Bioletics is a company that's focus is "Cellular Health" for optimal human performance: testing it, and improving it.
In this exchange, Rick Cohen and i talk about how a traditional approach to viewing cholesterol is often not an optimal approach to tuning personal performance. That's a long way of saying i was surprised by a normal but higher end cholesterol result, and started to wonder if perhaps the more fat-oriented practices of my diet over the previous 6 months were really not a great idea. But how could that be? So a lot of detail here about LDL, HDL, triglycerides, essential aminos and more - and some cool insights (i think) around triglycerides, glucose, starchy carbs and the all important, insulin resistance.Background
For context, as i've written about frequently here, my main approach to nutrition has been to follow the heuristics in Precision Nutrition (here's a free 40page overview of the program) A couple of key ones for me are: starchy carbs only after workouts; protein and greens with each feeding; good fats daily. I've had considerable success with this approach and thought i was doing pretty well. But to quote z-health's Eric Cobb, if we're not testing we're guessing. So i went to Bioletics to get a very thorough set of screens, including some a-typical checks from the standard GP blood panel, such as mineral balance, essential fatty acids, essential amino acids, vitamin d, i was not best pleased.
Part of the this screen was a dietary assessment and consult using metabolic typing. What the assessment with Tim Monaco encouraged me to consider was not a radical rethink, but a few big tweaks: upping protein, and, if doing dairy or related, not to avoid real whole fats. Indeed, fat could become a more core energy source. Right about this time, colleagues of mine were also exploring what might be called a modified paleo approach, the Perfect Health Diet. Fat was plainly the New Black. It was around this time i also started exploring medium chain triglycerides like coconut oil (see this post on Fat Tea), while also keeping my DHA supplementation at 1g a day in an Omega 3 dha/epa blend.
With that context, here's my conversation with Rick Cohen, first with a bit about cholesterol in general, then look at the specific test results as a worked example, then how omeaga's fit into this, and a final wrap.
Cholesterol: Overview
mc: Cholesterol and cholesterol levels are mad out to be a Huge Deal in health. Would you care to give a very brief overview of cholesterol's role in our lives and why it's a GOOD thing (perosnally i feel like fingernails on a blackboard when someone says "LDL" is "bad" cholesterol. - surely we wouldn't produce a substance that's bad for us - an abundance of it - i'm guessing - like too much insulin - indicates something's out of balance or broken; not that insulin is bad????)
RC: The first thing everyone should know is that cholesterol is not the cause of cardiovascular disease. In fact, cholesterol is critically important to human health. While hundreds of millions of people have literally been brainwashed to fear cholesterol, few of them even know what this substance is—or why it’s even in their bodies.
Cholesterol is an innocuous, waxy lipid that plays a critical role in maintaining the health and integrity of the body’s blood supply and every one of its cellular membranes. It also performs many valuable functions like insulating the nerves, allowing the body to utilize fat-soluble vitamins such as vitamin D; it detoxifies the body by producing bile and acts as a building block for the synthesis of all steroid hormones including DHEA, testosterone, estradiol and progesterone.
To make a long story short, it turns out that the original data on which the conventional cholesterol theory is based was both incorrect and incomplete. The conclusion of this flawed study (which pinpointed cholesterol as the cause of cardiovascular disease) is similar to that of attributing the cause of an auto accident to a backseat passenger who was left behind after the driver ran away. It’s a simple case of guilt by association.
We now know that chronic, systemic inflammation and oxidation are the cause of arteriosclerotic illness. And while the vast majority of lipid researchers have completely accepted that the cholesterol theory is a myth, medical treatment programs designed to address inflammation and oxidation are virtually non-existent. After years of anti-cholesterol propaganda, the pharmaceutical industry has firmly established itself as the provider of cardiovascular disease solutions. This large and profitable industry has become so entrenched that not even the government can extract itself from the resulting (but erroneous) health policies it has made. Unfortunately, nothing will change until the doctors in the trenches become educated, begin recognizing and measuring inflammatory markers, and are given a new pharmaceutical agent they can prescribe.
Cholesterol: The Test Results (cue Jaws theme music)
mc: Thats a quite strong inditement. it puts all the next questions nicely in context, but of course as you note this is info most of us don't have. So imagine my surprise as someone following a low carb hi pro/fat diet to get back cholesterol results and have my doctor advising me to see the nurse about dietary interventions because my cholesterol is *high* - and even the ration of Chol to HDL is poor at 3.1 - it *should* be lower than that. Oh no! is all this re-learned love of Fat, and its various chain lengths in my food from cocnut oil to Other Kinds - coming back to bite me? In the first box are US reference ranges recommended - in the right are my UK levels with the lab's recommended reference ranges.
Cholesterol 150 - 199 mg/dL 6.7mmol/L | nice <4 mmol/L
Triglycerides 75 - 100 mg/dL .4/mmol/L | <2.3
LDL < 99 mg/dL 4.38mmol/L | <2Imagine after this, Rick, when i ask you oh gosh, what's happening, you say "by the way, your lipid levels are awesome."
