Thursday 7 July 2016
Monday 4 July 2016
Darwin of the gaps just so stories re junk DNA becomoing harder to sell
Junk DNA: Is Preventing Breast Cancer a Function?
Evolution News & Views February 6, 2016 4:33 AM
Each time a function is found for a piece of non-coding DNA, the "junk DNA" myth gets more mythological. Here's a function that has been revealed for a certain long, non-coding transcript of DNA into RNA (lncRNA). It helps prevent breast cancer and ovarian cancer.
Researchers at the University of Bath explain why it is difficult to find these functions for non-coding parts of the genome:
The human genome contains around three metres of DNA, of which only about two per cent contains genes that code for proteins. Since the sequencing of the complete human genome in 2000, scientists have puzzled over the role of the remaining 98 per cent.
In recent years it has become apparent that a lot of this non-coding DNA is actually transcribed into non-coding RNA. However, there is still a debate as to whether non-coding RNA is just 'noise' or whether it serves any function in the cell.
Part of the reason for this uncertainty is that it is very difficult to knock-out non-coding RNA without damaging the DNA, which can lead to off-target effects and false results.
They are clearly aware of the "debate" about junk DNA and the results of ENCODE that found that the majority of the genome is actually transcribed (they referenced ENCODE in the paper). As we have reported often, some members of the evolution side of the debate expect most of the DNA is junk. The design side expects that much of it (but not necessarily all) is functional. Thanks to this research, we have a new case that may point the way to future discoveries.
The news release is titled, "'Junk' DNA plays role in preventing breast cancer." It's based on an open-access paper in Nature Communications. Most readers scanning the paper will see what researchers are up against. Discussion of the complex interactions of parts -- lncRNAs transcripts, small interfering RNAs (siRNAs), promoters, exons, introns, alleles, interference in cis and trans and all the rest -- gets into the technical weeds fast. Thankfully, the release simplifies the essence of the finding. Basically, a piece of non-coding DNA "keeps cells healthy" by preventing a genetic "switch" from getting stuck.
Dr Adele Murrell, from the University of Bath's Department of Biology & Biochemistry, led the study. She explained: "The number of cells in our body are balanced by the level at which cells replicate and replace the ones that die. Sometimes the switches that control this growth get stuck in the 'on' position, which can lead to cancer.
"As the tumour grows and the cancer cells get crowded, they start to break away from the tumour, change shape and are able to burrow through tissues to the bloodstream where they migrate to other parts of the body, which is how the cancer spreads. This process is called metastasis and requires a whole network of genes to regulate the transformation of cell shape and mobilisation.
Dr Lovorka Stojic, from Cancer Research UK Cambridge Institute, the first author of this work identified that GNG12-AS1, a strand of non-coding RNA, prevents the growth switch getting stuck and suppresses metastasis. The specific genomic region where this non-coding RNA is located often gets damaged in breast cancer patients -- this control is removed and the cancer cells spread.
The researchers found that the lncRNA GNG12-AS1 acts as a molecular "rheostat" (their term) that controls the expression of an adjacent gene, DIRAS3, a tumor suppressor. It does it by two mechanisms. One is by regulating the number of transcripts of the tumor suppressor. But if that gets out of control, it can even suppress the "network of genes that prepare cells to change their shape and prepare for metastasis."
By experimentally reducing the amount of GNG12-AS1 produced, either by preventing its transcription or destroying the transcripts, they found that cells start becoming cancerous. This explains why in cancer patients, the switch is stuck:
DIRAS3 is downregulated in 70% of breast and ovarian cancer, and its loss of expression correlates with cancer progression and metastasis. The mechanism responsible for DIRAS3 downregulation to date involves different epigenetic mechanisms and loss of heterozygosity. We hypothesized that TI [transcriptional interference] by GNG12-AS1 could represent an additional layer of regulating DIRAS3 dosage.
The interactions are far more complex than can be described here. Suffice it to say that this long non-coding RNA, which would have been considered "junk" previously, plays a crucial role in regulating the amount of an important tumor suppressor gene. It's a "stable lncRNA localized in the nucleus" with a half-life of 20 to 25 hours, meaning it needs to be transcribed often. Other processes regulate the amount of the lncRNA in a very complex choreography of enhancers, suppressors, and feedback loops. Levels of expression also vary depending on the tissue involved.
It has become increasingly clear that non-coding parts of the genome play vital roles in regulating the coding parts. Regulation is an important function. A system that generates parts without regard to the amount needed is a system out of control. How cool is it to find a code that codes for products that regulate the amount of products in other parts of the code? Not only do we see function emerging for the non-coding regions, we see design on a more colossal scale than anyone could have imagined.
The University of Bath is an internationally recognized center of excellence in biological research. It's encouraging to see their biologists actively challenging the "junk DNA" myth:
Dr Kat Arney, science communication manager at Cancer Research UK, said: "Only a tiny fraction of our DNA contains actual genes, and we know that at least some of the bits in between -- often dismissed as 'junk' -- play important roles in controlling how genes get switched on and off at the right time and in the right place.
When the Human Genome project found that only 2 percent of the genome coded for proteins, the right question should have been, "What is all the rest doing?" Some evolutionists were too quick to dismiss it as a pile of useless leftovers from time and chance. Cancer patients around the world can be grateful that these researchers didn't buy that explanation, but looked beyond the unknown for greater understanding.
"Research like this is helping is to unpick the precise details about how these regions work, shedding light on their potential role in the development [or prevention] of cancer and pointing towards new approaches for tackling the disease."
If a system works, it's not happening by accident. That's the intelligent-design spirit that promises to shed more light into the genomic black box.
Evolution News & Views February 6, 2016 4:33 AM
Each time a function is found for a piece of non-coding DNA, the "junk DNA" myth gets more mythological. Here's a function that has been revealed for a certain long, non-coding transcript of DNA into RNA (lncRNA). It helps prevent breast cancer and ovarian cancer.
Researchers at the University of Bath explain why it is difficult to find these functions for non-coding parts of the genome:
The human genome contains around three metres of DNA, of which only about two per cent contains genes that code for proteins. Since the sequencing of the complete human genome in 2000, scientists have puzzled over the role of the remaining 98 per cent.
