Namibia to the defence of religious liberty

Namibia Supreme Court Upholds Patients’ Rights and Religious Freedom:


The Supreme Court of Namibia has ruled to protect a patient’s right to bodily self-determination and personal autonomy in making treatment decisions. The Court also recognized the validity of a written advance directive informing health-care providers of the patient’s treatment wishes.

Childbirth and a Medical Emergency
The legal case before the Court concerned the health of Efigenia Semente, one of Jehovah’s Witnesses. In preparation for the birth of her third child, Mrs. Semente informed her physician that she would not accept blood transfusions because of her religious convictions. She also gave him an advance medical directive in the form of a durable power of attorney. In this document, Mrs. Semente expressed her unequivocal refusal of blood and designated her husband as her health-care agent to make decisions for her if she became incapacitated.

The physician safely delivered her daughter on September 8, 2012, but Mrs. Semente required postdelivery surgery. Her husband, as her health-care agent, consented. However, complications arose during the surgery, and the physician wished to administer a blood transfusion. Mr. Semente refused on his wife’s behalf, consistent with her advance medical directive. The doctor successfully operated without a blood transfusion, but Mrs. Semente came out of surgery with low hemoglobin levels.

High Court Intervention
On September 13, 2012, while Mrs. Semente was recovering from surgery, her eldest brother applied to the High Court of Namibia to be appointed as her legal curator so that he—instead of her husband—could direct her medical treatment. Although neither Mrs. Semente nor her husband received notice of her brother’s application, the court conducted a hearing in their absence and ordered her brother appointed as curator. Her brother thereafter directed the medical staff to transfuse Mrs. Semente against her will, but she repeated her refusal and resisted their efforts, thus preventing the transfusion.

When Mrs. Semente learned that the court had appointed her brother as her curator, she made an urgent application to the High Court to rescind the order. She argued that she was of sound mind when her brother applied for curatorship and that her brother’s authorization of a blood transfusion violated both her religious beliefs and her right to bodily self-determination. The court dismissed her application and allowed her brother to continue as her curator.

Although Mrs. Semente’s doctor testified that she would die without a transfusion, her condition improved with nonblood medical management, and she was discharged from the hospital on September 26, 2012, without being transfused. However, the High Court had appointed her brother as her curator indefinitely. Viewing the curatorship as a violation of her personal autonomy and basic human rights, Mrs. Semente appealed to the Supreme Court of Namibia.

“The facts of this matter concern some of [the] most essential human rights issues likely to arise in litigation. They relate to the right to bodily autonomy, the right to freely practice one’s religion, and the freedom from discrimination.”—Supreme Court of Namibia.
Supreme Court Judgment
On June 24, 2015, the Supreme Court of Namibia upheld Mrs. Semente’s fundamental rights and rescinded her brother’s curatorship. The Supreme Court condemned as “entirely inappropriate” the lack of notice to Mrs. Semente and her husband and the High Court’s one-sided hearing that appointed Mrs. Semente’s brother as her curator.

The Supreme Court highlighted that the Namibia Constitution guarantees personal liberty and human dignity as the basis of patient autonomy. The Court stated: “The principle of patient autonomy reflects that it is a basic human right for an individual to be able to assert control over his or her own body. . . . Medical practitioners must inform their patients about the material risks and benefits of the recommended treatment but it is up to the patient to decide whether to proceed with a particular course of treatment.”

“It is a basic human right for an individual to be able to assert control over his or her own body.”—Supreme Court of Namibia.
Ultimately, in reviewing Mrs. Semente’s competency to refuse blood transfusions, the Supreme Court concluded that the High Court gave insufficient weight to her durable power of attorney. The Supreme Court further stated: “Written advanced directives which are specific, not compromised by undue influence, and signed at a time when the patient has decisional capacity constitute clear evidence of a patient’s intentions regarding their medical treatment.”

The Supreme Court also addressed the question of whether a child’s right to be raised by her parents restricts her parents’ right to choose their medical treatment. After reviewing international case law, the Court concluded that “the right to choose what can and cannot be done to one’s body, whether one is a parent or not, is an inalienable human right.”


The Supreme Court of Namibia has strengthened the right to bodily self-determination and has recognized advance medical directives as evidence of a patient’s values and treatment choices. By upholding the rights to bodily integrity and religious freedom, the Supreme Court has protected basic human dignity and liberty for all Namibians.

