Why Doesn’t God Follow His Own Laws?!

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Why Doesn’t God Follow His Own Laws?!

James R. Aist

“But our God is in the heavens; He does whatever He pleases.” (Psalm 115:3)

Many people want to believe that what the Bible says about God is true, but they will do so only insofar as it conforms to their pre-conceived notions and/or they are willing to accept it as being true. Consequently, they believe in a god that is, at least to some extent, created in their own image. One major stumbling block for many such folks is the fact that God doesn’t always follow the laws that He commands us to follow. For example, in the Ten Commandments (Exodus 20:1-17), God has commanded us to not murder or steal, but He killed all the firstborn children in the land of Egypt (Exodus 13:15) and struck dead a Christian married couple (Acts 5:1-10), and, in effect, He stole the land from the inhabitants of the promised land and gave it to His chosen people, the Israelites (Leviticus 20:24)! So, they reckon, God is breaking His own laws and is, therefore, not the perfect moral being He claims to be. This leads them to the conclusion that such a god is a scofflaw, and therefore not worthy of reverence and obedience, much less worship.

But, there is a fatal flaw in that way of thinking about the God of the Bible. God’s laws were given to mankind for mankind to follow, not necessarily for God to follow. The God of the Bible is the supreme judge of what is right and what is wrong. There is no authority above God to whom one can appeal in order to lodge a valid accusation against God. Moreover, there is no need of someone to judge God, because all of His ways and thoughts are perfect. The psalmist stated it succinctly for us: “But our God is in the heavens; He does whatever He pleases” (Psalm 115:3). God is not subject to the laws He has given for mankind to follow. Rather, He does whatever He pleases. God’s perfect ways flow from His perfect, moral nature, whereas our imperfect ways flow from our imperfect, sin nature. Moreover, God forbids us to do some things that He does, even in those instances in which we are capable of doing so. For example, Paul states emphatically,”Beloved, do not avenge yourselves, but rather give place to God’s wrath, for it is written: “Vengeance is Mine. I will repay, says the Lord” (Romans 12:19). Judgement, in the sense of condemnation of a person, is another thing that God reserves for Himself. And, we can add the definition of right and wrong to this list. So, you see, God does not follow all of the laws that He laid out for mankind to follow, because He has reserved some functions and actions for Himself alone. He can do that, because He is God and we are not. We would do well to remember that.

The God of the Bible created, and therefore owns, all of creation, including us. He created us for His glory (Isaiah 43:7), in order for us to reflect back to him His glory (click HERE). Therefore, He has every right, even a moral obligation, to reward good and punish evil, as well as to be the sole judge of what good and evil are. And, He does with each human life whatever he pleases, without reproach. We can see this clearly in Romans 9:18, where Paul writes, “Therefore He has mercy on whom He wills, and He hardens whom He wills.”

So, whenever we accuse the God of the Bible of wrongdoing, we are deluding ourselves into thinking that we are morally superior to God and are, therefore, qualified to be His judge. But in reality, its the other way around: we will all be judged by God.  So let’s not judge Him because He doesn’t follow all of the laws He has given for us to follow. Rather, let’s make peace with the fact that as the heavens are higher than the earth, so are His ways higher than our ways, and His thoughts than our thoughts (Isaiah 55:8-9). This is the God of the Bible: morally perfect, beyond reproach and judge of all.

(To read more of my articles with biblical themes, click HERE)

How Could Jesus Have Been Born “Immaculate”?

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How Could Jesus Have Been Born “Immaculate”?

 James R. Aist

When Adam chose to believe Satan instead of God  and sinned (Genesis 3), two things happened that have affected all subsequent generations of mankind (Psalm 51:5; Psalm 58:3; Romans 5:12; Romans 5:17; and 1 Peter 1:18-19), not through a direct, genetic (biological) inheritance as we know it, but by a mysterious, spiritual inheritance that is associated with biological reproduction. First, we took on a “sin nature” (Colossians 3:9-10), or a predisposition to sin, that has been passed down to all subsequent generations, including ours. We have “inherited”, so to speak, from Adam, a “sin nature”, an inborn desire to reject God’s provision and follow our own path in life. This predisposition to sin is so pervasive as to render us, in our “natural-born” state, in rebellion against, and at enmity with, God. And second, we share in the guilt of the original sin of Adam that has been passed down to all of his descendants, because Adam was the representative of all mankind in his rebellion against God, just as Jesus, the second Adam, is the representative of all of Adam’s descendants who believe and trust in Him for their salvation (Romans 5:19; 1 Corinthians 15:22).