In recent years it has become apparent that a lot of this non-coding DNA is actually transcribed into non-coding RNA. However, there is still a debate as to whether non-coding RNA is just 'noise' or whether it serves any function in the cell.
Part of the reason for this uncertainty is that it is very difficult to knock-out non-coding RNA without damaging the DNA, which can lead to off-target effects and false results.
They are clearly aware of the "debate" about junk DNA and the results of ENCODE that found that the majority of the genome is actually transcribed (they referenced ENCODE in the paper). As we have reported often, some members of the evolution side of the debate expect most of the DNA is junk. The design side expects that much of it (but not necessarily all) is functional. Thanks to this research, we have a new case that may point the way to future discoveries.
The news release is titled, "'Junk' DNA plays role in preventing breast cancer." It's based on an open-access paper in Nature Communications. Most readers scanning the paper will see what researchers are up against. Discussion of the complex interactions of parts -- lncRNAs transcripts, small interfering RNAs (siRNAs), promoters, exons, introns, alleles, interference in cis and trans and all the rest -- gets into the technical weeds fast. Thankfully, the release simplifies the essence of the finding. Basically, a piece of non-coding DNA "keeps cells healthy" by preventing a genetic "switch" from getting stuck.
Dr Adele Murrell, from the University of Bath's Department of Biology & Biochemistry, led the study. She explained: "The number of cells in our body are balanced by the level at which cells replicate and replace the ones that die. Sometimes the switches that control this growth get stuck in the 'on' position, which can lead to cancer.
"As the tumour grows and the cancer cells get crowded, they start to break away from the tumour, change shape and are able to burrow through tissues to the bloodstream where they migrate to other parts of the body, which is how the cancer spreads. This process is called metastasis and requires a whole network of genes to regulate the transformation of cell shape and mobilisation.
Dr Lovorka Stojic, from Cancer Research UK Cambridge Institute, the first author of this work identified that GNG12-AS1, a strand of non-coding RNA, prevents the growth switch getting stuck and suppresses metastasis. The specific genomic region where this non-coding RNA is located often gets damaged in breast cancer patients -- this control is removed and the cancer cells spread.
The researchers found that the lncRNA GNG12-AS1 acts as a molecular "rheostat" (their term) that controls the expression of an adjacent gene, DIRAS3, a tumor suppressor. It does it by two mechanisms. One is by regulating the number of transcripts of the tumor suppressor. But if that gets out of control, it can even suppress the "network of genes that prepare cells to change their shape and prepare for metastasis."
By experimentally reducing the amount of GNG12-AS1 produced, either by preventing its transcription or destroying the transcripts, they found that cells start becoming cancerous. This explains why in cancer patients, the switch is stuck:
DIRAS3 is downregulated in 70% of breast and ovarian cancer, and its loss of expression correlates with cancer progression and metastasis. The mechanism responsible for DIRAS3 downregulation to date involves different epigenetic mechanisms and loss of heterozygosity. We hypothesized that TI [transcriptional interference] by GNG12-AS1 could represent an additional layer of regulating DIRAS3 dosage.
The interactions are far more complex than can be described here. Suffice it to say that this long non-coding RNA, which would have been considered "junk" previously, plays a crucial role in regulating the amount of an important tumor suppressor gene. It's a "stable lncRNA localized in the nucleus" with a half-life of 20 to 25 hours, meaning it needs to be transcribed often. Other processes regulate the amount of the lncRNA in a very complex choreography of enhancers, suppressors, and feedback loops. Levels of expression also vary depending on the tissue involved.
It has become increasingly clear that non-coding parts of the genome play vital roles in regulating the coding parts. Regulation is an important function. A system that generates parts without regard to the amount needed is a system out of control. How cool is it to find a code that codes for products that regulate the amount of products in other parts of the code? Not only do we see function emerging for the non-coding regions, we see design on a more colossal scale than anyone could have imagined.
The University of Bath is an internationally recognized center of excellence in biological research. It's encouraging to see their biologists actively challenging the "junk DNA" myth:
Dr Kat Arney, science communication manager at Cancer Research UK, said: "Only a tiny fraction of our DNA contains actual genes, and we know that at least some of the bits in between -- often dismissed as 'junk' -- play important roles in controlling how genes get switched on and off at the right time and in the right place.
When the Human Genome project found that only 2 percent of the genome coded for proteins, the right question should have been, "What is all the rest doing?" Some evolutionists were too quick to dismiss it as a pile of useless leftovers from time and chance. Cancer patients around the world can be grateful that these researchers didn't buy that explanation, but looked beyond the unknown for greater understanding.
"Research like this is helping is to unpick the precise details about how these regions work, shedding light on their potential role in the development [or prevention] of cancer and pointing towards new approaches for tackling the disease."
If a system works, it's not happening by accident. That's the intelligent-design spirit that promises to shed more light into the genomic black box.
Saturday 2 July 2016
Darwinism Vs.The real world.XXXVII
Puberty, Maturation, and Fertility: The Role of Information in Human Sexuality
Howard Glicksman
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 is delighted to offer this series, "The Designed Body." For the complete series, see here. Dr. Glicksman practices palliative medicine for a hospice organization.
The word sex comes from the Latin secare which means to separate or divide. Most one-celled organisms form offspring through asexual reproduction. It is asexual because there is no separation of genetic material. Therefore divided chromosomes do not need to be brought together and the new life produced is genetically identical to the original.
In contrast, most multi-cellular organisms form offspring in a much more complicated way called sexual reproduction. In humans, each of the chromosomes making up the 23 pairs containing the genetic material for life is separated from its partner and placed into gametes called male sperm and female eggs. Human reproduction involves sexual intercourse in which the male deposits sperm in the vagina of the female so they can move into the uterus and one of them can join its separated 23 chromosomes to the ones within the female egg in a process called fertilization. The fertilization of the female egg by the male sperm results in a one-celled zygote which then contains the full complement of genetic material and is distinct from its parents.
As difficult as it may be for evolutionary biologists to explain the blind and unguided development of the different organ systems and the body's ability to control them, because of the mechanism humans must use for reproduction they must also explain the simultaneous development of both males and females since neither is of any use to propagate the species without the other.
