Life Extension Magazine May 2014
As We See It
CDC Says: 200,000 Americans Die Needlessly Every Year
By William Faloon
The Centers for Disease Control and Prevention (CDC) deserve a level of respect that does not exist with most bureaucracies.
When the first cases of AIDS were reported in the United States in 1981, the CDC knew this country faced a contagious disease crisis and took action.
Despite interference by other government agencies, the CDC persisted with meticulous research. Within 18 months the CDC identified all the major risk factors for acquired immune deficiency syndrome (AIDS).1
The Food and Drug Administration (FDA), on the other hand, responded by organizing armed raids against those who sought novel ways to prevent the immune deficits that were ravaging AIDS patients.2
Life Extension ® was one victim of these police-state actions. We were fortunate that our early recommendations were vindicated before the FDA could incarcerate us.3-5
In 2013, the CDC released a report estimating that nearly 200,000 avoidable deaths occur each year in the United States from heart disease, stroke, and hypertensive disorders.6
According to the CDC, prevention of vascular disease can be as simple as following the “ABCS”, which stands for: “aspirin, blood pressure control, cholesterol management, and smoking cessation.”7
Life Extension does not question the accuracy of this CDC report. We in fact believe it to be understated. Our concern is that the CDC report contains omissions about other preventable causes of vascular disease overlooked by hurried physicians.
This article will show why the number of needless deaths is higher than the CDC estimates and how you can avoid being a victim.
Atherosclerosis is the term used to describe damage and obstruction to the linings of our arteries.8 When arterial blood flow is impeded or blocked, the result can be death or disability from a stroke or heart attack.8
A misconception about atherosclerosis is that it is a modern day scourge caused by unhealthy habits. I’ve heard so-called experts’ claim that people didn’t suffer coronary artery disease in the past because their diets were so natural.
These “experts” had no basis to claim that atherosclerosis is a modern day phenomenon. All they could cite was that few people developed heart disease in the past compared to today. The reason more people weren’t having heart attacks back then was that most died before age 50 from diseases that are now preventable/curable.
A study on this topic published in The Lancet last year attracted worldwide media attention. It documented that mummified human bodies dating back 4,000 years and spanning multiple geographic locations/cultures suffered from clogged arteries.9
As Life Extension has long argued, atherosclerosis is a disease of aging that has always been prevalent. It took MRI imaging to document clear signs of heart disease in 34% of mummified humans whose estimated mean age at death was 43 years. Those who died at an estimated mean age of 32 years were less likely to show signs of atherosclerosis.9
According to the lead investigator of The Lancet study:
“The fact that we found similar levels of atherosclerosis in all of the different cultures we studied, all of whom had very different lifestyles and diets, suggests that atherosclerosis may have been far more common in the ancient world than previously thought,”10
—Randall Thompson, MD
These findings help confirm that atherosclerosis has always been widespread. The encouraging news is that methods to prevent and even reverse it have been validated in modern clinical studies.
What Caused Atherosclerosis In The Mummified Bodies?
In seeking to identify what caused atherosclerosis in the mummified bodies, The Lancet researchers speculated that it could have been the high levels of inflammation these primitive people were exposed to from constant infections and a non-hygienic environment.10
People with severe inflammatory conditions (like rheumatoid arthritis and lupus) suffer accelerated atherosclerosis.11-13 Multiple studies on normal modern people link chronic inflammation as an independent risk factor for stroke and heart attack.14-16
A study published in late 2013 corroborate this. The investigators reported on a large group of older individuals who were followed for 17 years. Those with the highest levels of inflammatory blood markers were over 3 times as likely to suffer sudden cardiac death as those with the lowest levels.17
The recent CDC report did not factor in chronic inflammation as an “avoidable” cause of vascular-related death.1 That’s just one reason why the CDC’s number of avoidable deaths is an underestimate of how many lives could be spared.
It’s comforting to live in an era where chronic inflammation can be identified with blood tests and corrective actions taken to suppress elevated inflammatory markers.
Why Is Atherosclerosis So Common?