This sin nature and the guilt of Adam’s original sin that we are all born with present a dilemma that may seem irresolvable at first glance: the Lamb of God (Jesus) had to be “immaculate”; that is, without spot or blemish (1 Peter 1:19), entirely free of sin, the sin nature and the guilt of Adam’s original sin. So, how did Jesus escape inheriting the sin nature and the guilt of Adam’s original sin at His conception? All agree that Jesus did not inherit these from His Father, the Holy Spirit. But, what about Mary?

Let’s begin with the Roman Catholic solution to this dilemma.  According to Roman Catholic doctrine, Mary did not ever have a sin nature or guilt of original sin because of the direct intervention of God; Mary was immaculate as a divine privilege. Of course, there is no clear, unequivocal biblical evidence to confirm this view. It appears to me that the Roman Catholic Church invented this doctrine to resolve the dilemma, because they could not discover, in either the Bible or in Roman Catholic tradition, any other suitable resolution. Apparently, the main Bible verse they use is Genesis 3:15, which says “I will put enmity between you and the woman, and between your offspring and her offspring; he will bruise your head, and you will bruise his heel.” They claim that this verse refers to a battle between Mary and Satan, but a natural reading of the verse indicates that the actual battle will be, instead, between Jesus and Satan. Nonetheless, if God did, in fact, solve this dilemma in this way, then it is not for us to declare otherwise apart from the biblical witness.

Another solution, associated with Protestantism, posits that the sin nature and the guilt of original sin are inherited from Adam, generation to generation, through the fathers only, as seems to be implied by Romans 5:17 and 1 Peter 1:18-19 when taken together: Since Jesus did not have a human father to pass the sin nature and the guilt of original sin on to Him (His father was the Holy Spirit) and the sin nature and the guilt of original sin are inherited through the fathers only, then He could not have inherited either the sin nature or any guilt of Adam’s sin. Once He was conceived in Mary’s womb by the Holy Spirit, He would automatically be the Lamb of God “without spot or blemish” (1 Peter 1:19). Problem solved. I have addressed this viewpoint more fully elsewhere (click HERE), and it does have its foundation in the biblical witness.

But, there is yet another feasible solution to the dilemma that I believe may be even more strongly and clearly supported by the biblical witness. This explanation requires knowledge and understanding that the Jewish followers of God, such as Abraham (and, for our purposes, Mary)  had an opportunity to go to Heaven based on their looking ahead to the price to be paid by the Messiah for their sins (based on Old Testament messianic prophesies), just as we today have an opportunity to go to heaven by looking back to the price paid by the Messiah, Jesus, for our sins (based on New Testament fulfillment of Old Testament messianic prophesies). (For a more complete exposition of this biblical teaching, click HERE).

Now, to fully understand this third explanation, I will have to elaborate a bit, so bear with me if you will. Before Mary conceived, an angel spoke to her concerning who Jesus would be: “But the angel said to her, “Do not be afraid, Mary, for you have found favor with God. Listen, you will conceive in your womb and bear a Son and shall call His name JESUS. He will be great, and will be called the Son of the Highest. And the Lord God will give Him the throne of His father David, and He will reign over the house of Jacob forever. And of His kingdom there will be no end.” Then Mary said to the angel, “How can this be, since I do not know a man?” The angel answered her, “The Holy Spirit will come upon you, and the power of the Highest will overshadow you. Therefore the Holy One who will be born will be called the Son of God. Mary said, “I am the servant of the Lord. May it be unto me according to your word.” Then the angel departed from her (Luke 1:30-35, 38).”