The three things needed for a human to reproduce are: (1) either be male or female and have all of the right sexual parts, (2) be able to produce enough sperm or release an egg into a fallopian tube, and (3) be able to participate in sexual intercourse so sperm is released into the vagina or have a clear path for sperm to swim toward the fallopian tubes.
In my last article, I showed that for the first few weeks of life the human embryo is asexual. That is because the primordial gonads have not declared themselves to be testes or ovaries yet. Notwithstanding where the embryonic structures that develop into mature sexual organs came from, the human embryo is destined to become female by default unless acted upon by specific chemicals. These include the Testis Determining Factor (TDF) (usually found on the Y chromosome), the enzymes needed to convert cholesterol into testosterone and testosterone into dihydrotestosterone, the androgen receptor on the Wolffian ducts and the tissue that will become male external genitalia, Anti-Mullerian Hormone (AMH) and the AMH receptor on the Mullerian ducts.
If all of these chemicals are present and working properly the human embryo will usually develop into a normal male. But if the TDF is absent it will usually develop into a normal female. However, if the TDF is present, directing the primordial gonads to become testosterone-producing testes, but the androgen receptor is absent or defective (Complete Androgen Insensitivity Syndrome (CAIS)), the result in an XY female. XY females occur in about one in twenty thousand "male" births and have testes instead of ovaries, no genital duct system and female external genitalia. So for the first decade of life they look like normal little girls. However, experience teaches that although humans are sexually differentiated as male or female at birth, they are not able to reproduce. Most children begin to show signs of their sexual development to come by the end of the first decade. Over the following years they will undergo sexual and bodily development in a process called puberty. Puberty is a constellation of physiological changes that, except in, for example, XY females, not only enables human beings to reproduce but also prepares them for their natural role in the family. Let's consider how this happens.
The hypothalamus and pituitary work to control many different vital hormones in the body. For example, the hypothalamus secretes Growth Hormone-Releasing Hormone, which stimulates the pituitary to release Growth Hormone (GH). As its name implies, GH is very important in the overall growth and development of the body. The hypothalamus also sends out Thyrotropin-Releasing Hormone (TRH), which tells the pituitary to send out Thyroid Stimulating Hormone (TSH). It is TSH that controls the production of thyroid hormone from the thyroid gland, which mainly affects the body's metabolic rate. Furthermore, the hypothalamus sends out Corticotropin-Releasing Hormone, which tells the pituitary to send out Adrenocorticotropin Hormone (ACTH). ACTH stimulates the adrenal glands to produce cortisol, another hormone that is important in the body's metabolism, in addition to androgenic hormones.
The hypothalamus and pituitary together control the production of a hormone such as thyroid hormone, or others, through a process called feedback inhibition. For example, the hypothalamus and the pituitary have specific receptors that allow them to sense the blood level of thyroid hormone. If it rises above what is needed the hypothalamus reduces its output of TRH and the pituitary lowers its output of TSH. The feedback of the thyroid hormone level in the blood serves to inhibit the release of TRH and TSH to maintain control of the blood level of thyroid hormone.
The production of the sex hormones is regulated in the same way by the hypothalamus and the pituitary. The hypothalamus secretes Gonadotropin-Releasing Hormone (GnRH) which attaches to specific receptors on certain cells in the pituitary and tells them to send out the gonadotropins, Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH). It is FSH and LH that attach to specific receptors on the testes or the ovaries to produce the sex hormones, testosterone and estrogen, respectively.
In the first decade of life it appears that the hypothalamus and the pituitary are very sensitive to the feedback inhibition of the sex hormones. This means that prior to puberty, very low levels of testosterone and estrogen are able to prevent the hypothalamus from releasing its GnRH and the pituitary its FSH and LH. This results in the blood levels of testosterone and estrogen being very low prior to puberty.
A few years before puberty the adrenals increase their output of androgenic hormones which causes a small growth spurt and the development of pubic and axillary hair. What actually triggers the beginning of puberty is, as yet, poorly understood. However, what is known to happen is that the hypothalamus and pituitary start to become progressively less sensitive to the sex hormones. The gradually diminishing feedback inhibition of the sex hormones on the hypothalamus and pituitary results in their slowly increasing their output of GnRH and the gonadotropins, FSH and LH, respectively. By the time puberty is in full swing, the levels of gonadotropins and the sex hormones have risen significantly.
During male puberty, more FSH and LH attach to specific receptors in the testes and cause an increase in testosterone production, while at the same time giving them the ability to produce sperm. Puberty in the male also results in the progressive increase and coarsening of facial, chest, axillary, abdominal, extremity, and pubic hair, with enlargement of the vocal cords and deepening of the voice. Moreover, with the associated increase in the pituitary output of Growth Hormone (GH), the male experiences a significant linear growth spurt and the development of his musculoskeletal system as well. Furthermore, along with the capacity for sperm production, puberty brings on enlargement of the penis, scrotum, and testes. Finally, testosterone not only plays a major role in sexual differentiation, development, and maturation, but also in the desire for sexual relations. In addition, testosterone is important in giving the male the ability to maintain an erection for adequate penetration into the vagina and ejaculation during sexual intercourse. All these developments prepare the boy to become a man and later a father.
During puberty in the female, more FSH and LH attach to specific receptors in the ovaries and cause an increase in estrogen production while at the same time giving them the ability to develop an egg. Puberty in the female results in an increase in mainly pubic and axillary hair that is not as coarse as in the male. Moreover, breast development takes place so that the potential mother will be able to provide breast milk for her infant. In addition, an increase in Growth Hormone (GH) results in a significant linear growth spurt and development of her musculoskeletal system as well. Puberty also brings on enlargement of the external genitalia and increased mucous production within the vagina and uterus. Finally, along with the capacity for egg development, the increase in FSH, LH, and estrogen allows for ovulation, where the egg is released and can enter the fallopian tube.
Inside the fallopian tube the egg can meet and join with the sperm, which has been deposited into the vagina by the male during sexual intercourse, to form new human life. After ovulation, the ovaries mainly secrete the pregnancy hormone called progesterone. The estrogen before ovulation, and the progesterone after ovulation, attach to specific receptors in the lining of the uterus to make it thicken up and produce more mucous helping it to prepare for pregnancy. If a pregnancy does not take place, the gonadotropins (FSH, LH) and the female sex hormone levels (estrogen, progesterone) drop precipitously to cause the lining of the uterus to shed in the process called menstruation. The first menstrual period generally marks the beginning of female fertility and usually takes place on a monthly basis for the next thirty or forty years.
