuck

    9/15/2011 3:52:16 PM |

    @howard
    yes, based on the hour to hour, day to day, week to week, and month to month natural fluctuations of lipids in the blood it is difficult to make any real judgements about cholesterol readings without doing multiple panels over a period of time.  the whole medical community seems to be screwed up in this respect.

  • Kathy

    9/15/2011 4:13:20 PM |

    I have no idea what Dr. Davis' response will be, but if you're interested in getting an NMR profile done on your own dime (and if there is a convenient location near you), check out directlabs.com for their September special.  An NMR profile will only set you back $79 (reg $127).  I've been waiting for this "sale" and am getting it done to show my own doctor.  Your health is ultimately in your hands - keep up the good fight!
    Best,
    Kathy

  • edward white

    9/15/2011 5:02:18 PM |

    Dr D,
    I totally agree small LDL is driven by excess carbohydrate intake and postprandial
    triglycerides. However there is a substantial subset of people whose small LDL
    is genetically driven. I believe you are aware of this phenomena.
    Please let these folks know what their options are to address this important issue!
    There can be a good deal of frustration when carbs and triglycerides are addressed but
    with little lowering of small LDL.
    Please help this substantial number of people out by outlining their options...
    Gib

  • Unix-Jedi

    9/15/2011 5:22:13 PM |

    Thanks for that information, Kathy.

  • cancerclasses

    9/15/2011 5:57:26 PM |

    It ain't good,  just ask Wikipedia.   From the Wiki page re 'Chronic endothelial injury hypothesis':
    "Once LDL accumulates in the subendothelial space, it tends to become modified or oxidized.[5] This oxidized LDL plays several key roles in furthering the course of the inflammatory process. It is chemotactic to monocytes; oxidized LDL causes endothelial cells to secrete molecules that cause monocytes to penetrate between the endothelial cells and accumulate in the intima.[6]

    Oxidized LDL promotes death of endothelial cells by augmenting apoptosis. Also, through the activation of collagenases, ox-LDL contributes to a process which may lead to the rupture of the fibrous plaque[7] Oxidized LDL decreases the availability of endothelial nitric oxide (NO), which, in turn, increases the adhesion of monocytes to the endothelium.[8] Moreover, NO is involved in paracrine signalling between the endothelium and the smooth muscle that maintains vascular tone; without it, the muscle will not relax, and the blood vessel remains constricted. Thus, oxidized LDL also contributes to the hypertension often seen with atherosclerosis."

  • Bob

    9/15/2011 6:12:21 PM |

    Test reply

  • cancerclasses

    9/15/2011 6:13:54 PM |

    Yes, French cardiologist Guy-Andre Pelouze MD. at the recent Ancestral Health Symposium said in his presentation "Paleodiet and atheroma: A Cardiovascular Surgeon’s Perspective" that:

    1. Native (the reduced form of) LDL cholesterol is NOT atherogenic, only the oxidized form leads to atheroma, atherogenesis & arterial plaque formation.

    2. Without oxidized cholesterol it's very difficult to have arterial plaque formation

    3. Anti-oxidants are ineffective in preventing atheroma.

    4. SDLDL easily enter the subendothelial space because SDLDL are less than 25 nm in diameter and the subendothelial space is 26 nm.

    5. Subendothelial space in humans is very different in humans than other mammals due to the large amount of smooth muscle in the arterial media below the the intima layer.

    And there's much more.  To see a video of Dr. Pelouze's presentation hosted on the Ancestral Health page at Vimeo just google 'vimeo, paleodiet and atheroma', then scroll to video number 33 in the right side box.

  • cancerclasses

    9/15/2011 6:42:38 PM |

    Do you REALLY believe that? We have the ability to measure the distance between the earth and the moon almost down to the millimeter, and certainly down to the centimeter. We have the ability to measure individual atoms with electron and other types of microscopy used in materials engineering and computer chip manufacturing.  Medical, biochemical & physiological textbooks are full of descriptions of the sizes of white and red blood cells, bacteria and viruses, etc. ad infinitum.  Do you REALLY think we lack the ability to measure SDLDL?  Don't be so ready to believe something just because somebody says something about it.  Use your own brain, put together everything you know and can learn on your own and connect ALL the dots before drawing a conclusion.  