HDL 55 - 100 mg/dL 2.14mmol/L | 0.91-2.21
Chol/HDL Ratio < 3.1 3.1 | 1-4
RC: You do the following conversion:
HDL converts to 83 mg/dl.Ok, it seems we a few ratios going on here. First you are talking about HDL to TG and that with a goal being 1:1, and typical being .5 to 1, mine at 2.5 to 1 is actually really good? so a higher HDL to TG ratio is good; typical is that HDL is lower than TG. Is that right?
Triglycerids to 34
Your HDL to TG ratio is 2.5 to 1.
The goal is typically 1 to 1.
Most people are on typical diets around 0.5.
In order to describe why your labs while—on the surface—look bad are actually quite favorable: Cholesterol: 257 mg/dl
HDL 83 mg/dl
LDL 170 mg/dl
Triglycerides 34 mg/dl
Based on these numbers, these are the resulting ratios:Could we talk a little bit about fluffy LDL (pattern A)- because when i saw my numbers and thought "i don't get this" i started to look at the role of TG relative to cholesterol and seemed to see that if TG is low and LDL is up, that that *kind* of LDL is "fluffy" or "pattern a" and therefore no big deal.
Total Cholesterol/HDL 3.1
HDL/LDL .49
HDL/Triglycerides 2.5
Let’s discuss each of the variables.
Cholesterol: Current recommendations are for total cholesterol to be under 180 mg/dl. My recommendation is to simply ignore this number unless it is over 280mg/dl or under 160 mg/dl. As we have discussed, cholesterol is an innocent bystander. A higher cholesterol level may actually be beneficial to your health!
LDL: Current medical recommendations are to have LDL under 100 mg/dl. Some doctors prescribe medications in order to lower the LDL to less than 80 mg/dl. However, it is not the total LDL count but the levels of its sub-fractions (such as small dense LDL) that is significant. As a disease market, total LDL levels hint at a problem but don’t provide tangible insights.
HDL: Current recommendations are to be over 60 mg/dl. A high HDL (especially HDL2a and other sub-fractions) are indicators of a healthy metabolism and less inflammation. But as you will soon see, even HDL is best viewed in relation to the other markers.
Just a quick interrupt: what does low TG mean, by the way - why is that a good thing?
Triglycerides are essentially the glucose (from carbohydrates) that the body is converting to fat for longer-term energy storage.
The interesting fact is that there is really no direct relationship between triglycerides and cholesterol—even though they are always linked together. Like cholesterol, triglycerides (unless extremely elevated) are not a stand-alone risk factor for heart disease. They are, however, an indicator of inflammation and small dense LDL. This is because both elevated triglycerides and small dense LDL are caused primarily by the over-consumption or poor utilization of carbohydrates. A high carbohydrate intake will raise the body’s insulin level. And when combined with other biological imbalances (such as low vitamin D, omega 3, antioxidants, nitric oxide and magnesium), increased insulin will lower HDL and raise both small LDL and triglycerides. The end result is systemic inflammation.
So while your Cholesterol is 257 and your LDL is 170 if you fractionated almost all of the LDL would be really fluffly.
To better understand this it is important to understand that our working knowledge of HDL and LDL is wrong—they are not really cholesterol! HDL and LDL are the names we have given to a broad section of molecules called lipoproteins that have the qualities of both being fat and water soluble. They are not cholesterol but act somewhat like freighters, shipping cholesterol from one location in the body to the next.
In general, HDL moves cholesterol from the tissues back to the liver so it can eliminate it after we are done using it. And LDL has the job of transporting cholesterol after production in the liver to the tissues so we can use it for all its vital functions. As you can see, even the villainous LDL isn’t such a bad guy; [it] contributes in a positive way to both our cellular and hormonal health.
There’s another problem with HDL and LDL nomenclature. There are actually many sub-categories of both HDL and LDL, each with different functions. Among the many lipoprotein molecules, we now know HDL-2b is the most protective and the large less dense (fluffy) LDL-A particle has no significant role in heart disease but it is the smaller (more dense) LDL-B particles are the ones causing most of the inflammation. And we also now know that the number one cause of increased small, dense LDL is not fat but simple carbohydrates. In addition, small LDL is only a threat when it’s oxidized by free radicals that are increased due to improper diet, stress, toxins and lifestyle. In addition, there are other lipoprotein fractions including apolipoproteins, lipoprotein a, remnant lipoproteins which all are associated with cardiovascular risk.
I have to confess when i asked about getting a VAT test to confirm, i got a kind of funny look - it may not be a known thing in the UK.
Sadly, most people will never acquire this information. Comprehensive lipoprotein panels such as VAP and NMR assessments are not frequently ordered by doctors. Why? They are more costly and more complicated. And there simply aren’t many physicians who have the time, knowledge or experience to properly interpret their results. Having said that, anyone with a family history of cardiovascular disease should have one of these assessments done before the age of 35 in order to get a more accurate picture of their personal lipid profile.What is the role of Fluffy LDL then? As i understand it, ldl has an important role to play in shuttling nutrients from the liver to the blood stream, but fluffy vs tiny clumpy - i'm not so sure about.
