By Dr. Daniel Lombardo PhD
The Oxford dictionary tells us the word conspiracy means “a secret plan by a group to do something unlawful or harmful”.
Thought to be the number one cause of cardiovascular disease, in recent years cholesterol has come under significant scrutiny.
Various health lobbyists, doctors and members of the pharmaceutical industry now tell us it is not the enemy. Rather, it is a vital component for health. It is present in our cell membranes, is an essential building block for vitamin D, steroid hormones such as estrogen and testosterone, adrenal hormones such as aldosterone and cortisol, and plays a role in the communication of nerve cells.
Effect on arteries
Cholesterol is merely a symptom of cardiovascular disease, rather than the underlying cause. To understand why a person experiences a heart attack or stroke; we must briefly delve into the arteries.
Loosely termed, low density lipoproteins (LDL) and high density lipoproteins (HDL) are produced in our liver. The liver packages these proteins with cholesterol, various vitamins and triglyceride fats. Think of LDL and HDL as a taxi service; dropping passengers off at various parts of our body.
LDL runs the express service to our tissues and cells; delivering cholesterol. HDL acts as the night taxi service, returning the excess cholesterol safely to our liver to be recycled.
A problem occurs when pesky free radicals are lurking in our arteries. These cause havoc, targeting the small, helpless LDL taxis, causing them to break down (oxidise) in our arterial highway.
Macrophages at work
‘Free radicals… cause havoc in the body’s arterial highway’
Our bodies have their very own road-side assistance called macrophages that tow the LDL away to allow the arterial highway to continue to flow freely. If there are too many free radicals, this will lead a blockage of the immobilised LDL (plaque).
Our bodies’ road-side assistance simply cannot keep up with the number of breakdowns, and the outcome is a taxi pile-up in our arteries (refer to picture).
When this becomes too much to handle, the blockage bursts, resulting in the closure of the arterial highway. Simply put, the person experiences a heart attack or stroke.
Two studies come to mind which prove that inflammation and oxidation are the underlying cause, and not the presence of cholesterol itself. The first was conducted in 2009 and showed that a whopping 75 per cent of patients that experienced a heart attack had “normal” LDL cholesterol levels.2
Your C-reactive protein
The second study concluded that oxidised LDL levels had a “strong and graded association with the presence and extent of coronary heart disease”.3
The next time you visit your general practitioner, instead of asking for a standard LDL/HDL ratio test to determine your risk of a heart attack or stroke, request to monitor your oxidised LDL or C-reactive protein, the latter of which is an excellent marker for arterial inflammation.
Elevated levels of free radicals are a result of high stress and poor lifestyle choices. Diets rich in sugar, highly processed foods, cleaning products, treated water, smoking and heavy alcohol consumption are to blame.
The health industry may lead you to believe that statins are the answer to your cholesterol problems. Statins work by inhibiting the HMG-CoA reductase enzyme; lowering the amount of cholesterol produced in the liver. Remember, cholesterol is only the symptom: it is not the problem.
‘In 2010, it was estimated that… sales from statin drugs [were] amassing to billions of dollars’
As a former academic and pharmaceutical representative, I have seen statin promotion significantly increase. In 2010, it was estimated that about 2.6 million people were taking a cholesterol-lowering drug in Australia.4 That equates to nearly 10 per cent of our population; with the sales from statin drugs amassing to billions of dollars. Looking at this objectively, it is difficult to believe that the pharmaceutical industry does not have a hidden agenda.
The benefits of statins are minimal, in my opinion. If you do not believe me, request that your doctor share with you the product information of the statin you are administering. You might be surprised by the data.
Although statins have been shown to increase nitric-oxide production, which prevents platelets and white blood cells from sticking to the arterial walls,5 this is greatly out-weighed by the adverse effects of amnesia, nausea, memory loss and at worst case, impaired kidney function. Not to mention that a person’s CoQ10 levels decrease when administered statins.6
Your heart and CoQ10
We know that CoQ10 helps enzymes involved in energy production and plays a key role in protecting the heart against free radicals. Lowering CoQ10 actually increases the risk of a heart attack or stroke.
What is the alternative? Focus on changing your lifestyle. Exercise, stress management and mindfulness is a great start. Supplementation, more specifically high quality fish oil, a multi-vitamin with vitamin C, E and a broad spectrum anti-oxidant along with probiotics should all be considered.
One of my favourite studies was a meta-analysis comparing fish oil to statins. Fish oil was shown to reduce cardiac mortality by 32 per cent, compared to statins which was only 22 per cent.7 Supplements and healthy eating cost cents a day while statins can cost dollars a day. Supplements have minimal adverse effects, if any at all; statins have a plethora. The choice is yours. Just do not buy into the cholesterol conspiracy.
For further information: visit drdanlombardo.com, where you will find more information about supplements. Dr Daniel Lombardo PhD (Medicinal Chemistry).
DISCLAIMER: This article is not medical advice, and only provides information designed for you to engage in conversation with your general practitioner about the best option for your health.
- Oxford dictionary; 2017
- Sachdeva, A. et al. Am Heart J.2009. 157, 111-117
- Sotirios T. et al. Engl. J. Med. 2005. 353, 46-57
- The Conversation (derived from the Australian Government: Department of Health). Some things you should know about statins and heart disease.
- Tousoulis, D. et al. J. Cardiol. 2009. 123, 91-93.
- Folkers, K. et al. Natl. Acad. Sci. 87, 8931-8934.
- Studer, M. et al. Archives of Internal Medicine,2005. 165, 725-730