October 13, 2003
Remember last month? Clint Eastwood and his character, The Man With No Name from the movie The Good, The Bad and the Ugly, demonstrated to us the importance of fluid balance in the body. If you missed that column or youd like to review it first you can do so here. This month The Man With No Name has more to teach us as we read in Life on Earth is not for the Faint-Hearted (So how is it that we can stand up to gravity?).
Lets return to our hero, played by Clint Eastwood, in the movie, The Good, The Bad and The Ugly. He is weaving and staggering under the physical strain of heat prostration and dehydration as he is forced to trudge through the desert. Just when he is about to be put out of his misery by a bullet to the head, a black stagecoach appears on the horizon. Several scenes later, after our hero has learned the secret whereabouts of buried treasure, he conveniently faints, thereby preventing his torturer from further interrogating him.
Is this another example of Hollywood pointing a finger of affirmation toward the intelligent design of life? Well, yes and no. Yes; if one is inclined to try to understand how it is that the body is capable of standing up against gravity in order to be able to faint when things inside just dont work right. And, No; if one is not interested in how the body actually works and is happy to accept and trust the conclusions made by others. Are you ready to test what you believe to be true about macroevolution? Then read on my friend.
Quite simply, one faints when ones blood pressure drops so low that not enough blood is going to the brain. There are many mechanisms in the body that are involved in maintaining an adequate blood pressure and blood flow to the tissues. As you may have guessed by now, the bodys ability to stand up against gravity is more complicated than just considering its bones and muscles. One must have enough blood coursing through the vital organs of the body in order to provide them with water, nutrients and oxygen to allow them to function properly. The blood pressure, which is a measure of the force that the blood exerts against the arterial wall, plays a significant role in our survival. How do we know this to be true? In one word: SHOCK.
No, not the shock that you see portrayed in movies when someone faints or is in a catatonic state due to a sudden emotional or psychological insult. I mean circulatory shock or collapse, which is a medical emergency in which the body is not able to adequately supply the tissues with enough nutrients and oxygen to meet their metabolic needs. There are many signs that we see when someone goes into circulatory shock, but one of the commonest is a severe drop in blood pressure. And why is it such an emergency? In two words: irreversible damage, leading to certain death.
There are basically three fundamental components of the circulatory system: the circulating blood volume, the pumping action of the heart, and the vascular system which consists of the arteries, veins and the microcirculation which involves the arterioles, the capillaries and the venules. The arterioles and venules have small muscles around them that contract and relax to different degrees in order to control the flow of blood in the tissues. More to the point, if the arterioles did not provide some resistance to blood flow, then the blood pumped by the heart would freely enter the microcirculation and overwhelm the capillaries while at the same time severely diminishing the effective blood volume and lowering the blood pressure.
A breakdown in function of any of these three fundamental components can result in circulatory shock and death. For example, the blood volume can be seriously compromised if someone starts bleeding from an internal injury, such as from a car accident or from recurrent vomiting and diarrhea without adequate rehydration. The pumping action of the heart may be significantly reduced or even totally ineffective if someone has a heart attack, which causes damage and weakens the heart muscle, and then suffers a cardiac arrest. Lastly, there are many conditions, particularly septic shock from severe infection, that can cause the microcirculation to malfunction by dilating and allowing blood to pool within tissues and thereby be lost to the circulation which results in irreversible shock and death.
The body has many different ways of monitoring and controlling all three of these vital components of the circulatory system so that we may stay alive. It does this moment to moment and without us having to worry about it. When was the last time you checked if you had enough blood in your circulation, if your heart was pumping well enough, or your peripheral vascular resistance was up to snuff?
Having too low of a blood pressure can be life-threatening as weve just stated above. But what about high blood pressure? Im sure that many of you are familiar with it being a risk factor for stroke, heart disease and kidney failure. By investigating the various causes and thereby developing treatments for hypertension, modern medicine has stumbled upon one of the most important of these blood pressure/blood flow monitoring systems which Id like to briefly tell you about this month. Its called the renin-angiotensin system or RAS as its referred to in the business. Now dont be frightened by all of these fancy scientific names. By the time you finish this column, youll have a pretty good understanding of how all of this works to keep you alive and I suspect that youll be scratching your head as to how it could have all developed simply by the random forces of nature.
Say hello to the hormone called, angiotensin II, the strongest known arteriolar muscle tightener known to the body. Its constricting action is about five times stronger than adrenaline, the stuff youll often see injected into dying patients when youre watching a medical scene in the movies or on television. Angiotensin II also has the ability to stimulate the adrenal gland to produce and secrete another hormone that will make the kidney hold onto more water and sodium. So you can see that when angiotensin II is on the job, it is directly affecting two of the three fundamental components that maintain the bodys circulation. Its vasoconstrictor activity affects the peripheral downstream resistance applied by arterioles to increase the blood pressure, and its ability to positively affect sodium and water retention directly affects the blood volume. Lets look at where angiotensin II comes from and how the body controls its production.
In order for angiotensin II to be produced, the body requires the services of the liver, the kidneys, the lungs and the circulation. The liver produces an inactive protein called angiotensinogen, which floats around in the bloodstream doing absolutely nothing. But dont give up yet, the bodys got it all figured out already (see Figure 1).
