The Lipid Profile

Cholesterol is a term we hear all too often, given our beliefs in the ‘low-fat’ propaganda. Let’s have a closer look and improve our understanding of lipids (fats) and The Lipid Profile – the blood cholesterol check up that we have to undergo regularly. Some of the terms used in medical literature and in our reports need a better understanding.

Fats have many vital roles in the body. So much so, that no fats means no life. Fats (1) form the outer membrane of every cell in the body. (2) They are a compact dense source of energy. (3) They provide us with fat soluble vitamins, and are a part of the bile acids & several hormones within the body. (4) The liver creates most of the fats circulating within the body and dietary fats have little say in the matter.

Our blood is made up mostly of water. As you all know oils (fats) and water do not mix very well. So our fats (lipids) are transported within special carriers known as lipoproteins. Most of the fats that they carry are in the form of cholesterols or (TG) triglycerides. The lipoprotein outer membranes are made up of phospholipids – phosphate on the outside, and lipids on the inside. These can then freely mix in blood and go on in their buoyant way doing their duty of distributing fats to our cells. The density of the proteins in the lipoprotein carriers decides its name – HDL (High Density Lipoprotein), LDL (Low Density Lipoprotein) & vLDL (Very Low Density Lipoprotein).

When labs assess our blood for the lipids, they give us what is known as our Lipid Profile. These reports inform us of – Total Cholesterol (TC), HDL, LDL, vLDL, TG and the ratios TC/HDL & LDL/HDL. Actually the tests "are supposed to" measure the amount of cholesterol within each type of carrier. But they don't. Much of this science is assumptive and very outdated. The only actual assays (measurements) that they carry out are for the TC, HDL & TG. The rest is all guess work.

Decades ago, Dr. Friedewald found that each particle of vLDL carries typically 5 TG molecules within it. Using that information the vLDL is determined by TG/5. Then the LDL is calculated thus LDL = TC - (HDL + vLDL). Two out of 5 of the components within the report are calculated based on assumptions . Improvements in technology have resulted in newer labs giving us the direct measurement of cholesterol contained within the lipoproteins. In which case, “direct” is added to the type of the lipoprotein in the test report. 

In all of the above it is the cholesterol within the lipoproteins (example LDL-C) that is being reported, not the particle numbers (LDL-P) of the lipoproteins itself. There is no doubt that the sterols entering the artery walls and being internalized by macrophages cause atherosclerosis or plaque. But latest developments in the field have shown that it is the lipoprotein particle number and the size which is of critical importance. It is only the smaller and denser particles that can penetrate the arteries. The larger buoyant particles are largely benign & harmless.

The lipid trafficking in the body takes place within several lipoproteins, namely (from large to small) Chylomicrons, vLDLs, IDLs (Intermediate), LDLs and the HDLs. The HDLs are the reverse transporters of the lipids (back to the liver) and therefore supposed to be the good guys. Chylomicrons are used to transport lipids from the digestive tract directly through the lymph and have a very short life of a couple of hours, by which time they have delivered their stuff. The other lipoproteins wear out in order of their size after delivery of their goods. The LDLs live for about 3-1/2 days and form the predominant part of the TC that the lab reports. Therefore they are supposed to be the bad guys. It must be noted that among all health parameters, the lipids fluctuate the most and pretty fast. So they could be affected widely, by a lot of variables.

Newer studies have identified 4 different sizes of the LDL and as mentioned, it is the smaller denser variety that could cause harm. Hopefully in sometime this technology will also be available in India and we would benefit from better details. The ultracentrifugation technique known as the VAP profile is now probably available with Metropolis. The NMR (Nuclear magnetic resonance) spectroscopy is still a distant dream. But until then, I guess we’ll keep blaming all the fats equally.

If you are in Nutritional Ketosis and 'burning' fats for energy, you are bound to have higher fats in circulation. At least for some time. However, the tell tale sign of having the larger buoyant harmless LdL is that your TG levels will drop and your HdL values will go up. According to many prominent cardiologists, the TG/HdL ratio is a much more important cardiac disease risk marker. And the advice is to keep this under 2.0. Any value over 3.0 is of concern and the sooner this is brought down, the better. Unfortunately most doctors do not know of this, don't look at this, and none of the labs give you this ratio. So much so for the standard Lipid Profile.