The Watchtower Society's commentary on "patience"

LONG-SUFFERING:
The patient endurance of wrong or provocation, combined with a refusal to give up hope for improvement in the disturbed relationship. Long-suffering therefore has a purpose, looking particularly to the welfare of the one causing the disagreeable situation. It does not mean the condoning of wrong, however. When the purpose for long-suffering is accomplished, or when there is no point in further putting up with the situation, long-suffering ends. It ends either with good to those giving provocation or with action against the wrongdoers. In any case the one exercising long-suffering is not harmed in spirit.

The literal meaning of the Hebrew expression translated “slow to anger” (“long-suffering” in some translations) is “length of nostrils [where anger flares up].” (Ex 34:6; Nu 14:18; see ANGER.) The Greek word ma·kro·thy·miʹa (long-suffering) literally means “longness of spirit.” (Ro 2:4, Int) Both the Hebrew and Greek expressions denote patience, forbearance, slowness to anger. The English word “suffering” in the word “long-suffering” has the sense of “putting up with, permitting, tolerating, holding up, or delaying.” “Long-suffering” means more than merely enduring pain or trouble. It does not mean merely “suffering long” but involves deliberate restraint.

The Scriptures reveal God’s evaluation of long-suffering and point out the foolishness and bad results of not maintaining “longness of spirit.” The long-suffering person may seem weak, but he actually is using discernment. “He that is slow to anger is abundant in discernment, but one that is impatient is exalting foolishness.” (Pr 14:29) Long-suffering is better than physical mightiness, and it will accomplish more. “He that is slow to anger is better than a mighty man, and he that is controlling his spirit than the one capturing a city.”—Pr 16:32.

The man who is not ‘long in spirit,’ but who bursts forth without restraint, is open to the invasion of any and all improper thoughts and actions, for: “As a city broken through, without a wall, is the man that has no restraint for his spirit.” (Pr 25:28) “All his spirit is what a stupid one lets out, but he that is wise keeps it calm to the last.” (Pr 29:11) For these reasons, the wise man counsels not to be ‘short in spirit’: “Do not hurry yourself in your spirit to become offended, for the taking of offense is what rests in the bosom of the stupid ones.”—Ec 7:9.

Jehovah’s Long-Suffering. When Jehovah took Moses up into Mount Horeb and showed him some of his glory, he declared before Moses: “Jehovah, Jehovah, a God merciful and gracious, slow to anger and abundant in loving-kindness and truth, preserving loving-kindness for thousands, pardoning error and transgression and sin, but by no means will he give exemption from punishment.” (Ex 34:5-7) This truth about Jehovah’s slowness to anger was repeated by Moses, David, Nahum, and others.—Nu 14:18; Ne 9:17; Ps 86:15; 103:8; Joe 2:13; Jon 4:2; Na 1:3.

While long-suffering is an attribute of Jehovah, it is always expressed in harmony with his primary attributes of love, justice, wisdom, and power. (1Jo 4:8; De 32:4; Pr 2:6; Ps 62:11; Isa 40:26, 29) Justice is due, first of all, to God’s own name. That name must be exalted above all others in the universe; and this is essential for the well-being of all his creatures. The magnifying of his name is one of his chief reasons for long-suffering, as the apostle Paul explains: “If, now, God, although having the will to demonstrate his wrath and to make his power known, tolerated with much long-suffering vessels of wrath made fit for destruction, in order that he might make known the riches of his glory upon vessels of mercy, which he prepared beforehand for glory, namely, us, whom he called not only from among Jews but also from among nations, what of it?” (Ro 9:22-24) God, in exercising long-suffering, is taking out a people for his name. And by means of them he is magnifying himself in all the earth.—Ac 15:14; 1Co 3:9, 16, 17; 2Co 6:16.

God exhibited his long-suffering in the very early part of man’s history. Rebellion of the first human couple had brought violation of his law. But instead of executing them immediately, as God could have justly done, in love he displayed long-suffering. This was for their as-yet-unborn descendants, to whom such long-suffering meant everything (his patience means salvation for many [2Pe 3:15]). More important, God also had in view the magnifying of his glory by means of the Seed of promise. (Ge 3:15; Joh 3:16; Ga 3:16) And God not only was long-suffering at that time but he knew that he would have to put up with imperfect mankind for several thousand years of history, delaying punishment against a world at enmity with him. (Jas 4:4) Some have misunderstood and misused God’s long-suffering toward them, missing its purpose by viewing it as slowness rather than as loving patience.—Ro 2:4; 2Pe 3:9.

