Part 5: Size Does Matter: Fat Burning and Cholesterol for Cycling
Pipes and Clogging
What is wrong with this picture? If you eat fat and cholesterol it ends up in your blood, where it sticks to your arteries and if you do it long enough you get heart attacks. That begs the question, why are the biggest blood vessels with the fastest blood flow getting clogged, rather than the tiny capillaries? Therefore the seemingly simple explanation, requires a more thorough look and exploration. Yes, cholesterol is present in atherosclerosis, however, how it got there is a truly fascinating story.
Fats and Humans
As much as fat has been demonised, it has a pivotal place in us humans; we both structurally and functionally depend on this feared macronutrient. As an endurance athlete you put greater stress on your body, therefore, everything should be working better than normal, or injuries, frequent colds, chronic fatigue and overtraining come knocking very soon. An imbalance or deficiency оf fats is detrimental to both well-being and performance.
As this is the second half of the article about fat for cycling and endurance sports, it is a good idea to review the first instalment, since there I covered some historical data on how fat (wrongly) came to be the villain behind heart disease and obesity as well as I described some of the terms which are used here.
Therefore let’s continue (with a brief overview) about that often misunderstood relationship between fats, cholesterol and humans. Fats are not just that unsightly bulge under your shirt, rather they are essential in almost every process that goes on in our body.
- Inflammation and healing are controlled by different types of fats; scar tissue contains large amounts of cholesterol.
- Our cell membranes are composed of saturated and monounsaturated fats as well as cholesterol keeping the cells in a flexible shape. The brain is around 70% fat by composition, with the greatest concentration of cholesterol found in it as well the lining of neurons (myelin).
- Fat is our energy storage, put there by mother nature so that we can use in times of fasting since food was not always a block away. Fats contains more than double the energy found in carbohydrates. Even the leanest of us have ~30,000-40,000kcal of fat available for endurance activities (contrasted to ~2000kcal of glycogen).
- Cholesterol is a precursor in a lot of hormones, particularly testosterone, oestrogen as well as vitamin D (when exposed to the sun). Fats are converted to hormone-like substances – eicosanoids responsible for normal cellular function as regulating inflammation, hydration, circulation, and free radicals.
- Polar animals survive due to a layer of fat that insulates their inner organs from the cold environment, though not as extreme it serves a similar function in humans. In hot climates subcutaneous fat prevents excessive evaporation of water.
Just like for humans, fats are essential for the structure and function of other species on the planet. Mammals, humans included, require their fats to be relatively liquid and stable at body temperatures, in contrast most vegetable or seed oils of plants have to be liquid so that they can be used when the seeds are germinating during the colder months. Cold water fish (or more specifically their fats) face similar challenges. While more information is available in the first half on fats, in short the more double bonds a fatty acids has, the more unsaturated, unstable, prone to going rancid it is; it is also liquid at room temperatures. On the other end of the spectrum, plants in tropical climates need their fat to not be reactive (not go rancid) in the high temperatures and as such coconut and palm oil are very high in saturated fats. In general an organism has a combination of different fats with a majority determined/dictated by the factors described above.
Our cellular membranes are composed of fat – saturated one as well as monounsaturated and cholesterol. The fats provide a backbone, while the cholesterol gives membranes flexibility; can’t have one without the other. Cholesterol is not a fat, but a specialised form of alcohol that is not dissolved in water – it makes our cells water proof. Plants make their own versions of it – called sterols. Our bodies rely on the assumption that there will be enough saturated fat in our diets, unfortunately as “low-fat” snd deadly cholesterol has become the norm our bodies are not coping quite well with the changes.
Rabbits and Russian Scientists
While cholesterol is present within atherosclerotic lesions, we make quite a bit of it naturally and no matter how much or little we consume, or body adjusts the overall levels, therefore limiting dietary sources will not reduce blood levels. The circulating pool of cholesterol comes to ~14000milligrams, therefore the current recommendation of 300mg/day is less than 2% what we already have (egg yolk contains 25omg for a reference). The most famous example is president Eisenhower, who after his first heart attack went on to an extremely low fat diet; with his cholesterol levels constantly rising to the point his personal physician had to to resort to lying about the lab results. In the end Eisenhower’s cholesterol levels were above the norm and he died of another heart attack.
For good or for worse among the things that can be measured in blood, cholesterol was among the first test available to medical practitioners. If you can only measure one thing , it’s rather straightforward to use it to correlate it to many conditions – heart disease included. Such conclusions had its merits since a Russian scientist Nikolai Anitschkow in the early 1900s who wanted to reproduce the arterial lesions in animals and therefore gain a better understanding on how they form. He had a theory that it was inflammation in response to injury to the arterial walls that was the main culprit – similarly on how scars form when you cut your finger. On he went to test various causes mechanical injury to the blood vessels, increased blood pressure, severing or irritating nerves, not even salts and toxins could create human-like plaques in animals.
