Dietary Cholesterol Redeemed
Let’s establish something before we start our discussion – and bear with me for a moment even it violates everything that you’ve heard so far – dietary cholesterol (and cholesterol in general) is NOT bad for you.
Shocking, right? Isn’t dietary cholesterol responsible for cardio-vascular problems? Isn’t excess dietary cholesterol a major cause of death from heart attacks and strokes? Aren’t we supposed to stay away from fat, read meat, avoid cholesterol in eggs and other dangerous foods that make us obese and clog our arteries?
You would be surprised, but the answer to all of those is – NO.
For many decades, dietary cholesterol has been blamed for something it was not responsible for and this image is so deeply ingrained in most people’s brains that it is extremely hard to wipe out. But now even USDA and US Department of Health and Human Services may be ready to scrap the guidelines of avoiding high-cholesterol foods.
- The Case against Statins
- Why cholesterol is essential
- Can you lower your risk by consuming less dietary cholesterol?
- Does dietary cholesterol lead to plaques?
- If it is not dietary cholesterol – what really causes heart disease?
- Snacking – or why you shouldn’t really consume 6 smaller meals per day
- Conclusion: dietary cholesterol is not the cause of your problems!
The Case against Statins
Ironically, this enlightenment comes after decades of massive profits generated by pharmaceutical companies producing cholesterol-lowering statin drugs. Just one example – Pfizer’s Lipitor was the most profitable drug in history, with sales to date from this one particular drug exceeding $140 billion. In fact, even though Lipitor’s patents expired in 2011 and the market got flooded with other alternatives, Lipitor continues to generate $13 billion dollars per year.
This is despite the fact that even FDA’s advisories against statin drugs, warn against such side effects as: liver injury, memory loss, diabetes, and muscle damage.
Lipitor is only ONE specific drug out of many in its class. You can imagine how much money the industry generates (it is currently estimated to be around $20 billion a year). Still surprised that convincing people that dietary cholesterol is not the enemy is so hard? You shouldn’t be.
It would be one thing is statins didn’t prevent the risk of atherosclerosis. But this is not where it ends – to top it all off, statins are associated with a few added risks of their own. Here are only a few and most widely known side effects of statins:
- Muscle pain and damage
- Liver damage
- Digestive problems
- Increased risk of Type 2 diabetes
- Neurological side effects
The list doesn’t end there. A 2013 report summarizing Pubmed, EMBASE and Cochrane review databases states:
For every 10,000 people taking a statin, there were 307 extra patients with cataracts, 23 additional patients with acute kidney failure and 74 extra patients with liver dysfunction. Furthermore, statin therapy increased muscle fatigabilty by 30% with 11.3% incidence of rhabdomyolysis at high doses. What’s more, it induces inflammatory myopathy, including necrotizing autoimmune myopathy with immunosuppression and the statin-related myopathy can last for 12 months.
Some of the other risks the same review also mentions are:
- Erectile dysfunction;
- Parkinson’s disease in older patients (cholesterol is a critical component of neuronal cell membranes and synapses, and plays an important role in their proper functioning. A strong association between lower cholesterol and Parkinson disease risk has been reported);
- Non-melanoma skin cancers; and most ironically
- The evidence that statin use is associated with an increased prevalence and extent of coronary plaques calcification (just to be clear, this is what statins are actually supposed to prevent!)
Now the key point: most of the risks from statins are believed to be related precisely to the fact that statins inhibit production of cholesterol. Most people have no idea how important it is. So, let’s see what makes it so important. Discussions around cholesterol may fill whole books, so we will only try to stick to the important basics – but, hopefully, this would be enough to convince you.
Why cholesterol is essential
Cholesterol is essential for life.
In humans and animals, it is a major constituent of the cell membranes, modulating physical properties of these membranes (fluidity and structural integrity) that affect the function of membrane receptor and transporter proteins. When transporting stuff in and out of the cell is compromised because transporters and receptors cannot be properly expressed many cellular functions get crippled.
What else makes it essential? Here is a partial list:
- Cholesterol is a precursor to important sex hormones – testosterone, estrogen, androgen and progesterone. It is also a precursor to corticosteroids, hormones whose primary function is to protect the body against stress and disease – including cortisol and DHEA.
- Cholesterol promotes healthy nervous system, because it is used as an insulator around nerves – it is required for the formation of the myelin sheath, a fatty material that surrounds nerve fibers. It, therefore, helps prevent some diseases associated with the nervous system and is absolutely essential for brain function (it is not surprising, then, that inhibition of cholesterol production leads may lead to Parkinson’s and other neurological damage).
- Cholesterol is a precursor for bile salts, which actually aid in fat metabolism and, most importantly, facilitate absorption of fat-soluble vitamins A, D, E and K.
- Cholesterol is necessary for production of vitamin D in your skin when it is exposed to sunlight – we have discussed this vitamin in the article on the importance of sunlight (some actually equate it to a hormone) that controls the expression of about 1000 genes, helps absorb vital minerals, impacts immune function and does a lot more.
