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Cholesterol is a sterol which is mix between a steroid and an alcohol. It is NOT a fat as is commonly thought. It is essential to the formation of bile acids, vitamin D, progesterone, estrogens (estradiol, estrone, estriol), androgens (androsterone, testosterone), mineralocorticoid hormones (aldosterone, corticosterone), and glucocorticoid hormones (cortisol). Cholesterol is also necessary to the normal permeability and function of the membranes that surround cells.”

Therefore, without cholesterol we would not be able to sustain life.

As I have previously discussed, the lipid hypothesis/diet-heart hypothesis/cholesterol hypothesis has never actually been proven. Yet it is touted as fact by just about every government and government affiliated association. This is made abundantly clear through the recommendation of avoiding saturated fat and keeping our cholesterol intake to below 300mg per day. The low fat/diet industry is now worth billions of dollars so it’s understandable why the government keeps pushing this message. As consumers though, we need to start being more discerning about what advice we take. For me, all I have to do is look at the rising numbers of people with obesity, diabetes, heart disease, cancer, osteoporosis, depression etc. to know that something is not right about what we’re being told.

But I digress, back to cholesterol. Cholesterol is found in absolutely every cell in our body and is involved in the:

–          Formation of hormones (particularly testosterone, oestrogen and progesterone)

–          Cellular structure of all of our membranes

–          Control of our moods (cholesterol is needed to produce serotonin – our pleasure hormone)

–          Function of our immune system

Cholesterol also:

–          Works as an anti-inflammatory and antioxidant

–          Assists in vitamin D production

–          Has anti-ageing properties

Here’s some fun facts about cholesterol:

* Nearly every single cell in the body is capable of producing cholesterol

* it is needed for the integrity of every membrane of every single cell in our body (we have an approximate 100 trillion cells)

* additionally, 25 % of the cholesterol we produce is found in our brain of which is around 80% fat

* the more cholesterol we eat, the less the body makes

Interestingly, the numbers of people with Alzheimer’s and dementia are on the rise which really is a telling sign. But yeah sure, keep on with that low-fat, low-cholesterol diet.

It’s worth pointing out here that when you have your cholesterol checked, you’re not actually having your cholesterol checked. You’re having your lipoproteins checked. This is because cholesterol is simply cholesterol. The good vs. bad we’re always hearing about is actually in relation to the lipoprotein (i.e. HDL, LDL etc)  that carries the cholesterol around.

Just briefly; lipoproteins are classified into the following groups:

1. chylomicrons

2. very low density lipoproteins (VLDL)

3. low density lipoproteins (LDL)

4. high density lipoproteins (HDL)

Chylomicrons and VLDL have the highest percentage of triacylglycerols whilst LDL have the highest percentage of cholesterol and HDL have the highest percentage o f lipoproteins (see Table 1).

Table 1. Physical properties and lipid compositions of lipoprotein classes.
CM VLDL LDL HDL
Density (g/ml) < 0.94 0.94-1.006 1.006-1.063 1.063-1.210
Diameter (Å) 6000-2000 600 250 70-120
Total lipid (wt%) * 99 91 80 44
Triacylglycerols 85 55 10 6
Cholesterol esters 3 18 50 40
Cholesterol 2 7 11 7
Phospholipids 8 20 29 46
* Most of the remaining material comprises the various apoproteins.

So lipoproteins are simply carrier molecules. They carry cholesterol and fats around the body. HDL transports cholesterol from our cells to the liver and LDL transports cholesterol from the liver to the cells (where it is needed for so many functions as I just discussed). In this sense, neither is good nor bad, just moving in opposite directions. LDL is given its name as it tends to be less dense than other types of cholesterol particles whereas HDL tends to be denser. Approximately 80% of the blood cholesterol is taken around by LDL out to the cells where it is needed. The HDL is almost like a scavenger and it goes around collecting cholesterol that doesn’t get used by the cells and then takes it back to the liver where it is either excreted or recycled to be transported out to the cells again by the LDL.

This part is crucial (and sadly not discussed enough by doctors); there is a further division of the LDL. LDL can be broken into large and fluffy and small and dense. The problem with the small dense LDL is its susceptibility to oxidation (going off). If the LDL does oxidise it sets of a cataclysmic cascade inside the body where the immune system is activated which can ultimately lead to clot formation and the beginnings of atherosclerosis (the build-up of plaque in the arteries). Having a high amount of HDL in your blood stream is useful in this situation because HDL has anti-inflammatory and antioxidant properties. This means that it can combat the oxidised LDL. HDL may also reduce the risk of thrombosis by preventing clot formation (Bitzur, Cohen, Kamari, Shaish & Harats, 2009). I will discuss more on the differing types of LDL and HDL’s role in part 2.