The first point I want you to see here is that, in effect, the angel preached “the Gospel of Jesus Christ” to Mary: 1) He will be the promised Savior (The name “JESUS” means “savior” or “God saves.” See also: Matthew 1:21, “She will bear a Son, and you shall call His name JESUS, for He will save His people from their sins.”); 2) The Holy Spirit will be His father; and 3) therefore, He will be the Son of God. The second point is that, when Mary responded with “May it be unto me according to your word,” she was expressing agreement with, not only becoming pregnant by the Holy Spirit, but also with everything the angel had said concerning Jesus. Thus, it seems that Mary may have been the first person in the New Testament to hear the Gospel of Jesus Christ and accept it by faith. The third point is that Mary apparently was saved before Jesus was conceived. This is a critical point, because, if this is true, then, when she was born again through her faith in Jesus, she instantly “became an heir of the righteousness that comes by faith”, the righteousness of God in Christ (Genesis 15:6; Hebrews 11:7; Romans 3:22; 2 Corinthians 5:21). In other words, before Jesus was conceived, Mary may have already believed in Him (Luke 1:38) and, if so, she was already the righteousness of God in Christ and could not have passed on to Jesus either any guilt of Adam’s sin or a sin nature.

The gist of this explanation is that, if Mary was, in fact, saved before she became pregnant with Jesus, then there was no avenue whereby either the sin nature or the guilt of Adam’s original sin could have been passed on to Jesus, because  Mary’s new nature in Christ (2 Peter 1:4 speaks of the  “divine nature” of those who believe in Christ) would have already replaced her original sin nature (Colossians 3:9-10) and her righteousness of God in Christ would have erased her guilt of Adam’s original sin before He was conceived. If this explanation is, indeed, true and valid, then it’s a good thing the angel preached the Gospel to Mary before Jesus was conceived!

The “take home message” of this article is this, that one way or another, God saw to it that when Jesus was conceived, He was free of both the guilt of Adam’s original sin and of the sin nature. Add to that a sinless life (Hebrews 4:15) and we have a biblical explanation of how, when Jesus died on the cross, He could bear the sins of others (i.e., us). If He had had sins of His own to bear, then He would have died for His own sins, and our sins would still not be forgiven. In which case, it would not end well for us who believe and trust in Jesus for the forgiveness of our sins and the salvation of our souls!

(To read more of my biblical articles, click HERE)

New Theory: Homosexuality Is a Mistake of Nature

 

New Theory: Homosexuality Is a Mistake of Nature

James R. Aist

Introduction

Homosexuality is believed to be caused by some combination of biological and environmental factors. Several biological theories have been offered, the most feasible being the genetic, the hormonal and the epigenetic theories. In 2012, a new theory was introduced that combines aspects of the genetic theory with the hormonal theory. This is the epigenetic theory. Epigenetics is a relatively new and vigorously investigated field of biological science that deals with the regulation of gene expression (production of proteins) in cells. The components of chromosomes that regulate genes are called “epi-marks.” These include such things as methylated DNA and variously modified histone proteins, but do not include changes in the DNA sequences themselves that code for specific proteins.

The Theory

Rice et al. (2012) published a review article presenting a speculative and hypothetical model (theory) to explain the development of homosexuality in both male and female homosexuals. Their goal was to develop a model that would explain why 1) molecular studies have failed to conclusively identify “gay genes” and 2) concordance for homosexuality between identical twins is low (click HERE). The theory draws on research supporting the hormonal theory as well as known properties and functions of epi-marks. The model would explain homosexuality on the basis of epi-mark-controlled prenatal testosterone (a sex hormone) levels, to the virtual exclusion of a role for either a strictly genetic influence or post-natal environmental influences.

Normally, epi-marks regulating sexual orientation are “erased” after they have produced the intended sexual development (i.e., heterosexual males and females). But, occasionally, a mistake is made, and the epi-mark is not erased but is, instead, passed on to the next generation. According to the model, when this mistake is made, epi-mark regulated testosterone overexposure in a female fetus would result in a masculinized female who will prefer females (a lesbian), whereas epi-mark regulated testosterone underexposure in a male fetus would result in a feminized male who will prefer males (a gay). The low concordance in twin studies would be explained not by a low-level genetic influence, as is usually assumed, but by the occasional passing of testosterone-enhancing epi-marks from father to daughter (creating a lesbian) and of testosterone-limiting epi-marks from mother to son (creating a gay man).