    Furthermore, what's the point of a statement like that?  Should we just give up measuring and trying to understand how SDLDL causes atheroma just because ONE guy says we can't measure them to his degree of satisfaction?  Should we just give up worrying about what we eat, and what we are being sold as foods that are arbitrarily declared to be safe to eat by some anonymous bureaucrat at the FDA?  Should we just ignore the ever increasing incidence rates of cancer, heart disease and atherosclerosis that by all applications of observation and simple logic are known to be entirely due to the modern industrial foods diet in every society and the peoples that subsist on them?  

    I don't think so.  Homey don't play that anymore, at least this one doesn't.

  • cancerclasses

    9/15/2011 6:55:16 PM |

    @Bill,  Google and see this study: 'Detection of low density lipoprotein particle fusion by proton nuclear magnetic resonance spectroscopy'.    
    "Abstract: Recent evidence suggests that fusion of low density lipoprotein (LDL) particles is a key process in the initial accumulation of lipid in the arterial intima. In order to gain a better understanding of this early event in the development of atherosclerosis, it would thus be necessary to characterize the process of LDL fusion in detail. Such studies, however, pose severe methodological difficulties, such as differentiation of particle fusion from aggregation. In this paper we describe the use of novel methodology, based on 1H NMR spectroscopy, to study lipoprotein particle fusion."

  • Don

    9/15/2011 7:24:04 PM |

    Bill,
    You have no worry since your triglycerides are quite low and therefore your LDL particles are of healthy size.  Your correctly calculated LDL is only 161 using the Iranian formula (used if triglycerides low).  See LDL calculator here:
    http://homepages.slingshot.co.nz/~geoff36/LDL_mg.htm

    And never use statins, just cut carbs.
    Don

  • cancerclasses

    9/15/2011 7:34:54 PM |

    "About 80% of cholesterol is composed of fats and oils (Current Atherosclerosis Reports 2004). The
    majority of an arterial clog, 55%, comes from defective cooking oils, containing mainly damaged omega 6. Most of us unknowingly purchase these oils in the cooking oil section of the supermarket. These are the oils we fry with and the oils added to most packaged foods; both fresh and frozen.

    Here’s another shocker. It’s not the saturated fat —it’s the adulterated omega-6 from food processing that clogs arteries! Contrary to what we have heard for decades, it is not the saturated fat you eat that clogs your arteries! How do we know this? A 1994 Lancet article reported investigating the components of arterial plaques. In an aortic artery clog, they found that there are over ten different compounds in arterial plaque, but NO saturated fat. This means the bacon, eggs, cheese, steak, whipped cream, etc. isn’t the reason for a clogged artery. These natural saturated fats are actually good for you. You need them for body structure.

    With the consumption and transport of defective processed oils, LDL cholesterol acts like a “poison delivery system,” bringing deadly transfats and other ruined oils  into the cells. It is primarily the oxidized (adulterated) omega-6 that clogs the arteries, NOT saturated fat!"  

    For more just google 'Brian Peskin saturated fat' and read the day away to your heart's content.

  • Jack Kronk

    9/15/2011 8:37:50 PM |

    "just because somebody says something about it. Use your own brain, put together everything you know and can learn on your own and connect ALL the dots before drawing a conclusion. "

    lol. you must not know who CMast is.

  • cancerclasses

    9/15/2011 10:27:09 PM |

    Yeah, I do, and that's why I said that.

  • Dr. William Davis

    9/16/2011 2:40:13 AM |

    Hi, Gib--

    The strategies that reduce small LDL are the same whether it's genetically-driven or acquired. However, when (presumptively) genetically-driven, it's just harder and requires a more meticulous effort.

    We are now seeing more and more people achieve zero or near-zero small LDL with strict carb reduction. The big exception is apo E4 people, who can still struggle because of the peculiar physiologic effects of this pattern.

  • Dr. William Davis

    9/16/2011 2:42:32 AM |

    Big issue. Note that the real culprit in causing plaque may be glycated oxidized LDL.

  • Dr. William Davis

    9/16/2011 2:43:51 AM |

    Hi, Peter--

    No, I think that is wrong. It might be correct if small LDL is regarded in a dichotomous way, i.e., pattern A vs. pattern B. But, when viewed quantitatively, I believe the real culprit is quantity of small LDL.

  • Dr. William Davis

    9/16/2011 2:46:58 AM |

    No question: The various lipoprotein testing companies need to talk and standardize their definitions. But this does not invalidate the concepts.

