A Tale of 2 Heart Attacks, Thursday Nov 11th

Happy Veterans Day!!
Normal Class Schedule

2 rounds of:
5 empty-bar good-morning
10 jumping squats
15 Hip Extensions
Mobility:  Shoulders and Hips
Power Clean
3 @ 65%
3 @ 70%
3@ 80%
1@ 90%
1 @ 95%
1@ 101+%

Rest 5 minutes

For Max Total Reps (post 1 score…like yesterday)

2 minutes AMRAP Double Unders
Rest 1 minute
2 minutes AMRAP KB/DB swings (55/35)
Rest 1 minute
2 minutes AMRAP box jumps (30″/24″)

If you do singles instead of DUs, then divide your total singles by 3 for your score

Over the past month, I’ve learned of two people I know having heart attacks precipitated by blockages of 2 or more arteries.  One appears to match what most would envision as a heart-attack candidate (mid-50s, overweight, stressed, Standard American Diet (SAD), no exercise, drinks somewhat heavily).  The other does not match what most people would envision as a heart-attack candidate (early 40s, runner, not visibly overweight (but I can’t get an accurate hack on body comp), diet is mostly in-line with the USDA guidelines). 
So what gives?  Was one destined to a heart attack due to behavior and the other due to genetics? 
Regardless of what nutritional principles you subscribe to (sorry for the errant preposition), it should be evident that Person #1 (heretofore known as P1) was not helping his cause for avoiding disease.  Even a v*gan could see that (gotta give credit to a blogger on PaleoHacks for that reference).  P1 was, most likely, experiencing severe systemic inflammation due to persistent excess insulin, persistent cortisol exposure (stress), food sensitivities and fatty acid imbalance.  Visible body comp indicators (belly fat) indicated insulin resistance and metabolic derangement.  Lifestyle factors such as inactivity, high refined carb intake (persistent alcohol intake included), stress, etc. contributed, most likely (I don’t have bloodwork), to smaller/denser LDL…and lots of them and elevated triglycerides. Looking at these factors, along with bloodwork most likely showing elevated hsCRP (showing systemic inflammation) and the pending heart attack risk factors could all most likely have been seen clearly (i.e., bloodwork combined with known lifestyle factors would make it easy to predict pending heart issues.) 
Person 2 (P2) had a total serum cholesterol of less than 140 (that would make most Doctors very happy) and P2 has a family history of heart attacks.  So, is it P2’s genes that doomed him to a heart attack?  Is cholesterol a risk factor only if you don’t have a family history of heart disease?  What’s clogging the arteries?  On paper and in person, to most clinicians, P2 looked to be a low risk for heart problems.
I won’t go into the physiology of how arteries get blocked (you can read that under the Required Reading tab or the Nutrition Resources Tab at the top right of this blog).  But I will go into 2 things:
1)     This is not meant to be all-inclusive.  It is meant to be a wake-up call to take your health into your own hands.  Modern medicine is focused on treating, not on preventing.  Your doctor, while not devious or holding negative intentions may just not be up to speed on all information involving diet and lifestyle to prevent heart disease.  They may have the best science can offer to TREAT heart disease/artery blockages and to help you survive a heart attack if it occurs, but they may not be able to provide you steps to take that could vastly reduce your risk for getting that heart attack.  Here’s a great example.  Below, is a scanned image of the bloodwork from one of our athletes.   What’s the first thing we see:  Total Cholesterol: 212-HIGH.  Next, Triglycerides, 35, then HDL – 82, then LDL-122 HIGH.  OH DEAR GOD, SOMEONE CALL FOR SOME STATINS…STAT!  The number 200 as the upper limit for total serum cholesterol comes from the American Heart Association.  The problem is that total cholesterol > 200 is pretty much worthless as a predictor of heart disease (or risk of a heart attack).  I’ll skip down to the next section briefly where they say “Tips to Reduce Your Cholesterol.”  In there, they discuss some dietary changes and that the patient should exercise more.  The results of these changes (according to the paragraph) are that HDL will increase, Triglycerides will drop, but LDL may not change.  I think falling Triglycerides and rising HDLs are a good things.  But note that that doesn’t necessarily correlate to a reduced Total Cholesterol if your LDL doesn’t drop (so their “Tips to Lower Cholesterol” really may not lower total cholesterol below the Ultra-Deadly, Insano, Mega-Threatening 200).
Total Serum Cholesterol, as determined in this Lipid panel, is really just a math equation…not a direct measure of all Cholesterol carrying Lipoproteins.  In fact, the equation (called the Friedwald Equation) has serious limitations, especially when triglycerides are low (like in our stellar CFHR athlete’s case).  So we see LDL-122 HIGH in the bloodwork.  What we don’t see is the actual count (number) of LDL particles in the sample, and we don’t know what type they are (small, dense or large fluffy).  The Pattern (or type) of LDL tends to be a much more accurate predictor of risk of heart disease. 
So let me summarize, because I just verbally vomited a ton.  Without knowing his lifestyle factors, the Lab/Dr. is recommending our athlete alters his diet and exercise to : 1) Lower Triglycerides which are already AWESOMELY LOW by any standard; 2) Raise HDL which is AWESOMELY HIGH by any standard and to 3) maybe lower LDL which is most likely inaccurately calculated by the Friedwald equation used in this lipid test.   Not to mention his LDL pattern size is (I’m willing to bet my house on it), Large/Fluffy (the kind that won’t contribute to artery blockages) .  All of that should lower his cholesterol below 200 which will, miraculously, save him from pending heart doom.   Do you see how silly this is? 