It is interesting to note that this model posits homosexuality as an aberrant accident of nature, in which normal prenatal development of a fetus produces the intended effect (heterosexuality), and abnormal prenatal development produces an unintended effect (homosexuality) by mistake. Abnormal prenatal development results when a mistake is made and an epi-mark in a parent is not erased, but is, instead, passed on to the offspring, where its effect (homosexuality) is seen in the subsequent generation. Thus, according to this theory, homosexuality is a mistake of nature, and it is not biologically normal, as gay activists want us to believe.

Although this model is highly speculative and presently has very little, if any, direct experimental support, it does have merit as a scientific hypothesis, because 1) it would explain both male and female homosexuality, 2) it could explain the low concordance for homosexuality found in twin studies, 3) it seems to provide a feasible explanation for the long-term survival of a reproductively deleterious trait in the human population, and 4) it is, at least to some extent, testable. Only further research will determine whether or not this theory will join the many previous theories purporting to represent an almost exclusive influence on the development of homosexuality, all of which have failed.

Caveat

Twin studies have shown that the combined influence of all possible, pre-natal, biological factors (e.g., genetics, epigenetics, hormones, etc.) on the development of homosexuality in adults is only weak to weakly moderate (click HERE). Thus, post-natal influences (e.g., cultural, social and experiential factors) are far more influential than is epigenetics in the development of homosexuality (click HERE).

Reference Cited:

Rice, G., et al. 2012. Homosexuality as a Consequence of Epigenetically Canalized Sexual Development. Quarterly Review of Biology 87:343-368.

(For more articles on HOMOSEXUALITY, click HERE)

What Twin Studies Tell Us about Homosexuality: Nature vs. Nurture

What Twin Studies Tell Us about Homosexuality: Nature vs. Nurture

James R. Aist

(Note: Numbers in parentheses refer to specific, numbered references listed at the end of the article.)

Introduction

I presented a much broader treatment of possible causes of homosexuality elsewhere (click HERE). Most of the more recent research on possible biological origins of homosexuality has focused on the degree to which genes, along with other prenatal factors such as hormones and epi-genetics, may influence the development of homosexuality. In this regard, the most conclusive and telling results have come from studies of “identical” twins (who both have virtually the exact same complement of genes). Although it is commonly assumed that identical-twin studies reveal the influence of genes per se on a trait or behavior, the results of such studies have the unique advantage of reflecting, in fact, the combined influence of all possible, pre-natal, biological factors (e.g., genetics, epi-genetics, hormones, etc.) on the development of homosexuality in adults (1). This is because identical twins not only share the same complement of genes, but they also share the same pre-natal environment (their mother’s womb), where biological factors are postulated to operate.