All these developments prepare the girl to become a woman and later a mother. However, during puberty an XY female will develop normal breasts and in every way look like a normally maturing woman, except when she fails to menstruate. Investigation will then uncover her as yet unknown (even to her) secret.
Remember that an XY female has Complete Androgen Insensitivity Syndrome (CAIS). In this case, the testes form testosterone, but since the androgen receptors are absent or not working, the Wolffian ducts degenerate and the external genitalia become female. However, in addition to testosterone the testes also produce Anti-Mullerian Hormone (AMH), which attaches to specific AMH receptors on the Mullerian ducts and makes them degenerate as well. So the XY female has neither a male nor female genital duct system and her vagina ends in a blind pouch. If an XY female has testes instead of ovaries how can she develop breasts during puberty?
The answer lies in the fact that breast development does not, per se, depend only on estrogen but rather the ratio between estrogen and testosterone. Since during puberty the normal XY male produces lots of testosterone and relatively small amounts of estrogen, his breast tissue does not develop. During puberty the normal XX female produces lots of estrogen and only relatively small amounts of testosterone, so her breast tissue does develop. Although an XY female has testes that produce lots of testosterone, because there are no androgen receptors for it to take effect, this allows the small amount of estrogen she produces to dominate and cause breast development. In fact, without any androgenic effects in their bodies, XY females are some of the most femininely attractive women in the world.
As noted above, the human embryo is destined to become female by default unless several other chemicals swing into action to make it become a normal male. But that's only part of the story because for the first several years of life, humans, whether male or female, cannot reproduce. Puberty first involves an as yet unexplained reduction in feedback inhibition so there can be a significant increase in the release of GnRH from the hypothalamus and FSH and LH from the pituitary. This also requires the presence of specific receptors on their target tissues. It leads to the testes being able to produce sperm and more testosterone and the ovaries being able to release an egg and more estrogen (and progesterone) so males and females can reproduce.
It is information, wrapped in chemical signals, that makes the embryo become male or female and initiates puberty, thus making human reproduction possible. As Stephen Meyer observes in the Discovery Institute film The Information Enigma, the major discovery of the last half of the 20th century was that it is information that drives biology. In generating information, all human experience points to a mind rather than a random and unguided material process.
But clinical experience teaches that just having all of the parts present for reproduction doesn't automatically guarantee fertility and the natural ability to bring about new human life. That's what we'll begin to explore next time.
Howard Glicksman
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 is delighted to offer this series, "The Designed Body." For the complete series, see here. Dr. Glicksman practices palliative medicine for a hospice organization.
The word sex comes from the Latin secare which means to separate or divide. Most one-celled organisms form offspring through asexual reproduction. It is asexual because there is no separation of genetic material. Therefore divided chromosomes do not need to be brought together and the new life produced is genetically identical to the original.
In contrast, most multi-cellular organisms form offspring in a much more complicated way called sexual reproduction. In humans, each of the chromosomes making up the 23 pairs containing the genetic material for life is separated from its partner and placed into gametes called male sperm and female eggs. Human reproduction involves sexual intercourse in which the male deposits sperm in the vagina of the female so they can move into the uterus and one of them can join its separated 23 chromosomes to the ones within the female egg in a process called fertilization. The fertilization of the female egg by the male sperm results in a one-celled zygote which then contains the full complement of genetic material and is distinct from its parents.
As difficult as it may be for evolutionary biologists to explain the blind and unguided development of the different organ systems and the body's ability to control them, because of the mechanism humans must use for reproduction they must also explain the simultaneous development of both males and females since neither is of any use to propagate the species without the other.
The three things needed for a human to reproduce are: (1) either be male or female and have all of the right sexual parts, (2) be able to produce enough sperm or release an egg into a fallopian tube, and (3) be able to participate in sexual intercourse so sperm is released into the vagina or have a clear path for sperm to swim toward the fallopian tubes.
In my last article, I showed that for the first few weeks of life the human embryo is asexual. That is because the primordial gonads have not declared themselves to be testes or ovaries yet. Notwithstanding where the embryonic structures that develop into mature sexual organs came from, the human embryo is destined to become female by default unless acted upon by specific chemicals. These include the Testis Determining Factor (TDF) (usually found on the Y chromosome), the enzymes needed to convert cholesterol into testosterone and testosterone into dihydrotestosterone, the androgen receptor on the Wolffian ducts and the tissue that will become male external genitalia, Anti-Mullerian Hormone (AMH) and the AMH receptor on the Mullerian ducts.
If all of these chemicals are present and working properly the human embryo will usually develop into a normal male. But if the TDF is absent it will usually develop into a normal female. However, if the TDF is present, directing the primordial gonads to become testosterone-producing testes, but the androgen receptor is absent or defective (Complete Androgen Insensitivity Syndrome (CAIS)), the result in an XY female. XY females occur in about one in twenty thousand "male" births and have testes instead of ovaries, no genital duct system and female external genitalia. So for the first decade of life they look like normal little girls. However, experience teaches that although humans are sexually differentiated as male or female at birth, they are not able to reproduce. Most children begin to show signs of their sexual development to come by the end of the first decade. Over the following years they will undergo sexual and bodily development in a process called puberty. Puberty is a constellation of physiological changes that, except in, for example, XY females, not only enables human beings to reproduce but also prepares them for their natural role in the family. Let's consider how this happens.
The hypothalamus and pituitary work to control many different vital hormones in the body. For example, the hypothalamus secretes Growth Hormone-Releasing Hormone, which stimulates the pituitary to release Growth Hormone (GH). As its name implies, GH is very important in the overall growth and development of the body. The hypothalamus also sends out Thyrotropin-Releasing Hormone (TRH), which tells the pituitary to send out Thyroid Stimulating Hormone (TSH). It is TSH that controls the production of thyroid hormone from the thyroid gland, which mainly affects the body's metabolic rate. Furthermore, the hypothalamus sends out Corticotropin-Releasing Hormone, which tells the pituitary to send out Adrenocorticotropin Hormone (ACTH). ACTH stimulates the adrenal glands to produce cortisol, another hormone that is important in the body's metabolism, in addition to androgenic hormones.