We know that excess dietary intake of the wrong kinds of fats and sugars damages our arterial lining, as does tobacco smoke.18-23 Overlooked is the continuous toxic exposure arteries bear to cellular waste products that are released into our bloodstream for filtration and excretion primarily through the kidneys.24
Most of us are born with a flawlessly intact endothelium that lines our arteries and protects against formation of atherosclerosis. As we age, our arterial lining endures chronic insult from internal and external factors that results in loss of blood flow to the heart, kidneys, and brain. This is the leading reason why most aging people today become disabled and then prematurely die.
Those who understand the many causes of atherosclerosis should not be surprised it is so common. What’s appalling is the number of people who continue to succumb to atherosclerotic diseases because of widespread physician apathy and ignorance.
Endothelial Dysfunction: The Villain Behind Atherosclerosis
Multiple culprits initiate and promote atherosclerosis. They share in common an ability to damage the delicate endothelium that lines our vascular systems.25
An early step in the initiation of atherosclerosis is often reduced nitric oxide bioavailability that initiates endothelial dysfunction.26 Aging results in further impairment in the ability to synthesize endothelial nitric oxide that markedly accelerates atherosclerosis.27,28
We are grateful to the many scientists who have conducted research showing that consumption of plant polyphenol concentrates (such as those found in pomegranate,29-31 green tea,32-34 and red grapes)35-39 protect nitric oxide production, thus helping to restore youthful function and structure to our endothelial arterial linings.
It is somewhat contradictory, however, for one to gobble down capsule concentrates of pomegranate, green tea, berries, and grapes and then ignore other proven factors that silently destroy endothelial function.
Elevated glucose,40-42 insulin,43-45 triglycerides,46,47 LDL,48-50 homocysteine,51-53 C-reactive protein,54-56 oxidative stress,57-59 along with low HDL60-62 and low testosterone63,64 (in men) inflict their own unique forms of endothelial damage. It is thus critical to have one’s blood tested annually to ensure that none of these destroyers of endothelial integrity get out of safe ranges.
Vascular Toxicity Of Homocysteine
Elevated homocysteine has been linked to atherosclerosis via several toxic mechanisms.65-69 A few years ago, some studies questioned whether modestly-elevated homocysteine was really a health concern. Life Extension has published extensive information on the dangers of homocysteine as well as rebuttals to studies that the media portrayed in a highly misleading way.70-74
There is now a controversy in the mainstream as to what blood level of homocysteine really poses a vascular disease risk. Children who have a genetic defect that causes extremely high homocysteine levels show signs of impaired endothelial function as early as age 4.75
The question is what blood level of homocysteine should typical aging people strive for. The mainstream defines elevated homocysteine (called hyperhomocysteinemia) as greater than 15 micromoles per liter of blood.76 Other studies suggest that keeping homocysteine far below 15 is advisable.76
High homocysteine is associated with increasing age, consumption of animal protein, smoking, postmenopausal state, sedentary lifestyle, decreased kidney function, deficiencies of B-vitamins or with certain genetic abnormalities.77-83
Failure to test homocysteine blood levels can leave one vulnerable to silent vascular damage and increased dementia risks.76
When one understands the mechanisms by which homocysteine inflicts cellular damage, the importance of keeping it in lower ranges becomes abundantly clear.
Homocysteine Damages The Brain
Solid evidence connects the reduced cerebral blood flow with higher Alzheimer’s risk as well as its rapid progression.84-86
A study published in 2013 showed that people with homocysteine levels of 25.5 micromoles/L and higher were almost 4 times as likely to have severe shrinkage of the brain’s temporal lobe and had almost 5 times the risk for a severe brain white matter abnormality.87 This brain damage places people at increased risk of stroke, dementia, and death.88 This study is corroborated by previous studies showing brain benefits when B-vitamins are used to suppress homocysteine.89
The devastating impact that elevated homocysteine has on the brain alone should motivate maturing individuals to check their homocysteine blood level and take appropriate actions to suppress it if elevated.
Fortunately, most people can reduce elevated homocysteine levels by ensuring proper intake of folic acid, vitamin B12, and vitamin B6.90-92
A fatal assumption we have observed in people taking multivitamins is they assume their homocysteine levels are being adequately suppressed. Only a blood test can verify that homocysteine levels are in the safe ranges.
Some individuals, for instance, don’t absorb vitamin B12 well and require a sublingual or injectable route of administration. Others need to take extra vitamin B6 or the more metabolically active L-methylfolate form of folic acid to effectively suppress elevated homocysteine.