Nowhere is the long-suffering of God more evident than in his dealings with the ancient nation of Israel. (Ro 10:21) Time and again he received them back after they had fallen away, were punished, and repented. They killed his prophets and finally his own Son. They fought the preaching of the good news by Jesus and his apostles. But God’s long-suffering was not wasted. There was a remnant that proved faithful. (Isa 6:8-13; Ro 9:27-29; 11:5) He used some of such faithful ones to write his Word under inspiration. (Ro 3:1, 2) The Law he gave showed that all mankind are sinners and need a redeemer, and it pointed to that One who would give his life as a ransom price and who would be exalted to the high position of King. (Ga 3:19, 24) Patterns of that Kingdom and of Christ’s priesthood were provided (Col 2:16, 17; Heb 10:1), and examples for us to follow or avoid were set forth. (1Co 10:11; Heb 6:12; Jas 5:10) All these things are essential to mankind for the gaining of everlasting life.—Ro 15:4; 2Ti 3:16, 17.

Jehovah not long-suffering forever. On the other hand, God is long-suffering only as long as it is in harmony with justice, righteousness, and wisdom. The fact that long-suffering is exercised when a bad or provocative situation exists shows that it is meant to give opportunity for those involved in the bad situation to change, to straighten up. When matters come to a point where it is seen that there is no hope of such change, justice and righteousness would be violated if long-suffering should continue. Then God acts in wisdom to remove the bad situation. His patience comes to an end.

An example of this forbearance on God’s part and of its coming to an end is found in God’s dealing with men before the Flood. A deplorable condition existed, and God said: “My spirit shall not act toward man indefinitely in that he is also flesh. Accordingly his days shall amount to a hundred and twenty years.” (Ge 6:3) Later, regarding Israel’s misuse of Jehovah’s long-suffering, Isaiah said: “But they themselves rebelled and made his holy spirit feel hurt. He now was changed into an enemy of theirs; he himself warred against them.”—Isa 63:10; compare Ac 7:51.

For these reasons Christians are entreated not to “accept the undeserved kindness of God and miss its purpose.” (2Co 6:1) They are counseled: “Do not be grieving [saddening] God’s holy spirit.” (Eph 4:30, Int) Also, “Do not put out the fire of the spirit.” (1Th 5:19) Otherwise they may continue to the point of sin and blasphemy against God’s spirit, in effect outraging it, in which case there is no repentance or forgiveness, only destruction.—Mt 12:31, 32; Heb 6:4-6; 10:26-31.

Jesus Christ. Jesus Christ exemplified long-suffering among humans. Of him, the prophet Isaiah wrote: “He was hard pressed, and he was letting himself be afflicted; yet he would not open his mouth. He was being brought just like a sheep to the slaughtering; and like a ewe that before her shearers has become mute, he also would not open his mouth.” (Isa 53:7) He put up with the weaknesses of his apostles and the insults and discourtesies heaped upon him by bitter, vicious enemies. Yet he did not retaliate in kind, by word or action. (Ro 15:3) When the apostle Peter acted injudiciously in cutting off the ear of Malchus, Jesus reproved him with the words: “Return your sword to its place, . . . do you think that I cannot appeal to my Father to supply me at this moment more than twelve legions of angels? In that case, how would the Scriptures be fulfilled that it must take place this way?”—Mt 26:51-54; Joh 18:10, 11.

Why is it important for Christians to cultivate long-suffering?

From the foregoing it is evident that long-suffering originates with Jehovah God. It is a fruit of his spirit. (Ga 5:22) Man, made in the image and likeness of God, has a measure of this quality and can develop it by following God’s Word and the direction of his holy spirit. (Ge 1:26, 27) Christians are therefore commanded to cultivate and display this quality. (Col 3:12) It is an identifying mark of a minister of God. (2Co 6:4-6) The apostle Paul says: “Be long-suffering toward all.” (1Th 5:14) He indicates that it is essential to exercise this quality in order to be pleasing to God. But one’s long-suffering is not genuine if it is accompanied by grumbling and complaining. Paul shows that the commendable thing is to “be long-suffering with joy.”—Col 1:9-12.

Aside from the joy that one gets through the practice of long-suffering, the rewards are great. Jehovah is rewarded by having his name glorified. The challenge against the righteousness and rightfulness of God’s sovereignty is proved wrong, and he is vindicated. (Ge 3:1-5; Job 1:7-11; 2:3-5) What if he had put Adam, Eve, and Satan to death at the time of the rebellion? Some might have concluded that Satan had a point in his challenge. But by long-suffering, Jehovah gave men the opportunity to prove under test that they prefer his sovereignty over them and that they want to serve him because of his fine qualities, yes, to demonstrate that they prefer Jehovah’s sovereignty to complete independence, knowing that it is far better.—Ps 84:10.