Persistency is what keeps science going and another researcher form Antischkow’s lab succeeded in creating lesions in rabbits – by feeding them meat, eggs and cheese. While you think of this as the ultimate ‘a-ha’ moment, it wasn’t entirely clear which element of the diet was specifically responsible for the plaque formation. Further studies discovered that when the rabbits were fed pure cholesterol dissolved in sunflower oil, plaques developed that looked quite like the ones in humans. Even so, the rabbits never got heart attacks – the lesions never burst. Nobody could reproduce the results in animals that were not herbivores. Antischkow himself couldn’t make plaque form in dogs – natural meat eaters. The logical conclusion – since rabbits eat essentially zero cholesterol their bodies are not adapted to having it and species that are carnivores or omnivores (like humans) have mechanisms to protect against the ill effects of cholesterol. A reinforcing result was that the rabbits developed cholesterol build up in their joins and other organs as well. In 1946, a leading medical textbook stated that while fat deposits and cholesterol are present in atherosclerosis, there was no evidence that blood cholesterol had direct relationship. By 1950 the cholesterol-heart disease hypothesis had been burried for good. So how did it get brought back from the oblivion.
We come back to Ancel Keys yet again – a marine biologist who after 1939 was entrusted by the US government to come up with the minimum amount of calories that a soldier needs daily while still being combat worthy. Therefore he had a greenlight to perform some studies that are more than questionable today – or more precisely starving patients. To this day the US army’s food rations – the K-rations, although heavily modified, pay homage to their creator in 1941. Ancel Keys was the first expert on human nutrition and he had access to a significant amount of government population and health data from post-war Europe. When food supplies started to dwindle down and people faced starvation, death from coronary heart disease decreased substantially. Keys was aware of Antishkow’s experiments and subsequently formulated a theory that a full-calorie diet (ie one during time of plenty) contains more animals products and similarly to the cholesterol fed rabbits, well-fed Europeans had too much cholesterol in their diet. An aside here is that heart disease, diabetes and obesity was present mostly in the high classes and it is no surprise at that time they were the ones who had access to white sugar, white flour and white rice – items considered as luxurious in the early 20th century and before. Throughout the 1960s and 1970s Ancel Keys published a plethora of studies showing higher cholesterol in heart disease patients as well as that diets high in fat raise blood cholesterol. Keys’s ‘masterpiece’ was the 500-page 6-countries study demonstrating that Japan, Italy, England, Australia, Canada and the United States in that order showed a correlation between dietary fat and heart disease (i.e Japan the lowest fat and disease, the United States highest). The first huge gaping hole among the many (excellently detailed by Gary Taubes) in the study’s methodology is that Ancel Keys had data on 22, yes almost 4 times as many countries, and if he had plotted that data he would have gotten a scatter, ie absolutely no correlation even for the most creatively minded statistician. Yet he chose the 6 that nicely fit his hypothesis. Although hard to believe, [amazon text=bad science&asin=1400033462] can be the work of ‘experts.’
So Why IS There Cholesterol in Arterial Lesions????
We need to get fat from our food, the intestines and the liver to the rest of the body where it can be utilised. Blood is is an aqueous solution (ie water based) and fat doesn’t dissolve in water, therefore, fats and cholesterol are packaged in particles lipoproteins. The best way to describe these particles is trucks loaded with fats and similarly to our cell membranes the cholesterol keeps everything nice and flexible and in one piece. In more popular terms, these trucks are called Low-Density-Lipoproteins (LDL). They circulate and distribute their cargo around the body, however, ~20% of it remains in the periphery/blood vessels where it can get deposited and create lesions. As this is a process that occurs all the time inside each one of you, your blood vessels will be in pretty bad shape rather quickly. We have a garbage and recycling service that runs High-Density-Lipoprotein (HDL) trucks around scavenging any stray cholesterol so it is quickly transported back to the liver, and other organs such as ovaries, testes in order to make hormones. Ingenious things are simple. Why are HDL and LDL called simply cholesterol is beyond me; similarity the 90mile beach in New Zealand, that measures exactly…55miles. But I digress….
You can see why HDL is referred as the ‘good cholesterol.’ Why did LDL earn the name – ‘bad cholesterol?’ It does let those 20% slip by, however, it all gets swept up in no time.
Size Does Matter
LDL trucks/particles come in two patterns or sizes – Pattern A are large and fluffy, mostly because of adequate cholesterol content to keep them in shape (remember that cholesterol makes membranes flexible). Pattern B are deficient in cholesterol (have it in very low levels) and as such are small and dense. A study published in 1999 by researchers from University of California, Berkeley demonstrated that you can convert a person having mostly pattern A particles to pattern B by putting them on very low fat and low cholesterol diet (as president Eisenhower did). In addition sugar (fructose) and alcohol as well as unutilized carbohydrates not turned to glycogen, get directly converted to fat in the liver and since neither sugar, nor carbohydrates contain cholesterol, (see my article on sugar) the fat gets packaged into predominantly pattern B LDLs. That is why high level of blood lipids/triglyceride is a risk factor – those fats came from cholesterol deficient sources. Even if you have a high levels of Pattern A LDLs, it’s not an indicator of heart disease risk.