Using my favourite tool, the analogy, let's look at lipids in a more common sense sort of manner. Let's equate Cardio Vascular Disease with Pollution in a city. Pollution as we all know is caused by the number of vehicles on the road. More specifically, the number of ill maintained polluting vehicles. Any child can tell you, that the number of passengers in the different types of vehicles is not the cause of the pollution. Similarly our cholesterol (passengers) carrying vehicles (lipoproteins) are the reason for CVD, IF, they are polluting (oxidized) and not the cholesterol content per se. Simple to understand, isn't it ? 

It's not the fats, Silly

On a web blog there was this argument going on between an Indian member and others. The Indian was scared that if he ate way too many fats, the grease would end up in his arteries, which would then be clogged up, and he'd die of heart disease. That is how he had been scared (to death) by his doctors.

Let's ponder on that argument for a while. Does this line of thinking not lead to something like, if you drink more water, it'll end up diluting your blood and you'll die because of that. Nope, nothing could be far from the truth. Nothing that we eat or drink can or could end up directly in your blood. Survival would be impossible if that were true.

The nutrients are broken down in the digestive tract to their smallest components and then sent to the liver for re-packaging. By re-packaging I mean, that the liver uses these base components to make new stuff out of. What we consume does affect this re-packaging process. A scientific fact, that doctors are aware of is, that if the liver finds less fats in what you eat, it makes more fats out of the other stuff. Didn't you think that the body had it's own intelligence ? 

The lipids that we get evaluated for in the blood tests are approximately affected 85% by the body's own fats production and 15% by the fats in your diet. The 85% fats in blood come from our own bile juices. The 15% dietary contribution is also a vague estimate, it could be more like 10%. Wouldn't it be a better idea to control the 85% and not the 15%. That's why the lipid hypothesis which says the more fats you eat, the more fats you have circulating in your blood is completely wrong. It's the excessive carbohydrates in the diet which cause the liver to re-package more fats in your blood. 

It's not the fats silly.

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Nobody ever said that the body makes only fats and not proteins or the other stuff. It makes everything that is needed, in the quantity needed, and when it is needed. Every part of the body works to maintain ‘homeostasis’ – a state of balance within. The problems start when this homeostasis is disturbed.

The vitamins are not made in the body but come from diet. They are used as catalysts in (1) further synthesis of other substances and (2) in the actions of several enzymes and co-enzymes that the body uses in diverse functions. Proteins are what we are made up of, as are all organisms, including bacteria and viruses. Every cell uses it’s genetic code within the DNA to continuously make proteins that are required in body for build-up, repair and many other functions.

Our blood supply vessels are lined with a protective inner layer known as the endothelium. Due to chronic inflammation or for some other reasons as well, the endothelial cells do get compromised and lesions start to form. What causes chronic inflammation within the blood vessels – High levels of insulin. What causes high levels of insulin – High levels of glucose. What causes high levels of glucose – High levels of carbohydrates in diet.

So when the endothelium is damaged and lesions appear (cracks form up), the smaller, denser lipoproteins (mostly sdLDL or Lp(a)) are attracted to the injured portions and enter deeper into the artery for repair to the damage. Once trapped inside the intima (the internal layer) of the vessel, the cholesterol within the lipoprotein carriers gets oxidized by the action of free radicals. Free radicals are any type of molecules with unpaired electrons, which are always looking to join up and react with something or the other. This sets off a chain reaction as more and more of the cholesterol gets oxidized and begins to decay.

Here, the protective Immune system is asked to step in and respond to the threat/injury. Monocytes which are a type of white blood cells, meant to fight infection are sent in for the defence. Monocytes enter the damaged tissue through the endothelium. They undergo a series of changes in their action, to become a macrophage. The role of macrophages is to engulf and then digest the cellular debris or the pathogens. When they become loaded with the cholesterol debris they acquire a bloated appearance and are now known as Foam cells.