    Chris Masterjohn is a very bright guy. But on this I disagree. I believe it is wrong to assume that triglycerides and HDL behave in perfect tandem with small LDL. While they do indeed correlate, they do not correlate perfectly and demonstrate independent behavior depending on postprandial phenomena and genetic factors like apo E and apo C.

  • Joyce

    9/16/2011 5:17:54 PM |

    This has nothing to do with LDL, but I don't know where else to ask this, so I'll dive right in.

    I am reading and enjoying your book Wheat Belly, but don't understand why you lump chia seed in with other non-gluten grains to avoid or minimize. .  In my mind it is closer to flax.  Chia is truly an oil-seed and not a grain according to Dr. Coates, the "father" of chia seed research.  I have used it generously, and feel it aids in weight loss.  Chia seed is high in protein and fiber and low in carbs.  Why are you telling us to avoid or limit it?  I feel it is healthier than flax even.

    Please, can you clarify your stance on chia?  I was very disappointed to read that in your book.  Other than that, I really enjoyed Wheat Belly, having avoided gluten for a few years now.

  • Joyce

    9/16/2011 5:33:17 PM |

    P.S.  According to calorieking.com website, 1 oz. raw chia contains 0 carbs and 1 oz. dried chia contains only 1 gram of useable carb.

  • Adriana

    9/17/2011 10:16:37 AM |

    Not everybody who has good HDL, good TG and eats a low carb paleo diet will have low small particle LDL numbers which is why an NMR LipoProfile is important.  People with gut issues, yeast issues,  H. Pylori or an otherwise compromised liver can have unhealthy LDL despite doing everything right on the diet front.  Getting to the root of these issues is critical to resolving it.

  • Dr. William Davis

    9/17/2011 1:23:49 PM |

    Thanks, Joyce. But I don't remember lumping chia with the bad stuff.

    In fact, as you point out, chia belongs with flaxseed as one of the few truly healthy, low-carb foods.

  • Joyce

    9/17/2011 1:45:31 PM |

    Dr. Davies, on p. 212 of your book, chia is lumped in with other non gluten grains.  Maybe in future editions, the publisher can remove that?

    Although I have been gluten free for years, my husband is finally going gluten free..ALL BECAUSE OF YOUR BOOK!  He has some health issues, so for that I humbly thank you.

    Also, his next Toastmasters speech will be on "Wheat Belly"...how about that!

    Thank you so much for a wonderful book.  Your recipes are awesome.  I look forward to a Wheat Belly cookbook!!!!

  • Linda

    9/17/2011 2:57:40 PM |

    There are so many well read and brilliant posters here that I am going to jump in and ask a question totally off topic. This is not Dr. Davis' area of expertise, so I hope others may help.
    I do believe I am dealing with a bone/heel spur. Too much treadmilling, trying to increase speed, etc. I have done research on the condition and I read that turmeric, taken 2-3 times a day, is helpful. I just recently began taking D3 as well, 5000 IU a day. Will the Vit D3 help as well?
    Any thoughts? No, I am choosing not to visit a doctor for a cortisone shot. I am using NSAIDS for the pain and that works very well.

  • nina

    9/17/2011 4:48:56 PM |

    I've just spotted this post.  Never tried chia and wonder what you thought.  Have your patients reported similar effects?

    Nina

  • steve

    9/17/2011 7:26:34 PM |

    We are now seeing more and more people achieve zero or near-zero small LDL with strict carb reduction. The big exception is apo E4 people, who can still struggle because of the peculiar physiologic effects of this pattern

    Could you go in to more depth as to what strict carb reduction menas?  Is it no more than 50grams of starchy carbs such as rice or potatoes, or 100Grams?  I am guessing it is individualized, but some range of restricitons with those who have been successful would be helpful.  
    I have always had a low level of Trigs- never higher tnah 75 even on a hi carb diet, and was surprised to find the NMR showing all small particles!  So Dr. Davis is right to say low Trgs not always indicative of having large LDL.  Switched to elimination of most carbs and totally changed the profile.  Only issue that is while i produced lots of particles with carb diet, i also produce lots of LDL particles with carb restriction.  Genetics i guess!  I am an ApoE 3/3, which was a surprise.  
    Thanks for the good work Dr. D.  Have gotten several to buy Wheat Belly.  It will have an impact!