Jesus Christ, because of long-suffering in obedience to God, received a most marvelous reward, being exalted to the superior position of kingship and being given “the name that is above every other name,” by his Father. (Php 2:5-11) Besides this, he receives a “bride” made up of his spiritual brothers, the New Jerusalem, which is represented as a city, the foundation stones of which have on them the names of the 12 apostles of the Lamb.—2Co 11:2; Re 21:2, 9, 10, 14.


Likewise, the reward is rich for all persons cultivating long-suffering and maintaining it in harmony with God’s purpose. (Heb 6:11-15) They have the satisfaction of copying God’s quality, of doing God’s will, and of having God’s approval. Additionally, their long-suffering will bring accomplishment in helping others to know God and to gain everlasting life.—1Ti 4:16.

Lamarck's revenge III

Epigenetics, a Revolution with a Long Onramp, Poised to Accelerate Design Thinking
Some revolutions have long onramps. Modern epigenetics has been around for well over a decade, but its impact has yet to be fully explored. Which interpretation of biology -- evolution or intelligent design -- stands the best chance of advancing scientific understanding of genomics through epigenetics research?

Well, it is indeed a revolution; that's what senior reporter Heidi Ledford calls it in her Nature Outlook piece, "Epigenetics: the genome unwrapped." She ends with remarks by Tomasz Jurkowski, a biochemist and epigeneticist at the University of Stuttgart in Germany who is racing against other researchers to untangle DNA's secrets:

He takes the competition in stride -- it is the price of entry into the fast lane. Epigenetics is on the verge of a revolution, he says. "This is just the beginning," he says. With just a little more time, "It will develop into a completely new field." [Emphasis added.]

As with any field in such a revolutionary condition, the ultimate outcome is unpredictable. That's why Ledford's subtitle reads, "Epigeneticists are harnessing genome-editing technologies to tackle a central question hanging over the community -- does their field matter?"

There's reason to think it will matter -- a lot. Of the many epigenetic markers already identified, many have shown to affect an organism's phenotype. Some of them have been shown to be heritable, opening up new vistas of epigenetic inheritance. Now, with the updated CRISPR-Cas9 gene editing tool, despite its potential for ethical quandaries (see discoverer Jennifer Doudna in Nature worrying about the Pandora's box she opened), epigenetics researchers are pushing the accelerator pedal.

Ledford describes how CRISPR-Cas9 -- Science Magazine's 2015 "Breakthrough of the Year" -- has already allowed one research team to speed around another team that did things the old-fashioned way.

René Maehr, an immunologist at the University of Massachusetts Medical School in Worcester and his colleagues fused an enzyme called histone demethylase, which removes methyl groups from histones, to a deactivated Cas9 enzyme, and then programmed it to target regions of DNA believed to enhance the expression of certain genes. The result was a functional map of genetic 'enhancer' sequences that allows researchers to determine what these enhancers do, how strongly, and -- most importantly -- where they are located in the genome.

Question: Why were they seeking "to determine what these enhancers do"? Answer: They didn't believe they were junk. They watched the target gene increase its expression significantly. "That result started to convince me that the acetylation of histones may be a direct cause of gene activation." This suggests a new layer of specified complexity that supersedes the old Central Dogma that viewed DNA as the master controller. Functional mapping now steps up from genes to the epigenetic markers that regulate them.

Researchers don't know if all epigenetic marks have such dramatic effects. "For all we know, they might have very minor effects on gene expression except in a few special cases," a researcher at the Fred Hutchinson Cancer Center in Seattle opines. We may not have long to find out.

Now, however, researchers have a tool to pick apart the detail. Because of its simplicity and versatility, CRISPR-Cas9 opens up an opportunity to launch the kind of large-scale projects needed to reach that level of understanding. "If we want to target a region in the genome, we can have that targeting molecule here tomorrow for five dollars," says Reddy. "We're going to get to march through every single one of these modifications and figure out what they actually do."

You don't try to figure out what pieces of junk do. Whatever the outcome of the "ambitious projects" ahead, "the rapid pace of the field is already defying expectations," Ledford writes. Let's look at some other recent articles for clues.