The interior layer of our arterial walls are composed of epithelial cells that are packed closely together , however, there is small space to let oxygen and nutrients pass by (think fine mesh). Particulate matter in air pollution is small enough to pass through those spaces just as are Pattern B LDL. That is Step 1. What has also happened as ‘low-fat’ diets have become the norm is the switch from saturated (animal) fats towards vegetable (seed) oils. As mentioned earlier in this article seed oils are polyunsaturated and unstable – especially when combined with (body) heat and oxygen. In addition plants do not contain cholesterol. Now you have your small dense LDL trucks loaded with polyunsaturated fats, happily cruising around the bloodstream. The oxygen starts setting up the cargo on fire, releasing an extremely reactive free radicals. Not a problem since we have anti-oxidants to put the fire away as well as cells of the immune system recognise the oxidised LDLs. Unfortunately, when our metabolism evolved 2.5 million years ago, no huge industrial presses for extraction of seed oils existed; our inbuilt defences get overloaded with the amount of polyunsaturated fats present in our diets. Some of the trucks that were on fire can’t be saved; they crash and embed their oxidised cargo into the arterial walls. It’s never too late they say and the immune system tries to clean up, however, it also attacks the inside layer of the blood vessels causing inflammation. That is why cholesterol and LDL remnants as well as dead macrophages (immune cells) are present in plaques. Give it some time and atherosclerosis develops.
The three egg omelette and bacon for breakfast doesn’t seem like such a bad idea anymore, does it….?
That begs the question why are statins – cholesterol lowering drugs widely prescribed and what keeps many pharma companies in business.
Statins and YOU
As hard it is to believe today, before 1980 cholesterol wasn’t in the public view – patients were not concerned much about their blood values. Drug companies had been busy developing cholesterol lowering drugs – statins for quite a while though. In 1977 the Lipid Research Clinics Coronary Primary Prevention Trial or (LRCCPP) for short…had been testing the effect of cholesterol lowering drugs on two groups of patients – one receiving placebo, the other the said pharmaceutical product. The diets of all subjects not surprisingly were standardised to a low saturated fat and low cholesterol ones. For the eight year duration of the study 2% of the men in the placebo group died of heart disease, while in the controlled group the drugs did achieve a 8.5% reduction of cholesterol levels, however, 1.6% of the men still had fatal heart disease related outcomes. An unimpressive difference at best, I personally was surprised, however, when you look at the statistics just the right way it makes for decent advertising; more than 50% of drug companies’ budgets are for publicity rather than research. This data is available publicly, though the pharmaceutical industry doesn’t brag about it, especially that cancer related deaths increased in the treatment group….. Keep in mind that those were drug trial, NOT diet ones. It puts Ben Goldacre’s words “[amazon text=Medicine is broken. And I genuinely believe that if patients and the public ever fully understand what has been done to them – what doctors, academics and regulators have permitted – they will be angry&asin=0865478066]” in a whole new perspective.
Take Away Points
As early as the 1900s, the clogged plumbing model of how cholesterol causes atherosclerosis to develop was disproven and by 1950s the scientific community had put any discussion to rest. Even though it wasn’t clear why plaques in arteries contained cholesterol, blood and dietary cholesterol levels had no relationship with the development of (fatal) heart disease.
Unfortunately though as animal (saturated) fats were wrongly labeled, starting in the 1960s, as the cause and cholesterol got brought back from the oblivion. That fact coupled with the lucrative market for cholesterol lowering drugs, put an advertising machine into action, that to this day labels that highly important molecule in the human metabolism, as a villain. While atherosclerotic plaques do contain cholesterol, it has gotten there due to the shift toward vegetable fats and low fat diets with sugar (fructose) becoming the substitute for the missing calories. If there is one point that you need to take away from this article it is the following:
If a fat is liquid at room temperature at its natural non-human intervened state, with the exception of olive oil, avoid it and don’t buy into the “bad” saturated fats and cholesterol dogma.
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Cycling Nutrition Series
- Part 1: Fast Furious and Deadly – Carbohydrates
- Part 2: Sweet Little Lies – Sugar
- Part 3: Not by Bread Alone – Wheat, Pasta and Gluten
- Part 4: The Fat of The Land – Fats
- Part 5: Size Does Matter – Cholesterol
- Part 6: You Think You Know what Processed Food Is?
- Part 7: Putting it All Together: Recipes for Successful Cycling
[amazon text=Big Fat Lies&asin=0936077425] – David Gillespie
[amazon text=The Big Book of Endurance Training and Racing&asin=1616080655] – Dr. Phillip Maffetone
[amazon text=Good Calories, Bad Calories&asin=1400033462] – Gary Taubes
[amazon text=Fat Chance&asin=0142180432] – Dr. Robert Lusting
For further information check the ever-increasing Reading List
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