  • Joyce

    9/17/2011 7:30:40 PM |

    Nina, I am not Dr. Davis (wish I had his knowlege!), and I hope he doesn't mind me jumping in here, but I leaned about chia a few years ago when I read a book by Dr. Wayne Coates on the subject.  Chia has definitely helped me lose weight.  It is very filling.  When mixed with fluids, the chia seeds expand, and they really help to fill you up.  I've found all sorts of wonderful chia recipes on the web - from Chia "Tapioca" to beverages, etc.  I mix  it into many foods.  I think it enhances their taste.  I feel the chia seeds help with weight loss because of their appetite suppressant potential.  I hope this helped, and my apology to the good doctor for hogging the thread.

  • PeteKl

    9/17/2011 10:24:07 PM |

    Your post doesn't provide a lot of info, but if I were to guess I would say your problem is more likely related to walking/running incorrectly than nutritional (assuming you are in reasonable physical condition).  The human foot wasn't designed to be encased in the heavily cushioned shoes we typically wear today.   As a result many of us don't know how to walk or run correctly.

    Some of the better shoe stores will video tape you on a treadmill.  Just seeing the tape may be enough for you to realize what you are doing wrong.  If that doesn't help, there are professionals who should be able to figure out what might be happening.  

    Also consider reading "Born to Run" if you haven't already (it's a good read even for non-runners).  It probably won't give you a direct solution, but it may give you some ideas on where to look.  Good luck.

  • Louise

    9/18/2011 2:10:34 AM |

    Dr. Davis,
       I am 56 and have a strong history of heart disease in my family. I have been eating low carb for a couple of years... ( around 60 gms carb per day average..no pasta, no potato, almost no grain)  My most recent lipid panel showed LDL of 140. HDL 81, Triglycerides 43, CRP 0.2. .  I requested a test to show size of LDL. My doctor declined to order this, saying all LDL is bad.  Instead I was sent for a heart scan  ( paid out of pocket) and my calcium score was 0.  
      So now I'm trying to lower my LDL by lowering saturated fat.  Hard to do when you eat low carb. I wonder if I might be one of those Apo E 4 types that you mention, so thought I should try,.
      Here are my questions:
         Can I test my LDL size myself, through a home test? Or should I try to find out if I have Apo E 4?
          Do I really need to lower LDL if my calcium score is 0?
    Louise

  • Bob Goldstein

    9/18/2011 4:02:36 AM |

    For the last year I have eaten zero fruit, zero grains, zero sugar. Have mostly eaten beef, occasionally eggs cooked in butter. Have done two VAP tests the last year. When I started a year ago, trigs were 115, now 142. HDL was 50, now 46. My LDL did show a change of going from pattern A/B to pattern A.
    Any ideas why a diet for a year devoid of fruit, sugar, grains, would show an increase in trigs, and a slight decrease in HDL. If I have Apo E4 would my ldl go from A/B to A.
    I have lost 25 lbs. in the past year. Could this be a reason my numbers seem to be off?
    Thanks,
    Bob

  • Dr. William Davis

    9/18/2011 3:44:29 PM |

    Hi, Bob--

    Yes, blood drawn in the midst of weight loss can be very misleading.

    Transient effects include increased triglycerides, reduced HDL, even much higher blood sugar. Thankfully, it all gets much better once weight plateaus for a couple of months.

  • Dr. William Davis

    9/18/2011 3:47:39 PM |

    Hi, Louise--

    Sad that you have to educate your doctor.

    I find it unacceptable that a nice person engaged in health is refused a simple, helpful test. Tell your doctor goodbye and find one willing to act as your partner and advocate in health, not an obstruction.

    Yes, you can test it yourself through services like PrivateMDLabs.com. My view is to 1) identify how much, if any small LDL there is, then 2) reduce small LDL with diet. If you have only large LDL, you will absolutely need an LDL particle number by NMR or an apoprotein B to know what the REAL value is.

  • Dr. William Davis

    9/18/2011 3:49:52 PM |

    Thanks, Steve.

    There are a number of posts on this blog that detail how to gauge individual carbohydrate sensitivity. The best way is to check 1-hour after-eating blood sugars. Second best: count carb with the cutoff being determined individually. Just go back over the past 6 months and you will find several discussions.

  • Dr. William Davis

    9/18/2011 3:51:17 PM |

    Hi, Joyce--

    Thank you!

    If chia is listed as among undesirable non-gluten grains, that was my error. Remember what Mark Twain said: "Don't read about health, else you might die of a typo."

