Autopsies performed in the late 18th Century on patients who had died of heart attacks revealed “fatty streaks and deposits in the arteries that led to the heart [coronary arteries]” (text, pg. 19-2). Physicians performing the autopsies hypothesized that dietary intake of fats may have contributed to the fatty deposits, and eventually to the heart attack. This hypothesis has been well supported by subsequent research, and now it is considered to be clearly established that diets rich in some fats are a major risk factor in heart disease. Among other observations, in the recent past, the American diet was higher in red meat (and the fats in red meat) than in most other civilized countries, and American men had a higher risk of heart disease than did men in other countries. Then, in an unintended research protocol, we exported the “American diet” to Europe and Asia. As could have been (but was not) predicted, the incidence of heart disease rose among men in those countries as well. Even more recently, as we learned that women suffering heart attacks present with different symptoms than men, we have found that red meat fats increase the heart disease risks in all Humans. The opposite effect has also been observed; patients who have reduced their intake of fats from red meat exhibit a reduction in their risk of heart disease. With deaths attributed to heart disease accounting for 25% of all deaths attributed to disease processes [as opposed to deaths attribuable to accidents, crimes and wars], the role of diet in heart disease has become a major issue for Nutritionists.
Of the six major risk factors contributing to heart disease, five are life style
choices which can be modified, often by something as simple as education. Roughly in order of their
importance as risk factors, these are as follows:
risk factors
1. diet, especially fats
2. lack of exercise
3. obesity
4. smoking
5. hypertension
6. family history
The role of diet [defined as“Food actually
consumed on a regular basis”] as a risk factor in heart disease
is actually two separate issues. The more familiar issue is that diets high in saturated fats,
cholesterol, and omega-9 fatty acids increase the risk of heart disease. The less well known issue
is that diets rich in “poly-”unsaturated fats [more accurately omega-3 and omega-6 fatty
acids] reduce the risk of heart disease (and may “reverse” the damage caused by the
saturated and omega-9 fatty acids). Even less well known outside of Nutrition Science is that dietary
cholesterol is not an issue [although most Nutritionists still encourage reducing cholesterol, since
this will generally reduce saturated and omega-9 fatty acids as well]. As you are supposed to
remember from the lecture on Lipids, saturated and omega-9 fatty acids increase LDL (Low Density
Lipoproteins, or L for Lousy cholesterol which plaques out on arteries well); and omega-3
and omeaga-6 fatty acids increase HDL (High Density Lipoproteins, or H for Healthy
cholesterol which appears to dissolve arterial fatty plaque deposits) while decreasing LDL. Red
meats (pork, beef, …) are high density sources of LDL-producing fatty acids. Many vegetable oils
[except corn oil] are good sources of HDL-producing fatty acids, as are white fish [white fish flake
when cooked properly, non-white fish don't flake no matter how you cook them (even if they are quite
tasty as Cajun-style blackened fish)].
Exercise [defined as “Intentional physical
activity”] at any level above sedentary makes each muscle that is exercised stronger, and all
exercise exercises the heart muscles. This is part of the rationale for my suggestions that one
should always park farther from the door than is necessary, and that the best way to deal with
“drive-through” fast-food is to avoid it at every opportunity. It is far better to park
(farther than needed), walk in, order, sit down to eat, then walk back to the car.
This will provide minimal exercise and will be more relaxing than eating on-the-go, thereby reducing
stress (which may be a factor in heart attack risk in “Type-A personalities,” but is
probably not a factor in heart disease [that means at any given risk level for heart disease, the
timing of the heart attack depends on stress levels even if the risk level itself does not]).
Obesity, whether diagnosed or not diagnosed (although
diagnosable) contributes substantially to heart disease risk. It is the “belly fat,”
indicitive of internal (abdominal fat) that carries the highest risk because it is the best
predictor
of pericardial fat deposits [the only better estimator is the autopsy, but you probably are willing
to wait a few decades for that procedure]. If you think about advising patients on how to
reduce their heart disease risk by reducing their over-weight condition, what would you suggest? By
now, in this course, I hope you are thinking (a) reduce the dietary intake of those calories easily
converted to adipose (carbohydrate and lipid calories), and (b) increase exercise. The intervention
for the over-weight condition will also improve serum LDLs and strengthen the cardiac muscles. It
is
a win-win situation!
Smoking, for those patients who still smoke, is a high
risk activity for death due to your choice of causes: heart disease, COPD, cancer, …
Unfortunately as I understand smoking cessation programs, the one factor which will determine the
success or failure of the intervention is the smoker's interest in quitting. No one has ever been
known to quit smoking if they did not really want to, unless you consider death to be the ultimate
smoking cessation program. If you want to “nag” your smoking patients, go ahead as long
as you don't delude yourself into believing that they are planning to be compliant, or even
listening to your advice.
Hypertension, also known as elevated blood pressure, is
a medical condition the treatment of which continues for the remainder of the patient's life. Most
authors consider this to be one of the “life style choices” which the patient can
control,
but I disagree. The motivated patient can manage the life style choices which increase the
risk of hypertension, but for most hypertensive patients it is already too late to recover by life
style choices once they have been diagnosed as hypertensive.
One risk factor for heart disease over which the patient has absolutely no
control is family history. For assessing risks of death, the only
members of your family tree that count are direct ancestors and their siblings. Your first cousins
have one parent who is not “on your family tree,” and do not count because they
have some genetic information which you can't have. Your biological siblings do count, since they
have the same parents as you; your biological parents and their biological siblings count since
they
all have your grandparents as their parents. And so forth… [your fifth cousins are almost as
unrelated to you as are your next door neighbors]. Now that you know who is on the family tree, you
can make a rough guess concerning the age at which you can expect to die, and if you live that
long,
what natural causes could cause your death. You also need to know that this information and $1.50
will
not buy a cup of coffee at Starbucks™ it will not be until after you die that we can guess
accurately when and how you died.
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revised: 02 Oct 2009