The hypothalamus and pituitary together control the production of a hormone such as thyroid hormone, or others, through a process called feedback inhibition. For example, the hypothalamus and the pituitary have specific receptors that allow them to sense the blood level of thyroid hormone. If it rises above what is needed the hypothalamus reduces its output of TRH and the pituitary lowers its output of TSH. The feedback of the thyroid hormone level in the blood serves to inhibit the release of TRH and TSH to maintain control of the blood level of thyroid hormone.
The production of the sex hormones is regulated in the same way by the hypothalamus and the pituitary. The hypothalamus secretes Gonadotropin-Releasing Hormone (GnRH) which attaches to specific receptors on certain cells in the pituitary and tells them to send out the gonadotropins, Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH). It is FSH and LH that attach to specific receptors on the testes or the ovaries to produce the sex hormones, testosterone and estrogen, respectively.
In the first decade of life it appears that the hypothalamus and the pituitary are very sensitive to the feedback inhibition of the sex hormones. This means that prior to puberty, very low levels of testosterone and estrogen are able to prevent the hypothalamus from releasing its GnRH and the pituitary its FSH and LH. This results in the blood levels of testosterone and estrogen being very low prior to puberty.
A few years before puberty the adrenals increase their output of androgenic hormones which causes a small growth spurt and the development of pubic and axillary hair. What actually triggers the beginning of puberty is, as yet, poorly understood. However, what is known to happen is that the hypothalamus and pituitary start to become progressively less sensitive to the sex hormones. The gradually diminishing feedback inhibition of the sex hormones on the hypothalamus and pituitary results in their slowly increasing their output of GnRH and the gonadotropins, FSH and LH, respectively. By the time puberty is in full swing, the levels of gonadotropins and the sex hormones have risen significantly.
During male puberty, more FSH and LH attach to specific receptors in the testes and cause an increase in testosterone production, while at the same time giving them the ability to produce sperm. Puberty in the male also results in the progressive increase and coarsening of facial, chest, axillary, abdominal, extremity, and pubic hair, with enlargement of the vocal cords and deepening of the voice. Moreover, with the associated increase in the pituitary output of Growth Hormone (GH), the male experiences a significant linear growth spurt and the development of his musculoskeletal system as well. Furthermore, along with the capacity for sperm production, puberty brings on enlargement of the penis, scrotum, and testes. Finally, testosterone not only plays a major role in sexual differentiation, development, and maturation, but also in the desire for sexual relations. In addition, testosterone is important in giving the male the ability to maintain an erection for adequate penetration into the vagina and ejaculation during sexual intercourse. All these developments prepare the boy to become a man and later a father.
During puberty in the female, more FSH and LH attach to specific receptors in the ovaries and cause an increase in estrogen production while at the same time giving them the ability to develop an egg. Puberty in the female results in an increase in mainly pubic and axillary hair that is not as coarse as in the male. Moreover, breast development takes place so that the potential mother will be able to provide breast milk for her infant. In addition, an increase in Growth Hormone (GH) results in a significant linear growth spurt and development of her musculoskeletal system as well. Puberty also brings on enlargement of the external genitalia and increased mucous production within the vagina and uterus. Finally, along with the capacity for egg development, the increase in FSH, LH, and estrogen allows for ovulation, where the egg is released and can enter the fallopian tube.
Inside the fallopian tube the egg can meet and join with the sperm, which has been deposited into the vagina by the male during sexual intercourse, to form new human life. After ovulation, the ovaries mainly secrete the pregnancy hormone called progesterone. The estrogen before ovulation, and the progesterone after ovulation, attach to specific receptors in the lining of the uterus to make it thicken up and produce more mucous helping it to prepare for pregnancy. If a pregnancy does not take place, the gonadotropins (FSH, LH) and the female sex hormone levels (estrogen, progesterone) drop precipitously to cause the lining of the uterus to shed in the process called menstruation. The first menstrual period generally marks the beginning of female fertility and usually takes place on a monthly basis for the next thirty or forty years.
All these developments prepare the girl to become a woman and later a mother. However, during puberty an XY female will develop normal breasts and in every way look like a normally maturing woman, except when she fails to menstruate. Investigation will then uncover her as yet unknown (even to her) secret.
Remember that an XY female has Complete Androgen Insensitivity Syndrome (CAIS). In this case, the testes form testosterone, but since the androgen receptors are absent or not working, the Wolffian ducts degenerate and the external genitalia become female. However, in addition to testosterone the testes also produce Anti-Mullerian Hormone (AMH), which attaches to specific AMH receptors on the Mullerian ducts and makes them degenerate as well. So the XY female has neither a male nor female genital duct system and her vagina ends in a blind pouch. If an XY female has testes instead of ovaries how can she develop breasts during puberty?
The answer lies in the fact that breast development does not, per se, depend only on estrogen but rather the ratio between estrogen and testosterone. Since during puberty the normal XY male produces lots of testosterone and relatively small amounts of estrogen, his breast tissue does not develop. During puberty the normal XX female produces lots of estrogen and only relatively small amounts of testosterone, so her breast tissue does develop. Although an XY female has testes that produce lots of testosterone, because there are no androgen receptors for it to take effect, this allows the small amount of estrogen she produces to dominate and cause breast development. In fact, without any androgenic effects in their bodies, XY females are some of the most femininely attractive women in the world.
As noted above, the human embryo is destined to become female by default unless several other chemicals swing into action to make it become a normal male. But that's only part of the story because for the first several years of life, humans, whether male or female, cannot reproduce. Puberty first involves an as yet unexplained reduction in feedback inhibition so there can be a significant increase in the release of GnRH from the hypothalamus and FSH and LH from the pituitary. This also requires the presence of specific receptors on their target tissues. It leads to the testes being able to produce sperm and more testosterone and the ovaries being able to release an egg and more estrogen (and progesterone) so males and females can reproduce.
It is information, wrapped in chemical signals, that makes the embryo become male or female and initiates puberty, thus making human reproduction possible. As Stephen Meyer observes in the Discovery Institute film The Information Enigma, the major discovery of the last half of the 20th century was that it is information that drives biology. In generating information, all human experience points to a mind rather than a random and unguided material process.