  • nina

    9/18/2011 5:13:58 PM |

    Thanks for your response Joyce.  

    The part that fascinated me was the idea that chia triggers a drop in blood sugars without a pre-spike.  I can't find anything on the net about that and wondered if other people had similar experiences.

    Nina

  • Bob Goldstein

    9/18/2011 7:08:22 PM |

    Thanks for the reply Dr. Davis. I have a blood test scheduled six months from now, and hopefully I will see better numbers. My LDL shows pattern A so at least I did see one positive change.
    Love your blog. Have learned a lot and it was the reason I gave up grains and sugar. 1 full year, no cheats.

  • Annlee

    9/18/2011 10:41:56 PM |

    Consider also going barefoot as much as possible - around the house, etc. You don't necessarily have to run barefoot (unless you work into it *gradually* and choose to continue it). I've recovered from heel spurs with stretching my achilles, with emphasis on stretching the soleus, and letting my feet bear my weight without any props underneath. For stretches, Anderson & Anderson have a very good book - Stretching - available on amazon.com. You didn't develop the spurs overnight, and they won't clear that quickly, either. Be patient and work with your body.

    You may also wish to consider vitamin K2, very good for ensuring calcium deposition occurs in the correct locations.

  • Kira

    9/19/2011 6:52:43 AM |

    Hi Doctor Davis, I talked to your about a year ago and you were kind enough then to comment on my blood results saying there was nothing to worry about - according to the Iranian formula.  I would greatly appreciate if you looked at my new results, they scared my whole family, I certainly am not going to show to the family physician, and I don't even want to think about changing from paleo style of eating to some kind of low fat cholesterol lowering diet, and taking any drugs/supplements. But may be I have to? I am 36 y.o., 5'4 and weigh 104lb.
    Glucose 85
    VAP TEST:
    Lipids
    LDL Cholesterol 149!
    HDL 130
    VLDL 14
    CHOLESTEROL, Total 293!
    Triglycerides 48
    Non HDL Col (LDL+VLDL) 163!
    apoB100-calc 96
    IDL Cholest 4
    Remnant Lipo. (IDL+VLDL3) 12
    Sub-Class Information:
    HDL-2  35
    HDL-3  95
    VLDL-3  8
    LDL1 Pattern A 3.1
    LDL2 Pattern A 26.0
    LDL3 Pattern B  71.0
    LDL 4 Pattern B  31.4

    The ordinary, non-VAP Lipid panel shows:
    Cholest TOTAL 279 !
    Triglycerides 48
    HDL Cholest 144
    VLDL Cholest Cal 10
    LDL Cholest Calc 125 !

    Also, I can't understand how my vit. D can be so low - 29.0, when I have been sun tanning all summer here in Orange County, California, at peak hours. Is there anything that you know of that may inhibit the vit. D conversion from the sun?
    Again, I greatly appreciate any insight that you can give me on this situation...

  • Louise

    9/19/2011 4:52:38 PM |

    Dr Davis,
      Thank you for your reply.  For now, I found a lab I can go to and get myself tested. Two hours away.. (Oddly, I must leave NY state to get this done due to billing law.). I'm going to do this! Do you agree that my best choice is the NMR?

  • otterotter

    9/19/2011 5:43:51 PM |

    Hi Gib,

    Option 1 will be cutting the saturated fat and cholesterol from the diet in addition to cutting the carbs. I tried eliminating eggs and cheese and my total cholesterol down from 400 to 260. By adding back "one egg a day", it went back to 320 (that's the impact of the dietary cholesterol on me, confirmed twice). I am currrently trying to replacing all saturated fat with mono unsaturated fat (olive+canola), just want to see how big the impact is. I am also going to test coconut oil separately, it is a cholesterol-free plant based medium-chain saturated fat, there is a chance I might respond to it differently.

    Option 2 will be taking Statin drugs. I know it has side effects, but that's better than small dense LDL. Based on Dr Davis's previous response, for apoE, sometimes we have to go to Statin for the rescue. (My doc was pushing statin really hard on me, and I have been resisting that for the last year)

    otter

  • Joyce

    9/19/2011 5:50:45 PM |

    Dr. Davis, you are so funny.  We'll take your book....typos and all!  Now...how about a cookbook to compliment Wheat Belly/  PLEASE????