Some points worth considering:

– Polyunsaturated fats tend to oxidise more readily than saturated fats due to their chemical structure

– Saturated fat has never been proven to cause heart disease

– Sugar (particularly fructose) has been shown in numerous studies to increases blood triglyceride (fat) levels and LDL levels and be linked with heart disease

– Free radicals promote oxidation (smoking is a major free radial producer) which is the stimulus needed for atherosclerosis (plaque in the arteries)

– Antioxidants combat the effects of free radicals

– Vitamins A, C, E are antioxidants. Vitamin A and E are fat soluble which means eating them in a naturally fatty source (i.e. butter) ensures the body is able to utilise them

– When there is damage to the lining of blood vessels (i.e. due to smoking, high blood pressure, toxins etc), LDL takes cholesterol to the site of the injury to repair the damage (remember cholesterol is an integral component of cell membranes and everything is made up of cells)

– If the immune system has been triggered the area is pro-inflammatory which increases the risk for oxidising the LDL (this where the type of LDL you have determines your heart disease risk). If the LDL does oxidise, it becomes trapped in the lining where it becomes a part of a bigger fatty streak and over long periods of time will form a lesion (plaque).

– The amount of oxidised LDL in your blood directly correlates to your risk of a cardiovascular disease (CVD).

–  Inflammation closely correlates with CVD

– A highly processed diet (particularly processed carbohydrate and seed oils) are pro-inflammatory

– A grain based diet is also pro-inflammatory

 

So what does all this mean? Well simply put, when you get your blood checked by your doctor, you need to ask for either an oxidised LDL test or an LDL pattern test. A simple check of LDL to HDL levels is not enough. The following graphs explain why:

 (McNamara, 2013)

As you can see there is little relationship between LDL levels and coronary artery disease.

But in this next graph, you can see the STRONG linear relationship between oxidised LDL and coronary heart disease.

     (McNamara, 2013)

Finally, the ratio of real concern is the oxidised LDL to HDL ratio.

           (McNamara, 2013)

 

Of importance, is that you can have high levels of LDL and low levels of oxidised LDL and conversely low levels of LDL and high levels of oxidised LDL. Simply getting a reading of your LDL levels is not enough. The real issue is how much of your LDL is oxidised! If you can’t get your oxidised levels checked, ask for LDL pattern A/pattern B or ask about Lp(a). I will explain all of these in part 2.

I’ve now covered the basics of lipoproteins and their chemical composition, in part 2 I will discuss the differences between LDLs and what sort of diet promotes the right sort of patterning.

References

Bauer, J. (2012). How Food Affects High Triglycerides. Retrieved 18th July, 2012, from  http://www.joybauer.com/high-triglycerides/about-high-triglycerides.aspx

Bitzur, R., Cohen, H., Kamari,Y.,  Shaish, A. & Harats,D. (2009). Triglycerides and HDL Cholesterol: Stars or second leads in diabetes? Diabetes Care, 32(2): 373-377. Doi: 10.2337/dc09-S343

Cronau, C. (2012). The Fat Revolution: Why butter and real fats actually make us slim. Purple Lotus Publishing: Brisbane.

Disability Online. (2004). Cholesterol – In more detail. Retrieved 18th July, 2012, from http://hnb.dhs.vic.gov.au/dsonline/dsarticles.nsf/pages/Cholesterol_in_more_detail?OpenDocument

Gillespie, D. (2012). Big Fat Lies: How the diet industry is making you sick, fat and poor. Penguin Group: Victoria.

McNamara, L. (2013). Oxidised LDL cholesterol is the best predictor of heart disease. Retrieved 6th October, 2013, from http://www.laddmcnamara.net/2012/05/oxidized-ldl-cholesterol-is-the-best-predictor-of-heart-disease/

Nielson, N. S., Pederson, A., Sandstrom, B., Marckmann, P., Hoy, C. E. (2002). Different effects of diets rich in olive oil, rapeseed oil and sunflower-seed oil on postprandial lipid and lipoprotein

concentrations and on lipoprotein oxidation susceptibility. British Journal of Nutrition, 87:489-499, DOI: 10.1079/BJN2002567

Welsh, J.A., Sharma, A.,Abramsom, J.L., Vaccarino, V., Gillespie, C., Vos, M. B. (2010). Caloric sweetener consumption and dyslipidemia among US adults. Journal of American Medical Association, 303(15): 1490-97. Retrieved 18th July, 2012, from http://jama.jamanetwork.com/article.aspx?articleid=

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