But clinical experience teaches that just having all of the parts present for reproduction doesn't automatically guarantee fertility and the natural ability to bring about new human life. That's what we'll begin to explore next time.
On the collapse Darwinism's prima facie case.
Alleged Instances of Observed Speciation -- Evolution's Smoking Gun Is Still Missing
Editor's note: William Dembski and Jonathan Wells, leading figures in the intelligent design movement, are co-authors of The Design of Life: Discovering Signs of Intelligence in Biological Systems. Originally published by the Foundation for Thought and Ethics, this path-breaking work explores some of the most important arguments for intelligent design in biology. To celebrate the launch of Foundation for Thought & Ethics Books as an imprint of Discovery Institute Press, we will be publishing excerpts from the book here at Evolution News. Through July 8, we will also be making the book available for only $10 -- that's more than a 70 percent discount, and it includes both the full-color hardcover and an accompanying CD with additional materials. If you haven't read this classic book, now is your chance! Order now, because this special discount won't last long.
Despite the absence of evidence for the ability of reproductive isolation to harness the mechanisms of genetic change and thereby to produce new species, some Darwinists still claim that there are many instances of observed speciation.1 But most of these alleged instances are in fact analyses of existing species that are used to defend one or another theory of how they might have originated -- such as the theories of allopatric and sympatric speciation, or the bottleneck and founder effects. Analyzing existing species to support one or another theory of speciation, however, is not the same as observing speciation in action.
There actually are some confirmed cases of observed speciation, but these are due to an increase in the number of chromosomes, or "polyploidy." Such cases, however, are limited to flowering plants and result from hybridizing two species to form a new one.2 Furthermore, according to evolutionary biologist Douglas Futuyma, speciation that results from polyploidy (also called "secondary speciation") "does not confer major new morphological characteristics . . . [and] does not cause the evolution of new genera" or higher taxonomic levels.3 Darwinian evolution, by contrast, depends on taking a single existing species and splitting off new species from it (called "primary speciation"), which then in turn diverge and split, diverge and split, over and over again. Only primary speciation, and not secondary speciation, could produce the branching-tree pattern required by Darwinian evolution.
Of the many instances of observed speciation alleged by Darwinists, only five come close to claiming observed primary speciation. First, in 1962, from a single lab population of Drosophila (fruit flies), J.M. Thoday and J.B. Gibson bred only those flies with the highest and lowest number of bristles (the insect equivalent of hair). After 12 generations, the experiment produced two populations that not only differed in bristle number but also showed "strong though partial isolation." Yet Thoday and Gibson not did claim to have produced a new species. Furthermore, other laboratories were unable to reproduce their results.4
Second, in 1958 Theodosius Dobzhansky and Olga Pavlovsky started a laboratory population of fruit flies using a single female of a strain from Colombia. Crosses between that fly and several other strains produced fertile hybrids in the laboratory. In 1963, however, similar crosses yielded sterile hybrids. In 1966, Dobzhansky and Pavlovsky concluded that the strain they had introduced in 1958 had become "a new race or incipient species . . . in the laboratory at some time between 1958 and 1963."5 But Coyne and Orr, writing in 2004, suspect their results were "due to contamination of cultures by other subspecies."6 In any case, Dobzhansky and Pavlovsky reported only a "new race or incipient species," not a new species.
Third, in 1964 biologists collected some marine worms in Los Angeles Harbor and used them to start a lab colony. When they went back to the same location 12 years later, the original population had disappeared, so they collected worms from two other locations several miles away, and these were used to start two new lab colonies. In 1989, researchers found that the two new colonies could interbreed with each other but not with the Los Angeles Harbor colony that had been started 25 years earlier. In 1992, James Weinberg and his colleagues called this an observed instance of "rapid speciation," based on the assumption that the original colony had "speciated in the laboratory, rather than before 1964."7 A few years later, however, tests performed by Weinberg and two others showed that the original population was "already a species different from" the two new colonies "at the time when it was originally sampled in 1964."8 No speciation had occurred.
Fourth, in 1969 E. Paterniani reported an experiment on maize in which breeding was permitted only between individuals possessing two extremes of a particular trait. Paterniani noted the development of "an almost complete reproductive isolation between two maize populations" but did not claim that a new species had been produced.9
Fifth and last, in the 1980s William R. Rice and George W. Salt subjected a population of fruit flies to eight different environments. They then took the flies that preferred the two most extreme environments and allowed only them to breed. Within thirty generations the flies had sorted themselves into two populations that did not interbreed. Even so, Rice and Salt did not claim to have produced two new species. More modestly, they believed only that "incipient speciation" had occurred.10
So, of the five alleged instances of observed primary speciation, only one (Weinberg's) claimed to have observed actual speciation -- and it was later retracted. The other four (one of which could not be reproduced by other scientists and one of which was not controlled for contamination) claimed only some degree of reproductive isolation or "incipient speciation."
What is "incipient speciation"? Darwin wrote: "According to my view, varieties are species in the process of formation, or are, as I have called them, incipient species."11 But how can we possibly know whether two varieties (or races) are in the process of becoming separate species? St. Bernards and Chihuahuas are two varieties of dog that cannot interbreed naturally, but they are members of the same species. Maybe they are on their way to becoming separate species, or maybe not. The two varieties of Rhagoletis pomonella described in the previous section do not interbreed in the wild, but they look exactly alike and are still capable of mating in the laboratory. Like different breeds of dogs, they are still members of the same species. Calling them "incipient species" amounts to no more than a prediction that they will eventually become separate species. But maybe they won't. Short of waiting to see whether the prediction comes true, we can't really know. And given our limited lifespans, we don't have time to wait (at least not by conventional evolutionary timescales).