- Serotonin receptors in the brain require cholesterol in order to function properly. Serotonin is an important neurotransmitter that promotes a natural feeling of well-being and controls many different cognitive and behavioural functions, such as sleep, mood, pain, addiction, locomotion, sexual activity, depression, anxiety, alcohol abuse, aggression and learning.
- Cholesterol sulfate (which also gets produced in your skin from sun exposure) has protective functions for blood erythrocytes and is actually believed by some scientists to be protective from asthma and arthritis (read this very interesting article about important cholesterol sulfate functions by Dr. Stephanie Seneff).
There are some genetic disorders in which people cannot properly synthesize cholesterol (such as Smith-Lemli-Opitz syndrome), which lead to a number of problems including autism, mental retardation, lack of muscle, etc.
Insufficient cholesterol results in your brain not having the raw materials it needs to make biochemicals critical for memory and cognitive function, including coenzyme Q10 and dolichols, the latter of which carry the genetic instructions from your DNA to help create specific proteins in your body that are crucial for cognitive function, emotions and mood.
Doesn’t this demonstrate to you that limiting available cholesterol may have a profound negative effect on your biology? Doesn’t this explain why using statins, which disrupt cholesterol synthesis leads to so many dangerous side effects?
Can you lower your risk by consuming less dietary cholesterol?
What, you thought dietary cholesterol is the only source of cholesterol in your body? You thought it gets in with fats you eat?
That’s only part of the story. Only about 25% of our daily “intake” of cholesterol (dietary cholesterol, or exogenous cholesterol) comes from food we eat – the remaining 75% is synthesized by our bodies endogenously – typically by the liver and small intestine – but overall, most cells in our bodies can produce (and store) cholesterol as required, so very few of them require cholesterol “delivery”.
The synthesis of cholesterol is a complex process that includes multiple feedback loops that your body uses to regulate cellular cholesterol levels and keep it within a certain narrow range. If you have too much cellular cholesterol – it will crystallize and cause cellular apoptosis (programmed cell death) – which is a normal regulatory process that goes on all the time.
However, cholesterol in your blood (called “plasma cholesterol” or “serum cholesterol”) has little to do with cellular cholesterol – in fact, when you decrease the intake of dietary cholesterol, the body will either synthesize more or absorb (i.e., recycle) more of it from our gut. Moreover, your body has great mechanisms to regulate absorption and excretion of cholesterol (you can read this amazing detailed article by Dr. Peter Attia that describes the process in detail and also explains why much of cholesterol we eat doesn’t end up in your bloodstream because it is in a different (esterified) form and can’t get absorbed through the intestinal wall)
Does dietary cholesterol lead to plaques?
Cholesterol is naturally not water soluble, so to be transported through blood (which is water-based) your body packages it into lipoprotein molecules, where cholesterol is surrounded by protein shield. You have probably heard about High Density Lipoproteins (HDL cholesterol often called “good cholesterol”), and Low Density Lipoproteins (LDL cholesterol, often called “bad cholesterol”) – these are molecules that transport cholesterol (along with triglycerides – an important point to note for the discussion below): HDL is used to deliver cholesterol to the liver for further excretion, while LDL is used to deliver cholesterol to the tissues that need it.
Both HDL cholesterol and LDL cholesterol are a part of normal and important cholesterol transport throughout your body. If all systems function as intended, the mere presence of cholesterol in your blood (elevated or not) is not the cause to sound any alarms – in fact, as we have seen above with statins, when you start reducing cholesterol levels artificially by disrupting its synthesis in the liver, all sorts of system malfunctions start to happen all over the place.
When your arterial walls are inflamed and/or their structural integrity is compromised because of tiny lesions, however, LDL particles can get into the sub-endothelial space and gets “stuck” there. With little time, the lodged LDL particle starts to oxidize and this further triggers inflammatory response. When the number of such LDL particles becomes too large, your immune system (which typically can remove smaller number of LDL particles) cannot cope – the problem becomes chronic and expands into the neighboring space, involving macrophages, smooth muscle cells, microvascularization, calcification – and producing an inflamed plaque as a result.
(We should probably briefly pause at this point and emphasize that the structural damage to arterial endothelium is facilitated, to a large extent by sugar, which promotes glycation and free-radical damage).
Ultimately the growing plaque invades the arterial lumen or ruptures into the lumen inducing luminal thrombosis – this is what causes the arteries to narrow.
The chance of such occurrence increases with the sheer number of circulating LDL particles, which play a crucial role in plaque formation. In other words, elevated risk of heart disease is not because of dietary cholesterol (and not because of cholesterol in general) – it’s caused by the vehicle that carries it.
Interestingly, because LDL particles carry not only cholesterol, but also triglycerides within the same lipoprotein, an increase in the number of triglycerides molecules packaged within the LDL decreases the number of cholesterol molecules – which means that to transport a given amount of cholesterol (an important molecule for many processes, as we discovered above), your body necessarily has to increase the number of such LDL particles.
If it is not dietary cholesterol – what really causes heart disease?