Their recommendations are like this scenario:  You are behind a curtain.  You ask a person on the other side of the curtain to step on a scale.  You see only their weight displayed.  You see their weight is 250lbs, so you say, “you should lose weight…maybe start smoking because that can help you lose weight.”  What if that person was a 250lb 6’4″ lineman with 7% bodyfat?  We’ve taken an arguably fit/healthy athlete and ruined them because of a misguided recommendation based on an arbitrary number not tied to the actual health/well-being of that individual.  
For the record, I don’t disagree with a Dr recommending more exercise for general wellness and to increase HDL, but it would be good to know what the patient is doing prior to recommending more…what if the patient was a stellar CrossFitter putting up huge numbers?  Come on, “more exercise” is just a blanket printout recommendation base on cholesterol > 200 (which we’ve already covered).  More exercise could actually be an increased stressor and inflammatory factor, thus increasing his risk for heart disease.
Cholesterol is our body’s band-aid.  It helps us heal.  It is ABSOLUTELY ESSENTIAL in the synthesis of pretty much every hormone in our body.  EVERY cell can independently produce it.  If you eat less, your body will make up the difference by telling the liver to make more of it.  Statins prevent your body from producing sufficient cholesterol.  The most recent (and review of older) studies all point to any reduction in risk of heart disease via Statins coming from an anti-inflammatory response in the body…NOT to lowering cholesterol.  We can reduce inflammation with appropriate nutrition, sleep and stress control and avoid dangerously low Cholesterol and the multitude other possible side-effects of Statins.  The side-effects of Paleo are looking good, feeling good and kicking ass at life.  There is a stronger link to death from having cholesterol too LOW than there is to having it too high. 
Here’s a bit more info to paint the picture.  If we follow the “Tips to Reducing Cholesterol” from the lab, and we reduce fat, and eat protein to satiety (i.e. we don’t increase protein), then the calories to replace fat come from…..drumroll…..carbs.  And what carb sources does the AHA, USDA, FDA, ADA, CIA, FBI,  etc… recommend?  Well, of course, it’s our friendly whole grains, brown rice, oatmeal, etc…These are the dense, refined, gut damaging, irritant, inflammatory carb sources that elevate triglycerides and increase LDL count (and change those LDL to small/dense type contributing to artery blockages).  P2 told me he was told, specifically, to avoid meat and saturated fat (he told me this as I ate 3/4lb of ground meat mixed with butter and spinach) .  I’m guessing his protein intake won’t be increasing much (especially if he follows to 3 oz of fish per week recommendation from the lab work)
So, if we follow their recommendations, we’ll actually not achieve their goals.  There’s no guidance other than “limit fat…especially saturated fat.”  This makes me as frustrated as the fact that my 5 year old daughter already has homework every night in Kindergarten (might as well prep them for a society of 12 hour work days now…sorry…tangent).  I better stop with #1.
This athlete’s numbers are AWESOME.  Because one number (the total cholesterol) is above an arbitrary number (200) primarily driven by pharmaceutical companies selling statins, this lab report recommends reducing fat intake.  And actions caused by that reduction in fat intake will lead to increased number of “more-dangerous” LDL (if you can liken it to that), lowered HDL and increased triglycerides (the things we don’t want).  This is silly.
2)    GENETICS – We are all born with a Genotype:  a set of instructions for what to do with our genes.  This is our heredity.    For genes to express (and therefore carry out the genotype instructions), they require an environmental trigger.  This is called your phenotype:  your observable traits based on genes that have expressed due to environmental triggers or behaviors.  While P2 may have been born with a genotype that tends toward arterial blocking, it was environmental triggers (i.e. stress, nutrition, etc.) that caused that arterial blocking to happen.  The same stressors/nutrition may not have caused the same amount of arterial blocking for another person based on their genotype.  So, back to the question at the top:  was P2 doomed by his genetic makeup?  Did/does he still have control?  Was his low cholesterol not low enough?  Remember, our arteries are not like your sinks at home (despite how pharmaceutical companies want you to imagine it).  Eating fat and cholesterol doesn’t cause saturated fat and cholesterol to clog your arteries.  It’s just not how it works.  The inflammatory response of lots of long-distance running combined with a stressful job, combined with a high refined-carb intake may very well have been the environmental triggers that caused expression of P2’s potential for rapid and severe arterial blocking.  The point is that you are not a puppet to your genes.  It’s estimated that we control between 80 and 97% of our genetic expression (Gedgaudas) through our behaviors and environment.  It’s often the “well, I’m doomed,” attitude that stops us from truly seeking out answers beyond what a pharmaceutical, treatment-based medical industry provides.  Be pre-emptive.  Learn how your body works, not just how modern medicine can manage illnesses and diseases primarily caused by our own choices. 
I don’t really have a dramatic summary or ending to this story.  Instead I urge you to take your health into your own hands and form your own dramatically SUCCESSFUL, HEALTHY, VIBRANT AND ENERGETIC LIFE

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