Teeth are the gateway to good health
How Taking Care of your Teeth Reduces Heart Disease
The following article was excerpted from my book “All About Bacteria” first published by Harper Collins in 2013.
Have you seen the ads for statins? Those supposedly miraculous drugs that lower cholesterol? It is my belief that statins will one day come to be seen as cigarettes are today- causing all kinds of illnesses with long-term use.
The single greatest killer of Americans is heart disease, killing one in three people. Of course, we all have to die of something or the other, so this statistic in itself may not tell us much. But eighty-one million Americans have some form of cardiovascular disease (CVD), according to the American Heart Association.[i]
The good news is that deaths from CVD have declined in the last decade, as more and better surgical treatments have become available. The problem is that surgical treatments for CVD are horribly expensive. In 2009 alone, the economic costs of CVD in the US were US$475 billion[ii]. In the UK, the number for 2004 is £29 billion[iii]. This is truly one disease where an ounce of prevention is worth several billion pounds of cure!
There are all kinds of myths and theories regarding heart disease. The mainstream hypothesis is that high cholesterol, particularly high amounts of LDL cholesterol, is the root cause of heart disease. This hypothesis is so well-established that the pharmaceutical industry makes billions on a class of drugs called statins, which lower measurable cholesterol in the bloodstream. In 2006, the market for these drugs was US$18 billion in the US alone.
But let us look at exactly how this hypothesis works. Many studies have shown that people with naturally low cholesterol are less prone to heart disease than the general population. The science part of the cholesterol hypothesis ends here. From this data, someone decided that if you lower cholesterol using drugs in people who have naturally higher cholesterol through drugs, then you will lower the incidence of heart disease too.
This is like saying brown-skinned people are less prone to skin cancer, so if Caucasians used tanning beds regularly to become brown their rate of skin cancer would go down too! In fact, the process of tanning would more likely cause skin cancer!
The first question to ask is if artificially lowering cholesterol has any impact on heart disease. The answer is that it does not.
The second question is if the drugs themselves have huge side effects. The answer is that they do, from muscle weakness to impaired liver function to neurodegenerative illnesses[iv].
What does all this have to do with the human symbiote? Well, the symbiote has a big role to play in heart disease. The role is indirect and works like this: Heart disease, in reality, is caused by chronically elevated levels of cortisol, which is a chemical released in the bloodstream due to stress. The stress chemical, in turn, causes the body to increase the synthesis of cholesterol. The body does this because cholesterol is an antioxidant, which counteracts the free radicals caused by stress!
Now let’s think this through. The medical community wants us to take statins that lower the production of cholesterol, which is an antioxidant because increased levels of cholesterol are linked to heart disease. But cholesterol is the body’s medicine against stress compounds, so why would we want to lower the levels of this medicine? We should instead be getting to the root cause of the stress and eliminating it.
There is so much evidence of the effects of stress that these are now part of the medical consensus.
Let’s look at the biggest causes of cortisol release, which is the body’s response to stress. Probably the number one cause is a chronic inflammation of the teeth or dental disease. Remember that the teeth and gums are the one place where the skin is continuously being broken due to chemicals released when food particles that are stuck between the teeth decompose. The mouth symbiote is just doing their job, which is breaking down the food particles. But a side effect is that harmful chemicals known as endotoxins are released when this breakdown takes place and these endotoxins can enter the bloodstream and cause inflammation. The body fights this inflammation by releasing cortisol. This process can go on for decades before you see damage in the form of heart disease, which is why the dental disease has escaped attention in the past.
The healthy human mouth symbiote is made up of hundreds of species of bacteria[v] that belong to a group called ‘aerobic’ bacteria, meaning that they need oxygen to survive. These are normal inhabitants of the mouth symbiote and are quite harmless. In fact, just like the skin symbiote, they are there to fight off any pathogens that enter your mouth by preventing them from establishing a presence. When you clean your teeth and gums, these bacteria re-establish themselves very quickly, so there is no harm to the mouth symbiote. But when you fail to clean your teeth and tongue, and don’t floss regularly, a layer of plaque forms on your teeth, which then creates a barrier under which another class of bacteria, called ‘anaerobic’ bacteria set up shop and thrive. These bacteria are much more likely to be harmful, because they release endotoxins that cause inflammation, and stimulate the immune system to give a cortisol response.
The simple truth is that maintaining healthy gums and teeth is critical to preventing heart disease. Go to the dentist every six months and get your teeth professionally cleaned. Floss between your teeth every day, preferably at night before you go to sleep. Also, brush your tongue to remove the white coating of food underneath which anaerobic bacteria can establish themselves.
[iv] Vaughan et al, Statin Neuropathy Masquerading as Diabetic Autoimmune Polyneuropathy, Diabetes Care August 2005 vol. 28 no. 8 2082, http://care.diabetesjournals.org/content/28/8/2082.1.full
[v] Global diversity in the human salivary microbiome, Nasidze, I., Li, J., Quinque, D., Tang, K., and Stoneking, M., Genome Res. Published in Advance February 27, 2009, http://genome.cshlp.org/content/19/4/636