Life Extension Magazine November 2011
As We See It
Avoiding the Catastrophic Event
By William Faloon
By William Faloon
A question we are asked nowadays is, “What causes people to die who take extraordinary steps to remain healthy?”
Our response is that in many cases, there is one precipitating catastrophic event that ignites a cascade of degenerative changes that culminate in death.
A classic example is an otherwise fit elderly individual who sustains a bone fracture. The combination of trauma, systemic inflammation, loss of mobility, hospital confinement, and psycho-logical stress can result in several diseases emerging that conspire to kill the victim in a relatively short time.
Catastrophic events are by no means limited to accidents. Surgical trauma or the impact of temporary loss of blood flow can also initiate a downward spiral from which an aging person never recovers.
Aortic stenosis is a catastrophic event that strikes aging individuals, but may be thwarted by a supplement that was introduced in 1999.1,2
It is too early to know for sure, but there is provocative evidence that what members already do to protect against atherosclerosis and bone loss also prevents calcification of the aortic valve.3,4
The Aortic Valve
Blood exits the heart to nourish the body from the left ventricle. With each heartbeat, the aortic valve opens (to let blood out) and closes to enable the left ventricle to fill with fresh oxygenated blood from the lungs.
In aortic stenosis, the aortic valve narrows and does not open fully. The result is the left heart ventricle enlarges as it desperately tries to force blood out through the constricted aortic valve. If not treated surgically, the aortic valve may either constrict so tightly that blood cannot exit the heart, or congestive heart failure may set in as the left ventricle deteriorates in response to having to squeeze harder to push blood through the narrowed aortic valve.
In the case of aortic stenosis, the catastrophic life-threatening event can emanate from surgical trauma (which can inflict short- and long-term side-effects) and anti-coagulant drugs like warfarin5-8 that will slowly poison a person to death if not used properly. Aortic valve replacement also increases stroke risk even with warfarin.9-11
There is no validated therapy other than surgery to reverse advanced aortic stenosis. Many doctors and their patients have valiantly tried but failed to remove the calcium deposits that constrict the aortic valve. Prevention of this potential catastrophic disease is thus crucial.
Prevalence of Aortic Stenosis
While 2-9% of people over age 65 are diagnosed with aortic stenosis,12 48% of those over age 85 have aortic sclerosis, which is the calcification and thickening of the valve without left ventricular constriction.13
Aortic sclerosis is considered a precursor for eventual constriction (obstruction of blood flow out of the heart) that is ultimately diagnosed as aortic stenosis. Most of those with aortic sclerosis succumb to another disease before frank stenosis manifests.
Historically, most cases of aortic stenosis were thought to result from the “wear and tear” of aging.14 This perception is changing.
Taking steps to protect against calcification and thickening of the aortic valve would be expected to significantly reduce stenosis risk in one’s older years, when surgical procedures are of particular risk.
What Causes Aortic Calcification?
Calcium is always circulating in the blood. Our body goes to great lengths to maintain calcium blood levels in a very narrow range. Too much or too little blood calcium is invariably fatal.15,16
Lining our arteries and heart valves is a protein that regulates whether or not circulating blood calcium infiltrates (calcifies) our vasculature. The name of this calcium-regulating protein is matrix gamma-carboxyglutamic acid. To avoid having to repeat this tongue-twister again, we will refer to it from now on as MGP.
MGP is synthesized in the vascular walls and plays a key role in regulating vascular calcification.7,17-19 Whether MGP allows vascular calcification or inhibits it depends on its state of carboxylation. When MGP is under-carboxylated, vascular calcification spontaneously occurs.18,20 When MGP is fully carboxylated, it functions as a potent inhibitor of vascular calcification.21-23
Carboxylation of MGP is dependent on vitamin K. In fact, MGP is classified as a vitamin K-dependent protein because it cannot shield against calcification without adequate vitamin K.1,24,25
Epidemic of Systemic Calcification
In the aged population, vascular calcification is ubiquitous. Autopsy reports show that 75-95% of men and women suffer some degree of vascular calcification.26
Since calcification occurs in soft tissues throughout our body, including the kidneys, lungs, heart, and brain, this calcification epidemic is of great concern to those seeking to avoid a “catastrophic event” that precipitates a lethal downward spiral.27,28
It is fortunate that we are not dependent on a future breakthrough discovery to protect against vascular calcification as it may be prevented by correcting a vitamin K deficiency.29-32