Darwinists therefore discount the lack of observed instances of primary speciation by saying that it takes too long to observe them. But if it takes too long for scientific investigators to observe primary speciation, then there will never be anything more than indirect evidence for the first and most important step in Darwinian evolution. Darwinists claim that all species have descended from a common ancestor through variation and selection. But until they can point to a single observed instance of primary speciation, their claim must remain an unverified assumption, not an observed scientific fact. University of Bristol bacteriologist Alan H. Linton made precisely this point when in 2001 he assessed the direct evidence of speciation:
None exists in the literature claiming that one species has been shown to evolve into another. Bacteria, the simplest form of independent life, are ideal for this kind of study, with generation times of twenty to thirty minutes, and populations achieved after eighteen hours. But throughout 150 years of the science of bacteriology, there is no evidence that one species of bacteria has changed into another. . . . Since there is no evidence for species changes between the simplest forms of unicellular life, it is not surprising that there is no evidence for evolution from prokaryotic [e.g., bacterial] to eukaryotic [e.g., plant and animal] cells, let alone throughout the whole array of higher multicellular organisms.12
So except for secondary speciation, which is not what Darwin's theory needs, there are no observed instances of the origin of species. As evolutionary biologists Lynn Margulis and Dorion Sagan wrote in 2002: "Speciation, whether in the remote Galápagos, in the laboratory cages of the drosophilosophers, or in the crowded sediments of the paleontologists, still has never been directly traced."13 Evolution's smoking gun is still missing.
References:
(1) See Catherine A. Callaghan, "Instances of Observed Speciation," The American Biology Teacher 49 (1987): 34–36; Joseph Boxhorn, "Observed Instances of Speciation," The Talk.Origins Archive, September 1, 1995, available online (last accessed January 9, 2007); Chris Stassen, James Meritt, Annelise Lilje, and L. Drew Davis, "Some More Observed Speciation Events," The Talk.Origins Archive, 1997, available online (last accessed January 9, 2007).
(2) See Justin Ramsey and Douglas W. Schemske, "Neopolyploidy in Flowering Plants," Annual Review of Ecology and Systematics 33 (2002): 589–639; D. M. Rosenthal, L. H. Rieseberg, and L. A. Donovan, "Re-creating Ancient Hybrid Species' Complex Phenotypes from Early-Generation Synthetic Hybrids: Three Examples Using Wild Sunflowers," The American Naturalist 166(1) (2005): 26–41.
(3) Douglas J. Futuyma, Evolution (Sunderland, Mass.: Sinauer Associates, 2005), 398.
(4) J.M. Thoday and J. B. Gibson, "Isolation by Disruptive Selection," Nature 193 (1962): 1164–1166. J. M. Thoday and J. B. Gibson, "The Probability of Isolation by Disruptive Selection," The American Naturalist 104 (1970): 219–230. Coyne and Orr, Speciation, 138.
(5) Theodosius Dobzhansky and Olga Pavlovsky, "Spontaneous Origin of an Incipient Species in the Drosophila Paulistorum Complex," Proceedings of the National Academy of Sciences 55 (1966): 727–733.
(6) Coyne and Orr, Speciation, 138.
(7) James R. Weinberg, Victoria R. Starczak, and Daniele Jörg, "Evidence for Rapid Speciation Following a Founder Event in the Laboratory," Evolution 46 (1992): 1214–1220.
(8) Francisco Rodriquez-Trelles, James R. Weinberg, and Francisco J. Ayala, "Presumptive Rapid Speciation After a Founder Event in a Laboratory Population of Nereis: Allozyme Electrophoretic Evidence Does Not Support the Hypothesis," Evolution 50 (1996): 457–461.
(9) E. Paterniani, "Selection for Reproductive Isolation Between Two Populations of Maize, Zea mays L.," Evolution 23 (1969): 534–547.
(10) William R. Rice and George W. Salt, "Speciation via Disruptive Selection on Habitat Preference: Experimental Evidence," The American Naturalist 131 (1988): 911–917. See also Coyne and Orr, Speciation, 138–141.
(11) Darwin, Origin of Species, 111.
(12) Alan Linton, "Scant Search for the Maker," The Times Higher Education Supplement (April 20, 2001), Book Section, 29, available online with registration (last accessed January 9, 2007).
(13) Lynn Margulis and Dorion Sagan, Acquiring Genomes: A Theory of the Origins of Species (New York: Basic Books, 2002), 32.
Editor's note: William Dembski and Jonathan Wells, leading figures in the intelligent design movement, are co-authors of The Design of Life: Discovering Signs of Intelligence in Biological Systems. Originally published by the Foundation for Thought and Ethics, this path-breaking work explores some of the most important arguments for intelligent design in biology. To celebrate the launch of Foundation for Thought & Ethics Books as an imprint of Discovery Institute Press, we will be publishing excerpts from the book here at Evolution News. Through July 8, we will also be making the book available for only $10 -- that's more than a 70 percent discount, and it includes both the full-color hardcover and an accompanying CD with additional materials. If you haven't read this classic book, now is your chance! Order now, because this special discount won't last long.
Despite the absence of evidence for the ability of reproductive isolation to harness the mechanisms of genetic change and thereby to produce new species, some Darwinists still claim that there are many instances of observed speciation.1 But most of these alleged instances are in fact analyses of existing species that are used to defend one or another theory of how they might have originated -- such as the theories of allopatric and sympatric speciation, or the bottleneck and founder effects. Analyzing existing species to support one or another theory of speciation, however, is not the same as observing speciation in action.
There actually are some confirmed cases of observed speciation, but these are due to an increase in the number of chromosomes, or "polyploidy." Such cases, however, are limited to flowering plants and result from hybridizing two species to form a new one.2 Furthermore, according to evolutionary biologist Douglas Futuyma, speciation that results from polyploidy (also called "secondary speciation") "does not confer major new morphological characteristics . . . [and] does not cause the evolution of new genera" or higher taxonomic levels.3 Darwinian evolution, by contrast, depends on taking a single existing species and splitting off new species from it (called "primary speciation"), which then in turn diverge and split, diverge and split, over and over again. Only primary speciation, and not secondary speciation, could produce the branching-tree pattern required by Darwinian evolution.