Triglycerides are one of the forms fat takes to travel through your blood. We have seen how the amount of triglycerides may be correlated with the risk of cardiovascular disease (by increasing the number of LDL particles). But what raises the number of triglycerides?
You would think that eating more fat would increase triglyceride (fat) levels in your blood, but this is not the case. Surprisingly (or not, if you have been following this blog) – several studies in the past have concluded that the impact of sugar on cardiovascular risk markers is high precisely because fructose, glucose and high-fructose corn syrup (HFCS) increase triglyceride levels, as well as the number of LDL particles. In their purest form, fructose and glucose come from simple processed carbs consumed with junk food, candies, etc. But pretty much any source of carbs may trigger this problem when consumed in excess – and the reason for this is insulin.
Consuming carbs triggers the production of insulin to deliver glucose to cells. Basically, insulin flips the switch in your body and causes it to use glucose as opposed to fat. High insulin causes low utilization of triglycerides for energy (which may cause them to pile up in the blood) AND increased storage of triglycerides as fat in adipose tissue.
Some amount of carbohydrates is important and necessary – particularly when it comes from whole foods in a complex package including other nutrients, minerals, vitamins and fiber.
But, as we all know, “typical” average consumption of (especially simple) sugars throughout the world is quite disturbing. Statistics show that an average American consumes 126.4 grams of sugar per day, an average German – 102.9 grams, an average Dutch – 102.5 grams, an average Brit – 93.2 grams and an average Canadian – 89.1 grams.
These are higher than even conventional (and quite lenient) recommendations by the World Health Organization to reduce free sugar consumption (i.e. added sugars consumed as mono- and di-saccharides and not consumed in fruits and vegetables) to about 25 grams per day. For most people, these recommended levels should be even lower – especially for those who already consume carbs and starches in other foods and especially for those who are trying to reduce body fat and health risks.
Coming back to increased cardio-vascular health risks, the amount of circulating triglycerides can be quickly and significantly reduced by just removing simple sugars from your diet.
Snacking – or why you shouldn’t really consume 6 smaller meals per day
Another bad habit to guarantee elevated level of triglycerides is snacking. Remember (we have discussed this many times when talking about important dietary considerations in the past) – if you eat the right stuff in the right amounts (i.e. – do not starve yourself by making your lunch consist of only celery sticks and trying to create mythical “caloric deficit” in an effort to trigger body fat burn), you should not be feeling hungry between regular meal intakes. There is no reason why you should eat more than three times a day – this is true even for professional bodybuilders (who believe they have to eat every two-three hours) and endurance athletes (who typically rely on quick carbs to support their workouts).
Some athletes even get away with eating one or two times a day – with no significant detrimental impact on their performance. Perhaps you don’t get this very slight edge (even if there is one) by reducing the number of feedings per day to one or two, but I think your health is more important in the end.
When you snack constantly, you remain in the “fed” mode – with elevated blood glucose (and thus insulin). Because there is this constant supply of nutrients, your body may not want to utilize fatty acids in your blood (why would it, given then there is quicker fuel available in the form of carbs), which might cause elevated blood triglyceride levels (and, by extension – higher number of LDL and elevated risk of cardiovascular disease).
Once again, eating too much carbs wreaks havoc on your health.
Conclusion: dietary cholesterol is not the cause of your problems!
Long time ago, in 1950s, some tests showed association between early death by heart disease and arterial plaques. It was (mistakenly) concluded that dietary cholesterol was to blame simply because cholesterol it was found to be present in those plaques (naturally!).
But it seems that it was a case of being in the wrong place at the wrong time. In response to inflammation, cholesterol is being used as a temporary patch to cover lesions in the arterial wall and is supposed to be removed once the inflammation is resolved.
But when you constantly fuel that inflammation with carbohydrates (sugars, grains, starches, etc) – you contribute to both the increase in the number of LDL particles and to damages to endothelial lining of the arteries – a perfect situation for those extra LDL particles to get lodged in arterial walls.
What further exacerbates the problem is oxidation of these LDL particles by free radicals (from consuming bad foods, such as trans fats and even more sugar).
The damage inflicted by free radicals can be partially counteracted by consuming anti-oxidant-rich foods (most vegetables and some fruits), as well as Omega-3 fatty acids (such as those found in fish or krill oil). Conversely, if you diet consists of processed vegetable oils rich in pro-inflammatory Omega-6 fatty acids – you are really shooting yourself in the foot. This, by the way, makes the emergence of vegetable-oil-based hydrogenated (i.e. trans-fat laden) margarines a joke (a really bad one, too) when it comes to fighting heart disease.
As you can see from all of the above, elevated cholesterol (as typically measured by cholesterol containing particles, such as LDL) is merely an indication of a bigger problem with your diet – a problem that can be addressed and taken care of NOT by reducing dietary cholesterol and NOT by disrupting cholesterol synthesis by some artificial method, like taking statins), but rather by reducing other offending compounds that eventually lead to cardiovascular problems (among other things).
Remember – these are the real problems you have to address!