Epigenetic markers may shed light on the long-standing mystery of the molecular basis for caste-specific behavior in ant colonies. (Science Magazine):

These findings reveal the epigenome as a likely substrate underlying caste-based division of labor in eusocial insects. Furthermore, in light of the conserved role of CBP in learning and memory in both invertebrates and mammals, these data suggest that CBP-mediated histone acetylation may similarly facilitate the complex social interactions found in vertebrate species.

Epigenetic markers affecting the immune system change with habitat, researchers found when comparing methylation marks on forest-dwelling African tribes with sedentary farmers. (Pasteur Institute):

These results partly explain why some people are predisposed to certain diseases. "Our research shows that changing lifestyles and habitats have a major influence on our epigenome and that urbanization significantly affects the epigenetic profiles of the immune system. This demonstrates how important it is, alongside more traditional genetic research, to investigate how epigenetic changes could result in an immune system that is more prone to the development of autoimmune diseases, allergies, inflammation and so on," explains Lluis Quintana-Murci. [Italics in original.]

"Epigenetic discovery suggests DNA modifications more diverse than previously thought" (University of Cambridge):

The world of epigenetics -- where molecular 'switches' attached to DNA turn genes on and off -- has just got bigger with the discovery by a team of scientists from the University of Cambridge of a new type of epigenetic modification.... It's possible that we struck lucky with this modifier, but we believe it is more likely that there are many more modifications that directly regulate our DNA."

This is just a taste of the kind of high-level research that is attracting grant money. The project at Cambridge, for instance, was funded by the Biotechnology and Biological Sciences Research Council, Human Frontier Science Program, Isaac Newton Trust, Wellcome Trust, Cancer Research UK, and the Medical Research Council.

Four years ago, we discussed whether the epigenome is "Evolution's Newest Nightmare." Current Biology put up a brave front, claiming that epigenetics might promise "interesting new angles in the study of evolution." That's hard to support now. None of the articles quoted above had any use for evolutionary theory. Indeed, how could they? If epigenetic markers regulate genes; if they act like molecular switches; if they can be placed into functional maps -- then they represent a higher level of complex specified information that defies the neo-Darwinian mutation/selection story.


Stated explicitly or not, it's design-based thinking that leads scientists to build functional maps of epigenetic markers and motivates them to "figure out what they actually do." Who would waste time or money on junk? The downfall of the junk-DNA concept gives scientists encouragement to seek new levels of specified complexity in epigenetic regulation. The future of epigenomics looks bright -- for intelligent design.

Darwinism vs. the real world XXII

Hemostasis: Maintaining the Right Numbers Is Crucial

Howard Glicksman January 5, 2016 1:41 PM

Editor's note: Physicians have a special place among the thinkers who have elaborated the argument for intelligent design. Perhaps that's because, more than evolutionary biologists, they are familiar with the challenges of maintaining a functioning complex system, the human body. With that in mind, Evolution News & Views is delighted to present this series, "The Designed Body." For the complete series, see here. Dr. Glicksman practices palliative medicine for a hospice organization.

So far in this series, we have seen that evolutionary biologists can only speculate on how complex systems within the body came into being. As for the body knowing how to make sure it has the right amounts of oxygen, carbon dioxide, hydrogen ion, hemoglobin, iron, water, sodium, and potassium, the evolution of such a wonder similarly remains a black box.

The same applies to hemostasis, the process by which the body forms fibrin clots to stop bleeding and allow it to heal. Without this, a minor injury would be lethal. As noted previously, hemostasis involves mainly three processes, which are triggered when blood vessel damage occurs. Those are vasoconstriction, platelet aggregation, and activation of the clotting factors. However, since the presence of clots within a major vessel, like an artery sending blood to the heart, the brain, or the lungs, can result in sudden death, hemostasis must turn on only when it's needed and turn off and stay off when it's not.

In previous articles I've shown that chemicals released by the endothelium (the tissue lining the inside of the blood vessel), with the help of specific anti-clotting factors produced in the liver, combine normally to prevent clotting unless an injury takes place. The total absence of platelets, or any one of most of the clotting or anti-clotting factors, would have disrupted this delicate balance, making it impossible for our earliest ancestors to live long enough to reproduce. As with iron, potassium, and blood pressure, not having enough can be deadly, but so can having too much.

An Analogy from Nature

Consider Beavers build dams across streams to form large enough ponds in which to build their homes. When nature or a predator creates an opening in the dam, the beavers must quickly patch up the damage or lose their home. To prevent further leakage, the patch must seal the opening and be strong enough to withstand the force of water against it. Solid logs, flexible branches, and soft leaves packed together with lots of soft mud are the usual materials used by beavers to construct and repair dams. The size of the opening determines how much material must be used to complete the job properly. Even beavers "know" that real numbers have consequences for life. So too the body must have enough material to prevent traumatic blood loss through hemostasis.