Don’t worry if your doctor won’t order one of these tests. A number of laboratory assessments are now made available online; you can order your own tests and have the results interpreted for a reasonable (albeit out-of-pocket) price.
It is also possible to use the standard lipid panel of cholesterol, HDL, LDL and triglycerides to get a sense of your LDL particle size—and cardiovascular disease risk.
As we discussed LDL particles vary in size and density, and studies have shown that a pattern that has more small dense LDL particles, called Pattern B, equates to a higher risk factor for cardiovascular disease than does a pattern with more of the larger and less dense LDL particles (Pattern A). This is because the smaller particles are more easily able to penetrate the endothelium and are more susceptible to oxidation.Right, i've certainly heard for awhile that total cholesterol is a flawed marker, it's the ration that's important. But what i didn't know there were several ratios to consider with Cholesterol: and as said, we have several ratios floating around here: the lab has Chol to HDL say this ration should be lower than 3.1 and i have 3.1, but other sites i see have said it's hdl/cholesterol ratio, not chol/hdl ratio. they suggest that about .24 is ideal; mine is .31 so again, is someone just reading these number funny? are these reasons why these ratios - tg to HDL, hdl to chol rather than chol to hdl - are not better published/used?
Total cholesterol really is a non-meaningful number. If HDL is high and TG is low things should be fine.
While these each provide a bit more information, the only one you really want to pay attention to is the HDL/Triglyceride ratio. It is this ratio which you can get from the standard panel that will give you the most information on the levels of inflammation and predict your level of small dense LDL particles.Awesome. One further: since most labs in doctors offices do not test essential fatty acids but it is possible to get essential fatty acid tests (ie omega values) - indeed your group, Bioletics, offers this test - can you tell us a bit about the relationship of omega levels to this other lipid profile?My 3 to 6 ratio last test (dec) was 1.6 to 1, where it seems optimal levels are between 3:1 to 1:1 (improved from 3.3:1 in april).
Looking at the HDL to triglyceride (TG) ratio will give you the most cost-efficient and practically-available peek into both your insulin sensitivity (your body’s ability to use carbohydrates for energy) and overall inflammatory index. The goal is to have at least equal amounts of HDL to TG. Our 2:1 ratio example is a strong, but not foolproof, indicator of insulin sensitivity. Even though the LDL would be considered elevated by conventional standards, it is most likely confirming the presence of healthful (fluffy) LDL particles.
Increasing Omega 3 to Omega 6 will drive triglycerides down and HDL up. It will also increase insulin sensitivity.Is there anything else you'd like folks to note about lipid profiles?
[Indeed] one of the most important things you can do to assess the status of your cardiovascular—and overall—health is to check your essential fatty acid omega 3 to omega 6 ratio.
A balanced omega 3 to omega 6 ratio provides evidence of healthy, cellular function and low levels of the harmful, inflammatory, intracellular hormones that cause the blood to clot and blood vessels to constrict. In fact, studies have shown that the risk of sudden death in people with optimal omega 3 levels is 20 times lower. If you could do only one assessment and one thing to improve your cardiovascular health, maintaining a high (and balanced) omega 3 level would be it.
Measuring and optimizing your body’s ability to metabolize and utilize glucose will also keep chronic inflammation and oxidation at bay. Maintaining high vitamin D and nitric oxide/antioxidant levels are a must for anyone who wants to bullet-proof themselves from cardiovascular disease. The take home point here is that our bodies are very complex and we must not rely on one nutrient (or medication) to improve our health.
Yes. While the HDL: TG ratio and VAP or NMR lipoprotein assessments are helpful in determining your risk of cardiovascular disease, they tell us little about the cause. Using our accident analogy, we can identify the cars involved and know who the drivers were, but still don’t know if the accident was caused by weather, drinking, texting, fatigue or mechanical failure. Understanding the contributing causal factors will be the key to avoiding another accident—and reducing the risk of developing cardiovascular disease. In order to keep our cells healthy and avoid inflammation, it will be necessary to dig deeper than the results offered by a standard lipid profile.Cellular Health - that is a cool way of framing physiological aspects of wellbeing. How did you get focused here?
The take home point here is that our bodies are very complex and we must not rely on one number, nutrient or medication to improve our health. Whenever we do that we seem to always get it wrong. We must look at the whole picture and our best bet for now is to focus on the health of our cells.
My work is focused on knowing that it’s just not possible to follow a straight line toward perfect health. And we are only as strong as our weakest link. I am continuing searching on how can we practically give ourselves an advantage in improving our health and longevity odds.
A topic for another day would be discuss some of muy latest findings on how we are doing this using a unique nutritional program that combines synergistic cellular nutritional factors with regular at-home lab assessments to allow you to optimize cellular health.
Cool. Thank you so much for your time and detail on these questions, Rick. Awesome. You bet we'll be back.
So there you have it: putting cholesterol testing - and those results - in context. If you are interested in complementing your cholesterol results with your own essential amino acid levels to check your omega 3 levels, take a look at Bioletics EAA test - on its own and in combo with other test profiles.
Related Posts