Policosanol for Healthy Arteries
Atherosclerosis Can Rob You of Memory
Diseased arteries cause cognitive impairment
that can lead to vascular dementia
By Will Block
f you’ve ever seen the inside of an old, corroded drain pipe, partially clogged with scale and other gunk of indeterminate origin (you probably don’t want to know what that stuff is), you have some idea of what atherosclerosis looks like: not a pretty sight. The trouble is—and this applies equally to drain pipes and arteries—what’s out of sight is usually out of mind. Therein lies a bizarre irony when it comes to your arteries, namely, your very mind may be at risk from the out-of-sight stuff. The stuff we’re talking about is, of course, atherosclerotic plaque.
The risk is for impairment of memory and other cognitive functions, which depend critically on an adequate blood supply to the brain. When plaque deposits accumulate in your carotid arteries or in any other arteries that nourish your brain, blood flow is diminished. The result can be anything from mild cognitive impairment to full-blown dementia, especially vascular dementia, which, as the name implies, is dementia of vascular (blood-vessel) origin. The result can also be stroke, for which atherosclerosis is a major risk factor. And stroke is itself a major cause of vascular dementia.
Brain Plaque—A Very Bad Idea
No offense, but your brain is an energy hog, the biological equivalent of a gas-guzzling Hummer. Ounce for ounce, it burns more energy than your hard-working muscles. Although at 3 pounds it constitutes only about 2% of your body weight (assuming you’re of average size), it demands about 20% of your energy intake, primarily in the form of glucose and oxygen. And that means that it requires about 20% of your blood supply, which carries those nutrients to every cell of your body. Obviously, allowing plaque to build up in the arteries that supply this quintessentially vital organ is a very bad idea.
No offense, but your brain is an
energy hog, the biological equivalent
of a gas-guzzling Hummer. Ounce for
ounce, it burns more energy than
your hard-working muscles.
Not that anyone does it deliberately, of course—it just happens, mainly as a result of excessive eating and inadequate exercise, the hallmarks of the modern American lifestyle. When these conditions prevail, your bloodstream carries too much LDL-cholesterol (“bad cholesterol”), which contributes to plaque buildup, and too little HDL-cholesterol (“good cholesterol”), the vehicle by which excess cholesterol is removed from the blood. The idea, then, is to minimize LDL-cholesterol and maximize HDL-cholesterol. (Because there’s much more of the former than of the latter, reducing LDL-cholesterol by any given percentage usually has the effect of reducing total cholesterol too, unless HDL-cholesterol is going up by a much larger percentage, thereby offsetting the reduction.) It’s also important to keep your triglycerides (fats) under control.
Why Are You Depressed?
Anyway, let’s say you don’t have atherosclerosis, and you know you don’t have it. That should make you happy, right? And we’re happy for you. Keep up the good lifestyle! But what if, like millions of other aging Americans, you do have atherosclerosis? You have our sympathy, of course, but we both know that that isn’t worth the paper these words are printed on. You need to do something about it—that could be worth a great deal for your future health and happiness.
Meanwhile, perhaps you’re depressed. But is your depression caused by your knowing that you have atherosclerosis, or is it, perhaps, caused by the atherosclerosis itself? Inquiring minds (of medical researchers) want to know. It’s not easy, however, to untangle the symptoms of depression, as a condition caused by atherosclerosis, from depressive symptoms caused by thinking and worrying about having atherosclerosis.
Oh, What a Tangled Web …
To further complicate the problem, what if you’ve been led to believe (rightly or wrongly) the premise that people who know they have atherosclerosis are likely to suffer depression as a result—and you succumb to depression? Did you succumb because you thought you “should,” or would you have succumbed anyway? If you had not been led to believe the premise, perhaps you would not have succumbed, even though you knew you had atherosclerosis.
The number of cardiovascular
pathologies is related to the
severity of atherosclerosis,
measured as carotid-artery wall
thickness and arterial stiffness.
See how tricky this is? The power of mind over matter—or, in this case, perhaps, the power of one aspect of mind over another aspect of mind—can confound the best efforts of researchers to figure out true causes and effects. And that, of course, impairs the ability of healthcare providers to give their patients the best possible treatment for what ails them.
… But Scientists Keep Trying
The medical literature contains studies suggesting that atherosclerosis causes both cognitive impairment and depression in old age. Among other things, a thickening of arterial walls and the presence of atherosclerotic plaques in the carotid arteries have been associated with an increased risk for dementia and depression. But because the signs and symptoms of cognitive decline in old age can be difficult to distinguish from those of depression, researchers have had a hard time deciding whether these two conditions are: (1) different outcomes of the same disease process; (2) different diseases that have the same risk factors; (3) different diseases, one or both of which can cause the other; or (4) different but unrelated diseases that often occur together.