Due to the laws of nature, like friction, momentum, sheer, pressure, and gravity, the body experiences thousands of small vascular injuries every day. These trigger vasoconstriction and platelet aggregation to form a platelet plug. The body must have enough platelets to begin the process of hemostasis. Thrombopoietin is a hormone produced mainly in the liver and kidneys that controls platelet production in the bone marrow. The normal platelet count is 150,000-450,000 per microliter (uL = mm3) of blood. Platelet counts below 20,000/uL, and in particular, less than 10,000/uL, often result in moderate or severe spontaneous bleeding, which can be life-threatening if it occurs in the brain or the gastrointestinal system.

But having too many platelets isn't good for the body either. Platelets are cell-like structures that float in the bloodstream. Just like having too many food particles in the kitchen can clog the drain, so having too many platelets in the circulation can slow blood flow, particularly in the small arteries and arterioles, which can compromise organ and tissue function. Platelet counts above 750,000/uL can result in a heart attack, a stroke, or blood clots in other areas of the body. Thus, not just any number of platelets is needed to have controlled hemostasis. It looks like most of the time, the system that the body uses knows what it's doing.

During platelet aggregation, fibrinogen molecules attach to them and activation of the clotting factors takes place. The coagulation cascade involves several clotting factors using two different chemical pathways to form prothrombinase. Prothrombinase converts prothrombin into thrombin, which then converts fibrinogen into fibrin so a fibrin clot can form to seal the damaged site. In addition, the endothelium secretes chemicals that not only prevent platelet aggregation but also ones (heparan sulfate and thrombomodulin) that work with others from the liver (antithrombin and protein C) to prevent activation of the clotting factors.

When blood vessel damage takes place, these inhibitors of clotting are no longer present in sufficient amounts to prevent the clotting cascade from taking over to form a fibrin clot. Since the endothelium on either side of the injury site is functioning normally, these anti-clotting chemicals make sure that the clot only forms where it's supposed to, and doesn't propagate up or down the blood vessel. This is how the body is able to control hemostasis so that it turns on when it's needed and turns off and stays off when it isn't.

Thousands of Small Vessel Injuries Every Day

The liver produces most of the clotting and some of the anti-clotting factors, but as with most things made in the liver, medical science has very little understanding of how they are controlled. As noted above, thousands of small vessel injuries take place every day. This means that to prevent blood loss and promote healing, hemostasis is always working and, by necessity, is continually using the clotting factors. For hemostasis to function properly, it is not only important for all of the clotting factors to be present, but there must be enough of each of them to get the job done right

When there isn't enough of any one clotting factor, this puts the body at risk for excessive and sometimes spontaneous bleeding. These are called hemorrhagic or bleeding disorders. The normal blood level of fibrinogen is about 3,000 units, but if it drops below 1,000 units, excessive bleeding can take place with limited injury because there just isn't enough to go around. The normal blood level of prothrombin is about 100 units and if it drops below 30 units, the same thing happens.

For Factor V, the normal and critical numbers are 10 units and 2.5 units, for Factor VII, 0.5 units and 0.125 units, for Factor VIII, 0.1 units and 0.04 units (Hemophilia A), for Factor IX, 5 units and 1.5 units (Hemophilia B), for Factor X, 10 units and 2 units, for Factor XI, 5 units and 1.5 units and for Factor XIII, 30 units and 1.5 units.

Too Much of a Good Thing

But having too much of a good thing can cause problems as well. Prothrombin 20210 is an inherited gene mutation that occurs in about 1 percent of the U.S. population, when the liver produces about 30 percent more prothrombinthan normal. Having too much prothrombin significantly increases the risk of clotting and can cause what are known as prothombotic or hypercoagulable states. These conditions can often lead to thromboembolism in which a clot forms, usually in a leg vein, and then breaks off and travels to the right side of the heart and then to the lungs. Pulmonary embolism is a medical emergency that can quickly lead to death because the blood flowing to the lungs to pick up oxygen and drop off carbon dioxide is compromised.

Another mechanism that can cause a hypercoagulable state is a deficiency in the amount or function of the anti-clotting factors. Deficiencies of antithrombin and protein C are relatively rare, while their total absence is considered to be incompatible with life. However, the commonest inherited prothrombotic condition is Factor V Leiden. This occurs in about 5 percent of the U.S. population and may be responsible for up to 30 percent of the cases of thromboembolic disease.