  • nina

    9/19/2011 7:41:34 PM |

    Sorry I missed the link:

    http://suzanneloomscreativity.blogspot.com/2011/09/lowering-blood-sugar.html

    Nina

  • PeteKl

    9/19/2011 9:24:31 PM |

    Hi Kira,

    Just out of curiosity, could you summarize your "paleo style of eating".  I have a good friend of mine who has similar numbers (low trigs, high HDL, high LDL).  I would describe her diet as "low-carb (no sugar, no grains), low-veggie (under 15%), high meat, high sat-fat (particularly cheese, eggs and coconut)".  Is your diet somewhat similar?  I would be interested to know how the two of you compare.

  • Dr. William Davis

    9/20/2011 12:36:46 PM |

    NMR is my preferred method, since it yields the LDL particle number, what I believe should be the gold standard.

  • Dr. William Davis

    9/20/2011 12:38:12 PM |

    Thanks for asking, Joyce! I've had very preliminary conversations with my editor, but nothing firm yet.

    In the meantime, in addition to the discussion on this blog, see the Wheat Belly Blog, where I will publish recipes one by one.

  • Dr. William Davis

    9/20/2011 12:41:39 PM |

    Hi, Kira--

    You have a surprising dominance of small LDL particles, despite your slender build and lifestyle (LDL 3+4 divided by "real" LDL). This is likely genetically-determined. The means of correcting this is beyond the scope of this blog, unfortunately. You might consider joining the discussion in the Track Your Plaque website.

    The vitamin D issue is common, an impaired or lost ability to activate vit D in the skin. It means doing it orally.

  • Adam

    9/20/2011 6:40:19 PM |

    Dr. Davis. I'm a type 1 diabetic who is on a low carb diet (mostly primal-esque) with only meat and veg. No fruit, no grains, no legumes. I lost 14 kgs in the first three months, then stabalized at around 89 kgs. Granted my fat is going down a wee bit as muscle mass increases (doing the slow burn exercises, plus HIIT training and martial arts). That is the background.

    The reason I'm posting here is confusion about cholesterol. I just got my latest results back from the lab, and they are the same. While my HbA1C is 5.3 (not bad), my cholesterol numbers don't look hot. Tryglicerides are fine (as I've stopped losing weight quickly), but HDL is low at 39, and LDL (doctor forgot to put in particle size check, but it cna't be that good as I'm a diabetic) was 150 on the spot. This was measured, not calculated.

    I take ~7k miligrams (or whatever the measurement is) of fish oil a day. Well, 7k of EHA/DHA, more in total quanity including inert substances. With my exercise, low carb diet, and fish oil supplements, how is it that my HDL are still so low? Any advice?

    Thanks!

  • Dr. William Davis

    9/20/2011 11:08:46 PM |

    Hi, Adam--

    How timely! See the next post after the one you responded to in which I discuss the transient effects of weight loss, including drops in HDL that rebound over time.

    Also, have you address vitamin D normalization? I aim for 60-70 ng/ml, which usually requires around 6000 units per day (gelcaps or drops only); the HDL-raising effect develops over a year or longer.

  • Adam

    9/21/2011 1:01:18 PM |

    Dr Davis,

    A pleasure to make your (virtual) acquaintance! My vitamin D, according to my last test (results came in yesterday, as I mentioned) levels are 59. A wee bit low, but not too bad, I think.

    I've been consistently 88/89kg for three months (I've been low carb/primal for 6 months total), so haven't lost any weight in the past three months, but still my HDL levels are very low. Do you have any suggestions?

    Cheers,

    Adam

  • Adam

    9/21/2011 1:03:52 PM |

    P.S. I'm pretty sure I've stabalized, as my triglycerides were at 29 or 39 (can't remember off hand, but pretty low). But still I had the low HDL and high LDL?

  • Dr. William Davis

    9/21/2011 9:37:43 PM |

    Hi, Adam--

    Of course, you are wheat-free, low-carb in addition to your vitamin D? Omega-3 fatty acids?

    Note that doing the diet and taking the vitamin D yield rises over 1-2 years. Patience is required.

    Consider a little red wine and dark chocolate, as well.

  • Adam

    9/22/2011 5:10:38 AM |

    Thanks for the response! Yes, I am completely wheat free (and was before I read your book, which was excellent). I am very low carb due to the diabetes. My HDL did go from 29 to 39 this last test (after 6 months), so I suppose, as long as maintaining this diet will continue to increase my HDL, I am ok. My concern isn't immediate gratification but more continuous improvement.