Again we’re faced with questions that have no easy answers. Scientists keep trying to penetrate these mysteries, however, and one of their latest efforts was the “Leiden 85-Plus Study,” a 5-year-long evaluation of the health of elderly citizens of the city of Leiden, the Netherlands. The Dutch researchers recruited 599 men and women aged 85, and they monitored their health for the next 5 years (through age 90). At the outset of the study (the baseline), the researchers evaluated the subjects’ status with regard to atherosclerosis and history of stroke. Their objective was to assess the impact of these aspects of the subjects’ health on the development or progress of cognitive impairment and depression.
More Severe Atherosclerosis = More Cardiovascular Consequences
The level of burden imposed by atherosclerosis in each individual was rated by the number of cardiovascular pathologies, past or current, recorded at baseline. These included: myocardial infarction (heart attack); angina pectoris or myocardial ischemia (inadequate blood flow to the heart muscle via the coronary arteries); intermittent claudication (pain upon walking, owing to poor circulation in the legs); and arterial surgery for any reason.
The rationale for using the number of cardiovascular pathologies as a measure of atherosclerotic burden on the individual’s health was found in a previous study showing that this number is related to the severity of atherosclerosis, measured as carotid-artery wall thickness and arterial stiffness. In other words, the worse the atherosclerosis, the greater the number, on average, of serious cardiovascular consequences—which stands to reason. In the Leiden study, the median number of cardiovascular pathologies at baseline was one: 40% of the subjects had none, and 60% had one or more.* In addition, 10% of the subjects had a history of one or more strokes.
It’s Just a Little Nick …
What actually happens when your arteries become clogged? The key factor, initially, is not excessive cholesterol levels, but the occurrence of tiny nicks in the linings of your arteries, which consist of smooth, flat, tightly packed epithelial cells. If such defects occur in your Teflon-like arterial walls, they act as nucleation sites for the accumulation of materials—blood platelets, cholesterol, other lipids, cellular debris, calcium deposits, etc.—that gradually develop into atherosclerotic plaques. These, in turn, act as sites where blood clots can form—a perilous complication.
The delicate, one-cell-thick inner lining of our arteries is easily damaged, but such damage is largely preventable.
But what causes the nicks? Hypertension can damage the epithelial cells, causing them to pull away from one another and form gaps. Another cause is excessive glucose (blood sugar), which can also damage the cells. Also implicated are chronic inflammation caused by factors as diverse as periodontal disease, sexually transmitted diseases, anger, and stress. Note that all these factors are either preventable or controllable, which means that, by and large, atherosclerosis is too.
Toxins can also wreak havoc in your arteries. Among the worst are nicotine and the amino acid homocysteine, both of which belong in the physiological Hall of Infamy. Avoiding nicotine is easy: don’t smoke. But homocysteine is a natural product of protein metabolism, so we must deal with it constantly. As long as its levels are held in check by natural physiological processes, it poses no great risk.
As we age, however, these processes gradually fail, and homocysteine levels rise. If they become too high, they can lead to an ungodly variety of damage, including the injury, inflammation, and even death of epithelial cells, and the formation of life-threatening blood clots. (For more on this subject, see
“Fight Alzheimer’s and Heart Disease with B-Vitamins” and
“Folic Acid to the Rescue!” in the December 2001 and September 2002 issues, respectively; see also the
article on page 19 of this issue.)
That last sentence gives away the rest of the story, which is that the B-vitamin folic acid (it doesn’t have a number) is our knight in shining armor where homocysteine is concerned. Folic acid (also called folate) suppresses homocysteine very effectively and thus protects us from its ravages. In this noble task, its indispensable chemical ally is vitamin B12. These two vitamins should always be taken together, because too much of one can mask a deficiency in the other.
How to Test for Cognitive Impairment and Depression
The term cardiovascular refers to the heart and the general circulation, part of which serves the brain. That part is called the cerebrovascular system, and it’s there that atherosclerosis has the potential for causing dementia and, perhaps, depression. Although the methods are far from exact, various standardized neuropsychological tests and questionnaires can be used to measure the severity of these conditions. For example, one of the most widely used tests of cognitive function is the Mini-Mental State Examination (MMSE), which assesses global cognitive functioning. In addition to the MMSE, the Dutch researchers used four other tests of a more specific nature to assess attention, processing speed, immediate recall, and delayed recall. Together, these five tests have proved to be useful in detecting small differences in cognitive function in elderly people.