Normal endothelium secretes thrombomodulin, which joins to thrombin to activate protein C. Activated Protein C (APC) then deactivates Factors V and VIII, both of which are very important for clot formation. However, the amino acid structure of Factor V Leidenis such that it is resistant to being broken down by APC. This results in an increase in the presence of activated Factor V and the accumulation of more thrombin than usual. Having more thrombin can often lead to clots forming not only in the veins, but less frequently in the arteries as well. So a person with this condition is not only at risk for leg clots and pulmonary embolism but also heart attack and stroke.

The foregoing shows that the body's ability to prevent itself from bleeding to death from injury, while making sure it has enough blood flow to its trillions of cells, is a very delicately balanced process. The process, hemostasis, involves both pro- and anti-clotting factors. Not having enough pro-clotting compared to anti-clotting factors results in a bleeding disorder, like hemophilia, with its risk of hemorrhagic death (cerebral or gastrointestinal bleed). Not having enough anti-clotting compared to pro-clotting factors, like Factor V Leiden, results in a hypercoagulable state with its risk of a thromboembolic death (heart attack, stroke, pulmonary embolism).

Evolutionary biology speculates on how the many pro- and anti-clotting factors came into existence. But it never addresses how they could have worked together to allow an organism to survive long enough to reproduce. For that requires not only that an organism has all the parts of this irreducibly complex system, but that it also has the natural survival capacity to produce the right amounts of each.


Although medical science remains in the dark about such evolutionary mysteries, this does not stop some biologists from telling the public and teaching children otherwise. It takes a lot of imagination to believe that the ultra-complex and delicately balanced process of hemostasis came about by chance and the laws of nature alone. Advocates of intelligent design, who see the design seen in nature as real rather than an illusion, are on firmer ground, supported by what is already known about what it takes for life to survive under the laws of nature. In the next few articles in this series, I will look at how the body protects itself from invasion and what happens when its defenses break down.

On origin of life science's anthropomorphisms

What Origin-of-Life Researchers Forget
Evolution News & Views January 6, 2016 3:31 AM 

The origin-of-life field is often guilty of ascribing personality to molecules. You see this in the popular literature, but even the serious scientists slip into the habit. It takes the form of an invisible hand, directing the assembly of multiple parts like a foreman at a construction site. Need a membrane? Here are some fatty acids that can make a simple one for starters. Need a replicator? This RNA isn't great, but he can learn. Need proteins? We found some in this meteorite that are willing to lend a left hand.

A more realistic image would be an arena of dead runners surrounded by hurdles as high as mountains. They don't "want" to leap over the hurdles and win a race to become alive, because they can't. They're dead. So are molecules often dubbed "The building blocks of life." They have no interest in jumping over hurdles on a path to a protocell. Much as the origin-of-life researcher wants them to win the Protocell Prize, they couldn't care less. They'll just do whatever the unguided forces of nature make them do.

The only way dead runners can get over a hurdle without intelligent help is to wait for an earthquake, a tsunami, or a meteorite to launch them. With a lot of luck, one runner might land on the other side of the first hurdle. But then he won't have any interest in continuing on over the second hurdle. He is incapable of wanting.

This is the only realistic way for an origin-of-life researcher to approach the problem: molecules are dead things. They don't want to become alive. No amount of coaxing, sweet-talking, or intelligent interference will make them want to live. They will behave like the lifeless things they are, blindly following the laws of chemistry and physics, just as dead runners will obey the law of gravity and lie on the ground unless launched by a force strong enough to overcome gravity. Even if they make it over the top, they will fall back on the ground without any interest in making it over the next hurdle. This pessimistic outlook is true even after Darwinian natural selection enters the picture. Natural selection is just as dead as the molecules. It must not be personified; it has no goal, wish, or plan.

Origin-of-life researchers think they have done their job if they find a possible earthquake or tsunami that might get one body over a hurdle. This "sheds light" on the problem, they say. Different labs find additional earthquakes and tsunamis to help with the other hurdles. Accident #1 "might" work, accident #2 "might" get a body over the next hurdle, and so on. The series of lucky accidents "sheds light" on how life got here, the materialists assure us. They feel justified making up various scenarios because they think, "We're here, aren't we? It must have happened somehow." Having abandoned intelligence as a cause, they're stuck.