    I'll come bug you again in 3 months if my HDL doesn't continue to increase Smile

    Many thanks!
    ---Adam

    P.S. I've never been accused of not drinking enough red wine Smile While I've been beer free for 6 or 7 months now, I do go through ~2 bottles of red a week.

  • Adam

    9/23/2011 1:35:08 PM |

    Hah! Me too, because if my HDL doesn't start going up I'm gonna freak as I don't know what else to about my numbers. Diet is about as stripped down as it can be, and I'm exercising as much as is reasonable.

    --Adam

  • Kira

    9/24/2011 6:23:22 AM |

    HI Peter. I would say  that my diet could pretty similar, with the exception that I am still eating some low-glycmic fruit everyday (some cantaloup, grapefruits, berries) and eat lots of veggies.

  • Kira

    9/24/2011 6:29:11 AM |

    Dr. Davis, thnx for your reply. I understand this is a blog and it is hard to go into details here, but would you say that it is worth for me to try change this situation by changing the die to using less saturated fat? and would NMR test clarify anything?

    PS How do I further discuss this issue "by joining the discussion in the Track Your Plaque website"?

    Thnx AGAINSmile

  • ShottleBop

    9/25/2011 3:47:09 PM |

    My numbers are like Bill's.  I was diagnosed as pre-diabetic in February, 2008 (today, I'd have been diagnosed as Type 2; my A1c was 6.5, and my FBGs were 127 and 123).  Started low-carbing shortly after that:  cut out grains, starchy veggies, almost all fruit, all milk (still use heavy cream and eat cheese).   My most recent blood lipids (accounting for some variation, but roughly consistent in pattern over the past three years):

    TC:  381
    LDL (direct):  279 (291 calculated)
    HDL:  80 (was 40 at diagnosis)
    Trigs:  52

    (At diagnosis, my numbers were:
    TC: 281
    LDL (direct) 215
    HDL: 40
    Trig: 142)

    I lost 65 pounds in the first 9 months after diagnosis, and, since then, have regained approximately 25 pounds (mostly muscle).  Weight has been stable for months.  My doctor is talking statins, again--which I plan to continue resisting.  I have ordered an NMR test, and will see what it has to say about my particle size.

  • Dr. William Davis

    9/26/2011 12:39:56 PM |

    Hi, Shottle--

    Good plan. I wouldn't be surprised if NMR sheds an entirely different light on your values.

  • ShottleBop

    9/29/2011 4:23:57 PM |

    They drew the blood this morning.

  • Bob

    9/30/2011 11:14:10 PM |

    Dr. Davis, I had my NMR test and the doctor who looked at it suggests that I have familial hypercholesterolemia. My LDL-P 3158
    LDL-C 280 HDL-C 58, TGL 105, HDL-P 28.0 small LDL-P 1122,
    LDL 21.7, LP-IR-33. I have been on no carb, no sugar, no wheat, or fruit for the last 14 months. Have been eating fatty meat twice a day and also eggs. Before I started eating beef, I was eating low carb, very little sat. fat. I was eating a lot of skinless chicken breast, and canned salmon, veggies, nuts, fruit but almost no beef. My LDL according to the basic lipid test was a little high but not crazy high. My HDL was in mid 30's. and trigs were high. I changed to a high saturated fat diet to raise HDL and lower trigs. I have been taking 1 gram of fish oil 2X daily. Is it possible that the fish oil is having an effect on my LDL? Not sure what to do about my diet. Obviously I won't go back to sugar and wheat but what about all the meat I have been eating. Would it be better to go back to skinless chicken and egg beaters even if it means my HDL going down? Just not sure what to do. Doctor believes I am at high risk since my father died at age 62 of sudden death.
    Thanks,
    Bob

  • Dr. William Davis

    10/1/2011 1:48:14 PM |

    Hi, Bob--

    This is a tough situation that, unfortunately, cannot be remedied diet alone. I hate saying that.

    Like people with apo E4, familial heterozygous hypercholesterolemia people are fat sensitive. First order of nutritional business remains carb-restriction to minimize small LDL particles, but you can still show large increases in large LDL with fat intake. If apo E4 is present, too, then even something as great as fish oil can increase LDL measures. However, the dose of fish oil you are using is very small and not a likely factor.