Our body’s intelligence knows that in the vascular interiors, debris if offloaded into the circulation, may end up blocking some smaller vessel, somewhere. If that happens in the brain, you’d get a stroke. If it happens in the heart, you’d get an attack. So not taking that chance, the endothelium grows back over the foam cells deposited within, thus creating a mound within the blood vessel. Such damaged portions are then vulnerable to further attack, and over time the passage could become narrower and narrower. These are commonly referred to as “blockages” by heart surgeons. The reason why this happens only within certain arteries surrounding the heart which supply blood to the heart muscles is that because the blood gushes through these arteries under tremendous pressure and there are a lot of turns & forks in these arteries.

And when that happens, the blood supply gets restricted causing all sorts of problems. So the automatic question that follows – Is it the fats in the blood that are responsible for this damage. The correct answer is Yes & No. Yes because it is the fats within “some” of the LDL that get oxidized. And No, because it is the endothelial dysfunction that opens up the intima in the first place. Again, to control the serum fats, should we target the fats in our diet – Again Yes & No. Yes because there are ‘good’ fats and ‘bad’ fats, so obviously you have to choose well. And No because the fats in diet have no relation to the fats in blood serum. More fats are created and enter circulation when you eat a high carbohydrate diet.

So in a very nice circle, we have come back to – It’s not the fats silly.

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The question of fats in diet & fats in blood is so complex that it is very difficult to answer it in totality, while at the same time trying to keep the matter simple and understandable by everybody. Nevertheless a few points in a rejoinder were necessary and so here we go ...

Firstly it is important to note that when the endothelium is damaged and opens up to allow entry within, it's not just the lipoproteins that can enter and the fats within these lipoproteins that can cause damage. A whole lot of other stuff also can and does enter and do it's dirty work. Most known among these are calcium and some other minerals. And all of them are susceptible to further action of free radicals.

Further, in defence of dietary fats, it should be told, that most of the fats absorbed in the intestines through diet are too large in their composition to directly enter into circulation. Therefore they are packaged within larger lipoproteins known as "chylomicrons" and are sent into the lymph for circulation and delivery. The lymph is the other form of circulatory system within our body which is not completely enclosed as the cardiovascular (blood supply) system.

Chlyomicrons have a very short half life of a couple of hours and they enter into the CV supply  via the thoracic duct, somewhere near the neck. By that time they have lost most of their goods (cholesterol & TGs) and are much smaller in size and enter the CV system as vLDLs. This short life is the reason why a 12 hour fasting period is required when taking the lipid count in your blood tests. The chylomicrons, IDLs & vLDLs are mostly out of the way by then.

The fats that are packaged within lipoproteins in the liver mostly come from our own bile juices and leave in the form of vLDLs & LDLs. That is why we say that body makes it's own fats in a much larger proportion (approx 85%) than dietary fats.

I also want to add a disclaimer here. I started eating the way I do about 3 years ago and over these years have decreased my carbs & increased my fats. Assuming that this is the right way to eat, I could now potentially be preventing any inflammation and further damage within my CV system. But that does not erase 52 years of damage that I brought about in my system prior to this. Mounds / blockages once formed within arteries might not be reversed. The only way of tackling that problem is by either putting in a "stent" to increase the diameter of the artery or going in for a by-pass if the blockage is too severe. I have to live the rest of my life with that knowledge and hope that the past damage is not too severe to cause any future problems.

Another notable fact is that there are many risk factors where heart disease is concerned. Age is the foremost amongst them. As we age our functions and organs weaken and we are in a vulnerable stage. Added to that is the fact that by then the growth phase is over and we are now losing more cells than we are making. For no rhyme or reason, we blame the poor fats. They have so many important roles in the body No fats = no life, yet they take a solid beating time and again. As a matter of fact, it is the cholesterol in us that makes us animals different from plants and gives us mobility.

It’s not the fats, silly.

