Cholesterol. Cholesterol… Cholesterol!

What exactly does the number next to the words “total cholesterol” on your blood test really mean?

This number is a density reading, it displays the milligrams of lipoproteins per deciliter of blood. A non-specific, but reliable way to identify cholesterol related issues, such as heart disease—as we all know. As heart disease continues to rise in the US, scientists have been developing a better way of identifying cholesterol related issues. It is now common to not only identify the density of the lipoproteins, but also the particle size. Particle size is an important factor in understanding the function of the lipoproteins. The smaller the particle the more detrimental the lipoprotein; as the particle size decreases its ability to wedge into the inner lining of blood vessels increases. As a result of this information some blood screenings are incorporating the particle size measurements.

How does this effect the US perspective on cholesterol and heart disease?

As a result some are completely ignoring there total cholesterol readings and focusing only on particle size, which is only half of the equation. Our friend Jimmy Moore shares his opinion on this topic while openly displaying his lipoprotein reading:

Total Cholesterol 351


LDL-C 278


HDL-C 57


Triglycerides 79


LDL Particle Number 2130


Small LDL-P 535


LDL Part. Size 22.0


Large HDL-P 10.9


Large VLDL-P 0.4

Before dissecting Moore’s results, we should all commend him on his bravery for using himself as an example. And so, as shown his total cholesterol is well above the recommended range of below 200, and his low-density lipoproteins are well above any health standard. But, Jimmy Moore is not concerned, because the size of his LDL’s are large, and his triglycerides to high-density lipoproteins ratio is in the norm.

Although the above evidence supports Moore’s reaction—by focusing his attention towards the particle size and not at density—is it safe to say that he is free from potential arthrosclerosis? Even if we were to say that only smaller LDL’s contribute to heart disease, wouldn’t by increasing total cholesterol (which is a result of consuming a high cholesterol diet) increase the chances of producing more small LDL’s? And even if the smaller LDL’s are the only particles that can become embedded in arterial walls the larger LDL’s are going to contribute to the overall size of the clot as it continues to grow and trap more particles to the sides of the wall. Not to mention that the chemical make-up (steroid) of LDL’s—large and small—is what allows these lipoproteins to have the potential to stick. So, while chances of smaller LDLs sticking to the arterial walls are greater it doesn’t completely eliminate the potential for the larger ones to have the same effect.

In the end, as with most things, balance is key to the equation. Keeping cholesterol density low and the particle size high is going to be the best formula.

How is this accomplished?

The cholesterol made in the body is specific to the individual and sets the baseline, and it is very difficult to manipulate how much cholesterol the body makes naturally. What we can manipulate is total cholesterol, the ratio of HDLs to LDLs, and particle size. Cholesterol is found in animal products, and is higher in red meats, shellfish, and albumin (egg yolk). And, so total cholesterol can be managed easily through diet. In order to keep your HDLs high and your LDLs low exercise is the best prescription. Research has shown that low-moderate aerobic exercise will increase HDLs, and it is recommended to exercise 3-4 times a week for about 40 minutes a session. HDLs will increase and the LDLs will decrease as the cholesterol continues to recycle in the liver in a consistently exercising individual. Although research is relatively new, particle size has been shown to increase with a low carbohydrate diet. And, one theorist suggests a high fat diet to increase particle size, but no scientific evidence shows significant data supporting this theory.

Fitness and Motor Coordination

Every Friday my team of exercise science and physical therapy students head over to the local Boys and Girls Club to collect fitness data and to teach children ages 8-12 how to use a treadmill. Upon entering the club the children line up to have their turn on the treadmill with much enthusiasm, while they discover the dynamics of walking on a moving surface. Surprisingly, in these early stages our data has yet to form any distinct fitness trends related to body type. Before any experimentation had taken place, my initial assumption was that the older children were going to be able to maintain the endurance demands better than the younger ones, but the data did not show any significant evidence supporting this hypothesis. So, I then began asking more questions about the types of sports each child participated in and what their practice schedules were like. And, I began noticing that the children with athletic lifestyles were able to coordinate their posture on the treadmill better than the ones that did not participate in sport. Through this observation I began hypothesizing that the children with more athletic backgrounds were able to use less energy on the treadmill because of their ability to maintain the proper coordination pattern, which would lead to high fitness levels. Based on our data, this hypothesis has significance. Building on this hypothesis, my next assumption is that the assessment of children’s fitness levels could be inferred by their level of motor coordination, which could assist in identifying future fitness related illness—such as hypokinematic disease (disease related to sedentary lifestyle).

The next, and the current step I’m indulging in, is to research data that supports or disproves my hypothesis. Unfortunately, many of the articles I am finding have little to do with assessing coordination patterns as a precursor to sedentary-lifestyle diseases. Although, relevant research has been debating about the relationship between children with underdeveloped coordination and obesity. Some theorize, that the insecurities developed by lack of coordination inhibit these individual’s athletic aspirations, while others theorize that other personality traits (such as laziness) are the cause for the absence physical activity leading to underdeveloped coordination. So, the question remains: is lack of coordination due to lack of physical activity, or is a lack of physical activity due to underdeveloped coordination?

Based on my personal experience and brief observation, I lean towards the thought that coordination is developed through physical activity. Which opposes the thought that those with high coordination are drawn to physical activity. The unsettlement of this question propels me to inquire more information from personal testimonies. So, what do you think of this trend?