  • Bob

    10/1/2011 2:57:34 PM |

    Thanks for the reply Dr. Davis. I know I won't go back to carbs and sugar, but what about beef. I have eaten almost nothing but beef the last 14 months. Would I be better off going back to skinless chicken breast? Egg Beaters, instead of eggs? Olive oil instead of butter? I know in the past when I limited saturated fat my HDL dropped to mid 30's.
    Bob

  • Dr. William Davis

    10/2/2011 2:46:17 PM |

    Hi, Bob--

    I think we could make a strong argument in favor of variety in diet and that includes meat sources. Yes, I think a broader range of meats (if you eat them; I don't want to sound like a bloodthirsty carnivore; I don't even like meat, personally) is better--fish, shellfish, fowl, pork, as well as eggs.

  • ShottleBop

    10/3/2011 10:02:47 PM |

    Results came back today:
    TC:  373 mg/dL (ref <200)
    LDL-C:  282 mg/dL (ref = 40)
    Trigs:  47 mg/dL (ref < 150)
    Large VLDL:  <0.7 (ref <=2.7)
    LDL-P:  1793 nmol/L (ref = 30.5)
    Large HDL-P:  14.2 umol/L (ref >=4.8)
    Small LDL-P:  146 nmol/L (ref  20.5)
    HDL size:  10.0 nm (ref >=9.2)
    VLDL concentration was too low to determine a size
    According to the interpretive information:
    My HDL-P (total) of 39.1 places me in the lowest category of risk (it is beyone "high")
    My small LDL-P places me well below the 25th percentile (while slightly higher than the "low" level of 117), and is indicative of lower risk for CVD
    My LDL size places me well above the 75th percentile, and well into Pattern A territory (75th percentile level is 20.6), and is indicative of lower risk for CVD

  • ShottleBop

    10/3/2011 10:04:16 PM |

    Correction:  My LDL-C was 282, vs. a reference of " 40"

  • ShottleBop

    10/3/2011 10:06:37 PM |

    I give up.  I am typing things in correctly, and the comment system is dropping words (maybe it's interpreting my use of "greater than" and "less than" symbols as markup code?).  My HDL-C was 82.  The reference level is greater than 40.  My LDL-C was 282; the reference level is less than 100.

  • ShottleBop

    10/3/2011 10:09:37 PM |

    I see it dropped more information than I thought at first.  No matter, the conclusion stays the same: except for my LDL particle number and concentration, all of my lipid values indicate that I am at lower (or much lower) than average risk of CVD.  Now if only my body takes that to heart . . ..

  • ShottleBop

    10/3/2011 10:16:32 PM |

    LDL particle size was 22.1
    HDL-P was 39.1 umol/L

  • Dr. William Davis

    10/4/2011 2:41:25 AM |

    Hi, Shottle--

    Your values highlight this tremendous void we have in knowing just what to do about nearly "pure" large LDL particles.

    In other words, you have lots of LDL particles, but they are nearly all the more benign large variety. What level of large LDL particles are "allowable" before they contribute to atherosclerotic plaque formation? Not known. My preference would be, given the extreme abundance of large LDL, to reduce with statin drug. I hate to say this, but this is the occasional exception in which I believe that statins might indeed be beneficial. This is not to be confused with the general and absurd overuse of the drugs, but an application for a very specific genetic variant.

  • Louise

    12/5/2011 10:58:49 PM |

    At last I have had an NMR.  Thank you for the suggestion of PrivateMDlabs.com.  I can recommend this
    to others who find their doctor unwilling to order tests.
    I am pondering my results, trying to figure out if they are okay, or if I need to cut back on fat now, or go lower with carb reduction. What are your thoughts, Dr Davis?
       LDL Particle Number  1091  ( IS this too high??)
        Small LDL - P    129
          LDL size     21
        Large VLDL - P   < 0.7
           Large HDL - P        12.1
            HDL size           9.7
          LP - IR score    11
    Triglycerides are 32  ( lower since I"ve gone completely
    grain free since my last lipid panel)

  • Dr. William Davis

    12/6/2011 5:26:54 PM |

    These values are excellent, Louise! The only less than perfect value is the large HDL, but this tends to drift higher very slowly.

  • GoodStew

    5/11/2013 1:56:57 AM |

    Seems particle size doesn't matter as much as particle number. According to Dr. Peter Attia, a particle is a particle.  More than 1000 is a risk factor whether they're small, medium or large and fluffy.

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