Depression can be assessed with the 15-item Geriatric Depression Scale (GDS-15), a questionnaire developed as a screening instrument for depressive symptoms in elderly populations. Because the responses of individuals with serious cognitive impairment cannot be considered reliable or valid, however, the Leiden researchers did not administer the GDS-15 to subjects whose MMSE score was below 19 points (out of a possible 30). The median MMSE score at baseline in the Leiden study was 26, indicating a mild level of cognitive impairment. The median GDS-15 score was 2 (out of a possible 15), which is considered normal.
Atherosclerosis Correlated with Cognitive Decline
Not surprisingly, the researchers found that both atherosclerosis and a history of stroke at baseline in the Leiden study were significantly correlated with impairments in cognitive function. For depression, however, there was a significant correlation with stroke but not with atherosclerosis.
“… in old age, generalized athero-
sclerosis is related to cognitive
decline … Accumulating evidence
emerges that generalized athero-
sclerosis plays a pivotal role in
the etiology of dementia.”
During the 5-year follow-up period, all five measures of cognitive function declined significantly, and atherosclerosis was statistically associated with accelerated decline in the two tests of memory function: immediate recall and delayed recall. At baseline, the level of cognitive impairment had correlated with the number of cardiovascular pathologies, and during the follow-up period, the rate of further cognitive decline continued to show this correlation. The authors stated,
This prospective population-based study shows that in old age, generalized atherosclerosis is related to cognitive decline, especially to decline of memory function. … Accumulating evidence emerges that generalized atherosclerosis plays a pivotal role in the etiology of dementia. Perhaps the strongest argument is that treatment of risk factors for atherosclerosis, such as hypertension, may prevent dementia, although this has not been shown unequivocally.
What Do You Think?
In 1637 the great French philosopher and mathematician René Descartes famously wrote, “I think, therefore I am.” From this intriguing premise he built an intellectual edifice so imposing that he is sometimes called the father of modern philosophy. His wide-ranging interests included physiology, and he helped to popularize the still new, revolutionary, and hotly disputed theory regarding the mechanism and function of blood circulation, propounded in 1628 by the English physician William Harvey, who is now regarded as the father of modern physiology.
If either of those worthies had been able to see what the insides of the arteries of a typical older American of today would look like, they would probably have been appalled. One can only wonder whether it might have occurred to Descartes that the damage he was seeing could very well impair the person’s ability to think and, therefore, to be.
Policosanol Is an Atherosclerosis Fighter
Another risk factor for atherosclerosis, of course, is high cholesterol levels, which can be treated safely and effectively (and relatively inexpensively) with natural supplements, such as policosanol and niacin (vitamin B3). Policosanol, derived from sugar cane, has been found in numerous studies to rival—and sometimes exceed—the statin drugs in its ability to reduce total cholesterol and LDL-cholesterol levels, as well as triglycerides, while substantially increasing HDL-cholesterol levels. It has been the subject of many articles in this magazine. A companion
article in this issue (see page 9) describes research showing that, in addition to improving cholesterol and triglyceride levels, policosanol may be able to bring about functional regression of atherosclerosis in the carotid and vertebral arteries, which nourish the brain.
Atherosclerosis Did Not Correlate with Depression
Getting back to the Leiden study—during the same 5-year follow-up period, depressive symptoms increased significantly, but there was no statistically significant association between these symptoms and atherosclerosis. This result was somewhat surprising in light of general expectations that such an association would be found (as some previous studies had suggested). The authors’ speculations regarding the reasons for this finding are too involved for discussion here; suffice it to say that one more piece of a complex puzzle has been put in place, but a clear picture has yet to emerge.
Your Brain Certainly Deserves TLC
Although definitive results are common in research in the physical sciences, they are uncommon in the biological sciences, and rare in medicine. What we can say for certain, however, is that impaired blood circulation to the brain is harmful to the brain and, therefore, to its manifestation in that most splendid of natural phenomena, the mind. To preserve your ability to have thought, perception, emotion, will, memory, and imagination, give your brain the tender loving care it so richly deserves.
- Vinkers DJ, Stek ML, van der Mast RC, de Craen AJM, Le Cessie S, Jolles J, Westendorp RGJ, Gussekloo J. Generalized atherosclerosis, cognitive decline, and depressive symptoms in old age. Neurology 2005;65:107-12.
- Simons PCG, Algra A, Bots ML, Grobbee DE, van der Graaf Y. Common carotid intima-media thickness and arterial stiffness. Circulation 1999;100:951-7.
- Houx PJ, Shepherd J, Blauw GJ, et al. Testing cognitive function in elderly populations: the PROSPER Study. J Neurol Neurosurg Psychiatry 2002;73:385-9.
Will Block is the publisher and editorial director of Life Enhancement magazine.