Twin Studies: Overview

The design of research studies using identical twins has improved greatly since the mid-1990s, with the advent of large, twin registries which can afford much larger data bases and less biased sampling procedures. The former approach of recruiting identical twins via advertisements in gay and lesbian publications is now known to have a very strong “volunteer effect” that produced the appearance of relatively large genetic effects (1). Nevertheless, even with the use of large twin registries, the number of identical twin pairs found with homosexuality is often very small in individual studies, resulting in a standard deviation that is greater than the calculated genetic effect, meaning that the results are not statistically different from zero. In other words, the genetic influence or contribution in several of these studies may actually be zero, making definitive conclusions impossible. Whitehead and Whitehead (1) have presented and discussed, in some detail, these and other problems inherent in twin studies of homosexuality and have presented reasons to expect that the genetic influence on, or contribution to, homosexuality will eventually be agreed to be in the 10%-15% range (i.e., weak). One reason for this (anticipated) lower actual genetic influence is that epi-genetic effects operating through identical twins sharing one placenta probably represent about 15% of the total influence that has been attributed to genetics in published twin studies (2). Another reason has to do with the apparently predominant influence of post-natal environmental factors on the development of homosexuality (10). Schumm (9) found that children with homosexual parents are 12-15 times more likely than children of heterosexual parents to be homosexual as adults. This is the strongest environmental influence ever reported for the development of homosexuality, and it involves very close family members, the parent-child relationship. In a family environment, identical twins share a common bond and common experiences more so than do other siblings, including non-identical twins; siblings can’t be any “closer” than that. The results of a study by King and McDonald (8) illustrate how such a close, family relationship could inflate the calculated genetic influence on homosexuality in identical twin studies. They studied 46 twin pairs having homosexuality present in one or both of the twins in each pair and found that 54% of the twin pairs had discussed their sexual orientation with each other, 89% had “shared knowledge” of each other’s sexual orientation, and 30% of these twin pairs had actually had sex with each other. Because identical twins identify so closely with each other, and post-natal experiences  – especially close family relationships – strongly affect the development of homosexuality, it seems plausible, if not likely, that a homosexual member of a twin pair would influence the other member of that pair to embrace and explore homosexuality also, thus inflating the apparent genetic influence reported in identical twin studies. That is to say, a significant portion of what may appear, in identical twin studies, to be a genetic influence on the development of homosexuality may turn out to be, instead, a post-natal, environmental influence involving shared knowledge of sexual orientation and shared sexual experiences within identical twin pairs.

Twin Concordance Studies

The “pair-wise concordance” answers the simple question, “Where one twin of an identical pair is homosexual, what percentage of co-twins is also homosexual”. The mathematical formula for pair-wise concordance of identical twins is C/C+D, where C is the number of concordant (similar) twin pairs and D is the number of discordant (dissimilar) twin pairs found in the study. For example, if C=1 and D=9, then the pair-wise concordance would be 1/1+9=1/10 or 10%. This result would indicate that for every twin pair with both members being homosexual, there are 9 twin pairs with only one homosexual member.

Using data provided in several reports of large, twin registry studies in different countries, I performed a meta-analysis and calculated the range of pair-wise concordance to be 9.9% to 31.6%, with the average being 13.0% for males, 13.3% for females, and 13.2% when the raw data for males and females were combined. These pair-wise concordance values indicate that for every twin pair with both members being homosexual, there are 7 twin pairs with only one homosexual member. Now, compare this result to the range of theoretically possible outcomes where no twin pairs would both be homosexual (= 0%) and where all twin pairs would both be homosexual (= 100%) and you can see, intuitively, that a pair-wise concordance of only 13.2% would indicate a real, but relatively minor, contribution of genetics to homosexuality. This minor role is similar to the estimated level of genetic contribution to virtually any kind of human behavior (3) and is known to be non-determinative and, in many cases, treatable by therapy and/or counseling. For instance, the best example to date of a genetically related behavior (mono-amine oxidase deficiency leading to aggressive behavior) has shown itself remarkably responsive to counseling (3). Therefore, on the basis of pair-wise concordance in identical twins, it seems appropriate to conclude that there is, at the most, only a minor genetic contribution to the development of homosexuality, and that this relatively minor influence can be overcome (i.e., nullified) through behavioral therapy (1), which we know to be a fact (4, 5).

The other measure of concordance in twin studies is “proband-wise” concordance. This estimate of concordance is necessary in order to use both identical and fraternal twins in a study to disentangle the relative contributions to homosexuality of genetic and non-genetic (environmental) factors. The formula used is 2C/2C+D, which, compared to the formula for pair-wise concordance, gives much more weight to the individual twins (probands). The effect is to greatly increase, relative to pair-wise concordance values, the apparent genetic contribution to homosexuality in identical twin studies. To illustrate this point, if we use the example given above where the pair-wise concordance calculates to be 1/10 = 10.0%, the proband-wise concordance calculates to be 2/11 = 18.2%. Although it is less intuitive, proband-wise concordance is generally believed to give a better overall estimate of “genetic influence” than does pair-wise concordance.