Lipophilia

For the past several decades our dietary preferences have been largely influenced by two hypotheses, The Energy Balance Hypothesis & The Lipid Hypothesis. The theory of Energy Balance is based on the 1^st law of Thermodynamics which says that Energy can neither be created nor destroyed but it can only be transformed from one state to another. In terms of metabolism within the body it has been applied as

Energy Balance (Weight Gain/Loss) = Energy (calories) In  - Energy (calories) Out

We have already covered The Lipid Hypothesis in great detail in another post & I will explore The Energy Balance Hypothesis also in greater detail in another post. Here we must only ponder if the 1^st Law of Thermodynamics can be really applied to living organisms. If as a scientific truth, it must, then there must be other forces also at play, because the theory fails miserably to explain many observed facts.

Many writers, researchers, scientists & doctors agree that ‘a calorie is not a calorie’. Its more important where the calorie comes from. So basically they agree that the Energy Balance theory falls way short in trying to explain how & why some people get fat or some won’t put on an ounce for whatever they may eat. The absence of scientific & logical answers has given rise to The Lipophilia Hypothesis as a workable alternate. Simply put Lipophilia means ‘in love with fat’ or ‘fat loving’.

To better understand the concept behind Lipophilia it is first important to define obesity. The current definition of obese is any person having a BMI over 30. The BMI itself is a 2 dimensional measure and does not take into consideration many important factors like bone density, water and/or visceral or subcutaneous fat or lean tissue content. It is measured in kg/mtr² more or less meaning “mass per unit area”. I find that a little hard to digest because mass per unit area of say the ankles is very different to that of the stomach or chest. I simply love the new definition of obesity given by Steven O'Rahilly of the University of Cambridge, Metabolic Research Laboratories, Institute of Medical Science - “obesity is most simply defined as a state in which the total amount of triglycerides stored in adipose tissue is abnormally increased.”

To begin, let’s refresh a few facts. All fat in the body is stored in fat (adipose) tissue which is unevenly distributed in the body. The area of distribution is largely determined by the sex hormones and that is why men & women put on fat differently. Males develop more muscle and the females put on more fat for purposes of species proliferation, which is Nature working at it’s best. If the individual’s adipose tissue is Lipophilic (fat loving) then the person has a tendency for weight gain & vice-versa. That is the theory in it’s simplest form. But let’s look at some pathways to throw more light on the subject.

The Lipophilic mechanisms of obesity work as follows (1) When you ingest carbs, more particularly simple or refined or fast carbs (2) It breaks down to its base molecules of glucose (3) In response the pancreas secrete Insulin proportionately (4) Insulin helps circulate the glucose for (i) glycogen storage (ii) energy consumption in cells (iii) conversion to triglycerides & fat storage in adipose tissue (5) the conversion from glucose to TG leads to the creation of a byproduct “a glycerol phosphate” or activated glycerol (6) this substance disrupts the balance of the TG/FFA (triglyceride / free fatty acid) cycle. (7) Normally TGs are constantly breaking into FFAs and released into circulation to be further converted to ketones and used for energy (8) With the cycle disrupted a large TG bank is created in the adipose cells which gets locked in and cannot be released unless converted to FFAs (9) The adipose tissue starts to expand with the new TG deposits and we start to become fatter.

Only the FFAs in circulation can enter or exit the adipose tissue. TGs are normally much larger to be able to do that. The TG/FFA conversion happens only inside the tissue. On a high fat way of eating there is a large amount of FFAs in circulation. These can easily enter & exit the fat cells if and when required. The TG/FFA cycle continues to work normally and the result is a leaner body. This theory is able to better explain many of the anomalies observed and surely will find larger audience and acceptance in times to come.     

The Lipid Hypothesis

Lipids are a biological term for fats, and Hypothesis means a theory. It comes from the English verb ‘to hypothesize’ meaning ‘to theorize’. So, the “Lipid Hypothesis” is basically a “theory” that proposes that dietary fats result directly in the increase of circulating fats (cholesterol) in the blood. And further, that these circulating fats, infiltrate the walls of the arteries and cause the buildup of plaque (blockages). In medical terms these arterial blockages are known as atherosclerosis which can result in its known complications – heart attack & stroke.

The world’s nutritional preferences have evolved on the basis of this hypothesis. And sadly, so has chronic ill-health & disease. This hypothesis changed the way we, and our doctors, look at our health and decide on a course of medication, which most of the times is completely unnecessary, and many a times causes more harm than good. So let’s take a brief look into the genesis of the lipid hypothesis, and examine the merits or demerits thereof.

