It’s been quite a while since my last post.  I am neck deep in preparing for my PhD Comprehensive exam (early Dec 2013), working full time & caring for my almost 2 year old daughter as my wife and I have another child on the way (due Feb 2014).

I have to tell you honestly, that I am constantly disappointed by the current medical profession specifically when it comes to dealing with chronic diseases! As a registered dietitian I see it as my duty to constantly review the literature to see what new innovations might show promise. It’s my responsibility to understand these novel studies so that when clients inevitably ask about them, I will be able to give them legit advice & not just tow some antiquated party line!

Okay, enough venting!  Let’s dive into some of the newer evidence on Heart Disease Risk!

The Popular Dogma is Not Supported by Current Evidence

1)      Saturated Fat
a.       The current dogma is that eating too many saturated fats increases blood cholesterol, which in turn increases risk for heart disease.

b.      A few studies have shown that there increased levels of LDL increase risk for CHD.
c.       But, recent research concluded that there was in fact no association between dietary cholesterol and CHD.
d.      As of 1977 AMA/CMA recommended lowering fat intake to 30% or less in diet – result=significant change in diet composition – ­ Carb/­ PUFA (specifically vegetable oils – all ­omega 6).
e.      If we oversimplify and just ask two basic questions, we start to see the challenges that have arisen: i) What about evolution? Did we evolve eating more carbs and seeds & nuts or animal & coconut fats? ii) What about inflammation? Which is more inflammatory in nature: SFA or omega 6 + refined carbs?
2)      Apo lipoprotein Changes
a.       This change in diet comp – resulted in changes to our circulating lipoproteins that actually increase our risk for CHD (specifically – ­Triglycerides/ ¯ HDL particles).
b.      New technology explains why LDL amount is not as telling as once believed.  Particle size of   Think of cholesterol as the passengers in a car and the particle number is the number of cars on the road.  If there are more particles around then they are more likely to crash into the arterial linings and become trapped (atherosclerosis).  If LDL particles are smaller, there will be more of them present, when they are fluffy and big, and then there will be less of them.  Theoretically, the amount of LDL could be the same in both scenarios, but it’s the small, dense LDL particles (that are more abundant) that increase the risk for CHD.
LDL particle size is far more predictive of atherogenic risk.

3)      The Role of Carbohydrates in CHD
a.       Carbohydrates were pre-farming available in unrefined forms (vegetables & fruits) and only in the late summer and fall.  Today, we have year round access to the most highly refined carbohydrate sources we’ve ever seen.
b.      High carbohydrate intake shuts down fat burning & promotes fat storage.  This increased fat storage leads to an increased production of triglycerides.
c.       Hypertriglyceridemia is accentuated in people with abdominal obesity/insulin resistance.
d.      This insulin resistance occurs in the face of high carbohydrate diets & is now considered a protective measure by the liver to prevent substrate overload.
4)      The Role of Inflammation
a.       Athersclerosis does not occur in a vacuum (so to speak).  Inflammation and oxidation are required to promote infiltration of lipids within the arterial walls and the binding of minerals to them (plaque formation).
b.      High carbohydrate diets & especially refined carbohydrates are highly pro-inflammatory.

c.       Omega 6 fats are essential (small amounts) but in excess are highly pro-inflammatory.  They are highly available in Western diets (corn, soy & wheat oils) as well as most nuts & seeds.
d.      Recent studies have shown that low carbohydrate diets are effective at reducing cardiovascular risk factors.
Djousse, L and Gaziano, JM, 2009.
German, JB and Dillard, CJ, 2004.
Agius, L, 2013.

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