Classical Twin Studies

While pair-wise concordance gives an intuitive indication of the genetic influence on homosexuality as expressed in identical twins, it does not provide information on what factors may provide the remaining, non-genetic influence. To answer this question, researchers are using other measures, broader-ranging questionnaires and more sophisticated statistical procedures to evaluate such things as heritability, additive genetic effects and postnatal environmental influences. In order to be able to put the results of classical twin studies into perspective, it is important to keep in mind that, by convention in the twin study literature in general, a genetic contribution of around 25% is considered weak, of around 50% is considered moderate and of 75% or more is considered strong (6).

In a meta-analysis, Whitehead (6), using the results from seven of the recent twin registry studies that were designed to reveal contributions of both genetic and non-genetic factors to homosexuality, found that the mean contribution of genetics to male homosexuality was around 22%, and to female homosexuality, around 33%. Because of the relatively large standard deviations in the data, these two values were not statistically different from each other.  Thus, the mean genetic contribution to male homosexuality in these studies is weak and to female homosexuality is weakly moderate. Such levels of genetic contribution indicate a real but weak-to-weakly moderate and indeterminate role of genetics in the development of homosexuality. For comparison, other traits that have around 50% (moderate and indeterminate) genetic contribution in twin studies include such things as divorce and alcoholism, while puberty has a 90% (strong and determinate) genetic contribution (1). Furthermore, the non-shared, post-natal environmental contribution to homosexuality is moderate to strong, around 64%-78%, has a relatively small standard deviation and is consistently around the same percentage (6), indicating that homosexuality is influenced primarily by post-natal environmental factors and experiences that are not directly related to prenatal, biological contributions of any kind or combination.

The recent study by Zietsch, et al. (7) can be used to illustrate representative research results obtained with large samples from twin registries. They used a very large sample (9,884) of twins from the Australian Twin Registry, one of the largest samples to date for twin studies of homosexuality. In this sample, there were 1,840 identical twin pairs (1,133 female and 707 male). Their calculated value of only 24% for the proband-wise concordance for homosexuality indicates a weak genetic influence. Moreover, their calculated figure of 31% for heritability of homosexuality also indicates a weak genetic component. This leaves around 68% of the variance represented by post-natal, “shared environment” and “residual” environmental influences combined.

Summary

In view of the fact that twin studies have shown that the combined influence of all possible, pre-natal, biological factors (e.g., genetics, epi-genetics, hormones, etc.) on the development of homosexuality in adults is only weak-to-moderate, it is important to understand that all of the biological theories combined can address only this weak-to- weakly moderate amount of influence, while ignoring the far more important post-natal influences (e.g., culture, parental divorce, and having a homosexual parent). Furthermore, twin studies clearly support the inference, based on results obtained through therapy and counseling (4, 5), that post-natal, environmental influences have a far greater role in the development of homosexuality than do pre-natal, biological influences. Thus, where the development of homosexuality is concerned, twin studies have demonstrated that nurture is far more important than nature.

(For more articles on HOMOSEXUALITY, click HERE)

References Cited:

1. Whitehead, N. and B. Whitehead. 2016. Chapter 10. Twin studies: The strongest evidence.(click HERE)

2. Whitehead, N. and B. Whitehead. 2016. Chapter 1. Can genes create sexual preferences? (click HERE)

3. Whitehead, N. and B. Whitehead. 2016. Summary. (click HERE)

4. Whitehead, N. and B. Whitehead. 2016. Chapter 12. Can sexual orientation change? (click HERE)

5. Aist, J. 2012. Homosexuality: Good News! (click HERE)

6. Whitehead, N.E. 2011. Neither Genes nor Choice: Same-sex Attraction is Mostly a Unique Reaction to Environmental Factors. Journal of Human Sexuality 3:81-114. (click HERE)

7. Zietsch, B., et al. 2012. Do Shared Etiological Factors Contribute to the Relationship between Sexual Orientation and Depression? Psychological Medicine 42:521-532.

8. King, M., and E. McDonald. 1992. Homosexuals who are Twins. British Journal of Psychiatry 160: 407-409.

9. Schumm, W. 2010. Children of Homosexuals More Apt to be homosexuals? A Reply to Morrison and to Cameron Based on an Examination of Multiple Sources of Data. Journal of Biosocial Science 42:721-742.

10. Aist, J. 2012. Are Homosexual People Really Born Gay? (click HERE)