With this in mind, let's examine a paper in Current Biology by Saha and Chen, "Origin of Life: Protocells Red in Tooth and Claw." First, they recognize a couple of hurdles:

What is life, and how can we make it? NASA's Exobiology Program uses the working definition of life as "a self-sustaining chemical system capable of Darwinian evolution". Several research labs have undertaken the task of synthesizing an organism that meets this definition. It seems clear that some propagating genetic information is necessary, whether it is a self-replicating RNA or a system of enzymes and DNA. In addition, there are convincing arguments for encapsulating the genetic system inside self-replicating vesicles, creating a primitive entity called a 'protocell'. [Emphasis added.]

There are many more hurdles in the track beyond the two they mention, (1) genetic information and (2) a container. But did you catch the intelligent interference? They speak of labs run by intelligent agents who "have undertaken the task of synthesizing an organism." They ask, "How can we make it?" It's not their job, but even if they were to succeed, it would prove intelligent design, not the origin of life by natural processes.

Origin of life research is sometimes abbreviated OOL. According to their definition, NOODLE would be more apt: Naturalistic Origin of Darwinian Life Evolving. Their job is going to be harder than pushing a NOODLE through a needle. They have to keep their intelligent hands off, and the noodle doesn't want to go there. "But," they might reply, "what if there are billions of noodles and billions of needles? One or more might wash through the eye of a needle by chance and natural forces." OK, but there are more needles on the pathway to life, and the noodles are still dead, uncaring, and uncared for.

Saha and Chen make a big deal of protocell models based on phospholipid membranes (fat bubbles). These could encapsulate floating molecules of DNA or RNA and then merge with other fat bubbles, creating a game of competition. Follow the personification in their figure caption:

(A) A scheme for evolution of protocells from coacervates. (B) In the competition among protocells, the 'rich get richer' as the larger vesicle grows more quickly and fuses with the feeder vesicles. (C) In a virus-like strategy, a parasitic genome (red) lurks within a small vesicle and awaits fusion. Once inside an actively metabolizing protocell, the parasitic genome replicates rapidly and overtakes the host's genome (black).

It's hard to take this seriously. The molecules don't want to get rich. They aren't competing. They aren't lurking, awaiting, and overtaking. If the richest fat bubble outlasts the others, the only ones celebrating are the researchers.

It's not necessary to wade through the weeds of their paper, hearing about "zwitterionic or anionic membranes" and other jargon, because their approach is fallacious throughout. They are hoisting the dead bodies over the hurdles against their natural inclinations. Example:

Therefore, the membrane composition became increasingly dominated by the (non-phospholipid) cationic lipid, which could not form stable vesicles on its own. In addition, there was no way to add more nucleotides and enzyme. Ultimately, a mechanism to supply phospholipids and nucleotides to the protocells was required.

The solution to this problem has recently been reported by the same group, through delivery of nucleotides, enzyme and phospholipids by fusion of 'feeder' vesicles to the protocells....

They picture the fat bubbles cannibalizing one another. No kidding: "These protocell cannibals thus gain direct access to their victim's contents.... Vesicle cannibalism raises the stakes of the competition between protocells -- inactive protocells do not merely fail to grow, they are actually eaten by others."

These fat bubbles are sheer barbarians! They're waging war in some kind of Malthusian struggle. It's Darwin time now:

Feeding through fusion also opens the door to a pageant of evolutionary phenomena. Strategies to preferentially sequester resources (e.g., enzymes or membrane catalysts) during division or rapidly produce or acquire anionic mass could evolve. In addition, the conveyor vesicles need not be devoid of a genome. Fusion of vesicles containing different genomes would create intracellular competition between unrelated genomes, and could lead to genetic novelty through recombination. Parasitic genomes could lurk within conveyor vesicles, awaiting fusion to a target vesicle susceptible to takeover (Figure 1C).

Nothing in this story is realistic when you demand "plausible prebiotic conditions" and exclude investigator interference. Fat bubbles don't mind who wins the alleged "competition." A "genome" is not a random assortment of mixed-handed nucleotides inside a fat bubble. It's dead, too. It won't care about preserving "novelty" for future generations. It isn't lurking to take over a target vesicle.

It doesn't matter that the scenario is highly unrealistic; storytelling is fun! Everybody wins, and all must get a prize:

Although these protocells are rather advanced compared to the prebiotic milieu, further study of this evolvable system promises to be a rewarding endeavor.


If you find it troubling that scientific journals can publish stuff like this and be rewarded for it -- with no complaints from sensible realists or opportunities for rebuttal -- you're not alone.