The kidney contains specialized cells which are located near where it starts the filtering process on the way to forming urine, that are sensitive to the pressure of blood flow. These specialized cells secrete a hormone called renin at a rate that is inversely proportional to the blood flow that they detect. So if the blood flow is very low they will secrete more renin and if it is adequate they will reduce the flow to maintenance levels and if the flow is above what is necessary, they will reduce the production and secretion of renin. OK so far? Then lets continue.
Now comes the interesting part. Remember that apparently useless protein called angiotensinogen that is produced in the liver? Well, when it comes in contact with renin it is chemically converted into another protein called angiotensin I which is also inactive in the body. Close but no cigar! How do we eventually get the vasoactive hormone called angiotensin II ?
The cells that line the blood vessels in the lungs secrete a protein called angiotensin converting enzyme, which when it acts on angiotensin I that is floating in the circulation, chemically converts it to angiotensin II. And voila, we now have the most powerful arteriolar muscle tightener in the body. A chemical messenger that is vital for maintaining the blood pressure and thereby allowing the circulation to meet the bodys metabolic needs.
But the story doesnt end there. For the muscles surrounding the arterioles and the adrenal cells cannot be affected by the angiotensin II molecule unless their cell membranes contain angiotensin II receptors where the hormone locks on and causes the desired effect. The system works much like what you may have seen in the movie True Lies where Arnold Schwarzeneggers character has his right handprint and right retina analyzed to verify his identity. The arteriolar muscle cell and the adrenal cell wont play with strangers!
But remember, that in order for the body to be able to adequately control each vital function, once it turns on a switch it needs to be able to turn it off as well. Otherwise, the reactions set in motion by a given amount of angiotensin II could result in marked elevations in blood pressure and sodium retention. The combined actions of renin and angiotensin converting enzyme on angiotensinogen and angiotensin I, respectively as they travel in the circulation results in the turning on of the switch. What turns it off?
In fact, the effects of angiotensin II are short-lived because there are many other proteins contained in the tissues and red blood cells that are able to chemically break it down so that a given amount in the circulation is only effective for about ten minutes. These proteins, that are enzymes, are collectively known as angiotensinases.
Now when you consider all of the components that are necessary for the RAS to work, it seems to me that the NeoDarwinian mechanics of macroevolution just dont stand up to scrutiny. Lets look at what macroevolutionists must scientifically be able to prove here before anyone should even consider macroevolution as a truth of science.
There are six major factors at play here:
As a scientist, I believe that those who promote and teach macroevolution as a well-proven theory must explain the development of each and every one of the proteins involved in this system. But its not sufficient to only explain how they each came into being. One must also explain how this system could have been functional absent any combination of the above vital components; for that is how macroevolutionary mechanics works, one step at a time over many generations. For if the body were not able to properly control its blood pressure and blood volume, then theres no use in discussing further generations because the body would not be able to survive.
Based on the current understanding of human physiology and the pathological processes that undermine bodily function, we have ample clinical evidence of what happens when one or more of these vital components for our survival are compromised, never mind being totally absent. One need only theorize on how the system one step beforehand worked and then continue the process backwards in order to confirm macroevolutions thesis.
Any discrepancy between known data and a given theory is sufficient to undermine that theorys validity no matter what has supported it in the past. It must either be abandoned or amended to fit the data. This is much akin to how Copernicus improved upon Ptolemy and Kepler improved upon Copernicus when considering astronomical data. Or how Newton improved upon Aristotle and Einstein improved upon Newton regarding physics. ID may be an alternate theory to macroevolution. But one has to let go of the currently held theory of macroevolution before one can even begin to consider any other alternative.
Now here are some examples of questions that I think need to be answered before anyone should be embracing macroevolution as a well-proven theory.
Maybe you can come up with some answers or further questions on this subject. Let me know, Id like to hear from you. Why not post me a message at the ARN Discussion Forum? I cant promise to respond to every message but I will attempt to read them all.
Critics who have written to me so far have helped make me organize my thoughts better on this issue and I thank them for their efforts.
Taking into account my knowledge of how the human body works, it is my humble opinion that these questions are indeed unanswerable. In addition, it is my opinion that it is more difficult to believe that these complex, interdependent systems could have developed by random chance than it is to believe that they have come about by intelligent design. One critic commented that IDists have a vested interest in proving ICness. Having been on both sides of the fence at one time or another, I think that the same could be sincerely said of macroevolutionists regarding their theory as well. Finally, what will constitute proof to any one individual of the impossibility of a given event other than the intellect and beliefs of that one individual? Intelligence is often in the mind of the beholder! And by the way, so is the lack of intelligence!!
The next two columns are going to touch on a subject and substance that is very important to paleontologists. Does the fact that similar species having similar bone structure prove the theory of macroevolution? Not quite when you consider how those bones were actually formed by those bodies. One might similarly ask if the fact that bicycles and motorcycles being very similar in structure proves that they came into existence by the random forces of nature? I think youll find the study a fascinating one that should leave you with questions you can ask your science educators to answer in order to verify the validity of macroevolution.
Dr. G.
Howard Glicksman M.D. graduated from the University of Toronto in 1978. He practiced primary care medicine for almost 25 yrs in Oakville, Ontario and Spring Hill, Florida. He recently left his private practice and has started to practice palliative medicine for a Hospice organization in his community. He has a special interest in how the ethos of our culture has been influenced by modern sciences understanding and promotion of what it means to be a human being.
Copyright 2003 Dr. Howard Glicksman. All rights reserved. International
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File Date: 10.13.03