What is the Real Deal behind Preventing Cardiac Risk?

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.

Citations:

http://www.stlawrencedentistry.com/wp-content/uploads/2013/07/heart-disease.jpg

Djousse, L and Gaziano, JM, 2009.

German, JB and Dillard, CJ, 2004.

http://www.mayoclinic.org/news2011-mchi/6264.html

http://chriskresser.com/the-diet-heart-myth-why-everyone-should-know-their-ldl-particle-number

http://www.longevitytesting.com/pub/images/PARTICLES_web.jpg

http://img.springerimages.com/Images/ImagesMD/AHD/10/10/WATER_AHD1004-10-032.jpg

Agius, L, 2013.

http://www.realw8site.com/images/brochureillustration_clr.jpg

My Take on Hormesis, it's good or bad, depending on the dose!

Hormesis

Today, I want to chat briefly about the concept of Hormesis.

Hormesis is a biological phenomenon likely best known from Toxicology in which a beneficial effect results from a low dose exposure to an agent (or a practice) that can become otherwise toxic or lethal when given at higher doses.  You will often see Hormesis denoted by a U or J shaped curve (often inverted).  Here is a nice image that I think illustrates Hormesis well.  You can clearly see that there is a range of dosing that produces beneficial (healthy) results, and then either too little or too much produces negative outcomes.  This, in a nutshell is Hormesis.

To clarify, let's examine a couple examples.

1) Exercise.  It is widely known that exercise can have a plethora of benefits to human health & longevity, including altering gene expression over the long run to make humans more efficient at partition energy for expenditure and hence improving overall health.  However the dosing is key, and everyone's tolerances and genetic propensities are different.  Take running and cardiovascular disease prevention.  This has been a long-standing recommendation, and often dosing specific recommendations are avoided in Medicine, because "not enough is known".  If we explore the literature on this topic we see that mild endurance activity seems to be protective against cardiovascular disease, but higher doses of endurance training actually increase risk for cardiovascular disease.  A working theory of the benefits obtained from exercise is that exercise stresses our system through oxidative stress and our body has to mount a response to this.  As long as we can respond adequately, we gain benefit from exercise.  If the stress load is too great to mount a response (i.e. too high exercise volume) then it ceases to be beneficial and become toxic.

2) Antioxidants.  We see another example of hormesis from studies showing that high dose antioxidant supplementation (i.e. >1 g Vit C/day) while exercising actually blunts the beneficial gains from that exercise by blocking adaptation to the exercise conditions.  This is another example of hormesis, because lower antioxidant supplementation helps to speed recovery and even contribute additive health benefits to the exercise, however, when the dose is too great, then the adaptation goes away and it becomes toxic.  Additionally, high level supplementation with many antioxidants has been shown to be pro-oxdiative, again because our bodies respond to mild oxdiative stressors within compounds we call antioxidants by producing increased levels of antioxidants.  If the load of the stress is too great then we can't respond adequately and the result is increased oxdiative stress and negative health consequences.

3) Ketosis.  This is one of my favorite examples and I was first made aware of it from the Robb Wolf Paleo solution podcast in which he and Greg Everett interviewed Dr. Kurt Harris.  Be sure to check out their blogs and podcasts for a ton more info on cutting edge nutrition research! The concept of the benefits of ketosis has been bounced around for some time, especially revolving around fat loss.  Certainly, most conventional health circles avoid it or chastise it due to confusion with the potentially life-threatening ketoacidosis that can occur in diabetes.  However, in and of itself ketosis can be extremely beneficial in that it facilitates adaptation by the human body to a fuel source other than glucose, specifically ketone bodies produced by breakdown of fatty acids.  There's more to this and perhaps I will discuss more details in a later post, but I think this is adequate to briefly introduce the concept of Ketosis for the purposes of this discussion.  Anyway, this is also an example of hormesis, as there is literature supporting ketosis for fat loss, stimulating autophagy, starvation of tumors in cancer and reversal of the symptoms of the metabolic syndrome (insulin resistance, low HDL, elevated triglycerides, central adiposity and high blood pressure).  As a Dietitian, I've counseled many people who were staying in ketosis for various reasons and what was interesting, was that once people corrected a metabolic derangement or achieved a fat loss goal, if they persisted with ketosis year round, with no increase in (good quality) carbohydrate intake above 50 g per day, then they started to face some issues counter productive to health, performance and longevity.  Most often, this would arise in individuals who perform a glycolytically demanding activity (i.e. crossfit or high intensity training or other sport) in which the lack of carbohydrates causes them to crash during their activity due to failure to replenish muscle stores of glycogen for the next bout.

Please feel free to comment with your questions or any topics you would like to see in future posts.

Great blogs that define Hormesis.

http://gettingstronger.org/hormesis/

http://www.dose-response.org/pdf/HETDEFININGHORMESIS.pdf 

Figure represented from: http://www.nutritionandmetabolism.com/content/7/1/87/figure/F1?highres=y