The first seeds of the hypothesis were sown in the late 19^th century, when Dr. Rudolph Virchow, a German pathologist, performed chemical analyses on arterial plaques taken from corpses. He discovered that they contained large amounts of cholesterol. His post mortems could not have ascertained how and why the cholesterol was deposited there in the first place, since he was dealing with dead bodies. Then, in 1925, it was found that the human body produces 80-90% of its own cholesterol and that diet is relatively unimportant. But the ensuing tensions of the World War II subdued the importance of this revelation, and this vital discovery was silenced by the guns of the big war.

After the war, in 1950, the hypothesis was revived by Dr. Ancel Keys an American epidemiologist. His Six Countries Study showed that the percentage fat in the national diet of six countries proportionately correlated with the incidence of death from coronary heart disease (CHD). His graph showed a near perfect correlation between the two. Much later it was found out that the same data was, in fact, available with him, for 22 countries at the time of his study. He picked the six that fit his theory and omitted the 16 that didn't. This is virtually a text book example of statistical fraud. In a later article (1997) he said - “Cholesterol in food has no affect on cholesterol in blood and we’ve known that all along.” But by then, the Lipid Hypothesis juggernaut was unstoppable.

Then came another well known advocate of the low fat diet called Dr. Nathan Pritikin. In fact what Pritikin advocated was the complete elimination of sugar, white flour and all processed foods from the diet. He recommended the use of fresh raw foods, whole grains and a strenuous exercise program. However, it was the low fat aspects of his regime that received the most attention in the media. Adherents found that they lost weight and that their blood cholesterol levels and blood pressure declined. When Pritikin died of cancer at a young age, many doubts were cast on his dietary doctrine.

The final proverbial nail in the coffin was delivered by a U.S Senate Committee on Nutrition headed by Sen. George McGovern. It was the first time in history for a government to officially advise its citizens on what to eat and what to avoid. Be that as it may, the Committee actually recommended an elimination of sugars & fats from diet, but “somehow” the sugars were erased from the final draft. It is said to have been the “hard work” of the sugar lobby which ensured that. Thus were born the U. S. Dietary Guidelines, which continue till today and maintain the same anti dietary-fats approach.

During the first meeting of the 2010 Dietary Guidelines Advisory Committee, Dr. Eric B. Rimm from Harvard testified that he is concerned about "the artificial limit on fat" in the Dietary Guidelines. He mentioned that “there is some concern” about excess carbohydrates elevating triglycerides because the ratio of TG to HDL is emerging as one of the most reliable risk factors for heart disease. Dr. Rimm's testimony was greeted with silence and he did not bring up the subject again!

In keeping with the guidelines, not just American citizens, but the world population deviated towards a diet based on High Carbs – Low Fat foods. The rate of chronic disease skyrocketed inspite of following this “sound advice”. Heart disease, the core concern of the Hypothesis has also refused to slow down as it was supposed to. Even though science and technology have grown by leaps and bounds, they have not succeeded in addressing the acceleration of the problem. Figures for obesity & chronic illnesses, like diabetes and hypertension, have also zoomed. Infant obesity has gone up over 6 times. Has infant diet changed from mother’s milk & formula foods to something new ? Do we expect them to start exercising more to reduce weight ? And what exercises would that be ?

Study after study, research after research, has failed to establish any link between dietary fats, cholesterol and heart health. But the dogma continues. At best, high cholesterol levels in the blood are one of the 300+ risk markers for heart disease. That is not the cause and so reducing those levels artificially, certainly is not the cure, neither an answer to the problem. Arterial plaque has been observed in 2500 year old intact bodies discovered in the snowy Alps, and in young 25 year old dead soldiers. The real issue is not the cholesterol in the plaque, but how it gets there, and why. I believe Dr. Rimm is right. I believe that elevated blood sugar & elevated triglycerides oxidize cholesterol and they are the real culprits. The cholesterol is just a poor victim – of our dietary choices.    

Healthy Regards.