Of the many instances of observed speciation alleged by Darwinists, only five come close to claiming observed primary speciation. First, in 1962, from a single lab population of Drosophila (fruit flies), J.M. Thoday and J.B. Gibson bred only those flies with the highest and lowest number of bristles (the insect equivalent of hair). After 12 generations, the experiment produced two populations that not only differed in bristle number but also showed "strong though partial isolation." Yet Thoday and Gibson not did claim to have produced a new species. Furthermore, other laboratories were unable to reproduce their results.4
Second, in 1958 Theodosius Dobzhansky and Olga Pavlovsky started a laboratory population of fruit flies using a single female of a strain from Colombia. Crosses between that fly and several other strains produced fertile hybrids in the laboratory. In 1963, however, similar crosses yielded sterile hybrids. In 1966, Dobzhansky and Pavlovsky concluded that the strain they had introduced in 1958 had become "a new race or incipient species . . . in the laboratory at some time between 1958 and 1963."5 But Coyne and Orr, writing in 2004, suspect their results were "due to contamination of cultures by other subspecies."6 In any case, Dobzhansky and Pavlovsky reported only a "new race or incipient species," not a new species.
Third, in 1964 biologists collected some marine worms in Los Angeles Harbor and used them to start a lab colony. When they went back to the same location 12 years later, the original population had disappeared, so they collected worms from two other locations several miles away, and these were used to start two new lab colonies. In 1989, researchers found that the two new colonies could interbreed with each other but not with the Los Angeles Harbor colony that had been started 25 years earlier. In 1992, James Weinberg and his colleagues called this an observed instance of "rapid speciation," based on the assumption that the original colony had "speciated in the laboratory, rather than before 1964."7 A few years later, however, tests performed by Weinberg and two others showed that the original population was "already a species different from" the two new colonies "at the time when it was originally sampled in 1964."8 No speciation had occurred.
Fourth, in 1969 E. Paterniani reported an experiment on maize in which breeding was permitted only between individuals possessing two extremes of a particular trait. Paterniani noted the development of "an almost complete reproductive isolation between two maize populations" but did not claim that a new species had been produced.9
Fifth and last, in the 1980s William R. Rice and George W. Salt subjected a population of fruit flies to eight different environments. They then took the flies that preferred the two most extreme environments and allowed only them to breed. Within thirty generations the flies had sorted themselves into two populations that did not interbreed. Even so, Rice and Salt did not claim to have produced two new species. More modestly, they believed only that "incipient speciation" had occurred.10
So, of the five alleged instances of observed primary speciation, only one (Weinberg's) claimed to have observed actual speciation -- and it was later retracted. The other four (one of which could not be reproduced by other scientists and one of which was not controlled for contamination) claimed only some degree of reproductive isolation or "incipient speciation."
What is "incipient speciation"? Darwin wrote: "According to my view, varieties are species in the process of formation, or are, as I have called them, incipient species."11 But how can we possibly know whether two varieties (or races) are in the process of becoming separate species? St. Bernards and Chihuahuas are two varieties of dog that cannot interbreed naturally, but they are members of the same species. Maybe they are on their way to becoming separate species, or maybe not. The two varieties of Rhagoletis pomonella described in the previous section do not interbreed in the wild, but they look exactly alike and are still capable of mating in the laboratory. Like different breeds of dogs, they are still members of the same species. Calling them "incipient species" amounts to no more than a prediction that they will eventually become separate species. But maybe they won't. Short of waiting to see whether the prediction comes true, we can't really know. And given our limited lifespans, we don't have time to wait (at least not by conventional evolutionary timescales).
Darwinists therefore discount the lack of observed instances of primary speciation by saying that it takes too long to observe them. But if it takes too long for scientific investigators to observe primary speciation, then there will never be anything more than indirect evidence for the first and most important step in Darwinian evolution. Darwinists claim that all species have descended from a common ancestor through variation and selection. But until they can point to a single observed instance of primary speciation, their claim must remain an unverified assumption, not an observed scientific fact. University of Bristol bacteriologist Alan H. Linton made precisely this point when in 2001 he assessed the direct evidence of speciation:
None exists in the literature claiming that one species has been shown to evolve into another. Bacteria, the simplest form of independent life, are ideal for this kind of study, with generation times of twenty to thirty minutes, and populations achieved after eighteen hours. But throughout 150 years of the science of bacteriology, there is no evidence that one species of bacteria has changed into another. . . . Since there is no evidence for species changes between the simplest forms of unicellular life, it is not surprising that there is no evidence for evolution from prokaryotic [e.g., bacterial] to eukaryotic [e.g., plant and animal] cells, let alone throughout the whole array of higher multicellular organisms.12
So except for secondary speciation, which is not what Darwin's theory needs, there are no observed instances of the origin of species. As evolutionary biologists Lynn Margulis and Dorion Sagan wrote in 2002: "Speciation, whether in the remote Galápagos, in the laboratory cages of the drosophilosophers, or in the crowded sediments of the paleontologists, still has never been directly traced."13 Evolution's smoking gun is still missing.
References:
(1) See Catherine A. Callaghan, "Instances of Observed Speciation," The American Biology Teacher 49 (1987): 34–36; Joseph Boxhorn, "Observed Instances of Speciation," The Talk.Origins Archive, September 1, 1995, available online (last accessed January 9, 2007); Chris Stassen, James Meritt, Annelise Lilje, and L. Drew Davis, "Some More Observed Speciation Events," The Talk.Origins Archive, 1997, available online (last accessed January 9, 2007).
(2) See Justin Ramsey and Douglas W. Schemske, "Neopolyploidy in Flowering Plants," Annual Review of Ecology and Systematics 33 (2002): 589–639; D. M. Rosenthal, L. H. Rieseberg, and L. A. Donovan, "Re-creating Ancient Hybrid Species' Complex Phenotypes from Early-Generation Synthetic Hybrids: Three Examples Using Wild Sunflowers," The American Naturalist 166(1) (2005): 26–41.
(3) Douglas J. Futuyma, Evolution (Sunderland, Mass.: Sinauer Associates, 2005), 398.
(4) J.M. Thoday and J. B. Gibson, "Isolation by Disruptive Selection," Nature 193 (1962): 1164–1166. J. M. Thoday and J. B. Gibson, "The Probability of Isolation by Disruptive Selection," The American Naturalist 104 (1970): 219–230. Coyne and Orr, Speciation, 138.
(5) Theodosius Dobzhansky and Olga Pavlovsky, "Spontaneous Origin of an Incipient Species in the Drosophila Paulistorum Complex," Proceedings of the National Academy of Sciences 55 (1966): 727–733.
(6) Coyne and Orr, Speciation, 138.
(7) James R. Weinberg, Victoria R. Starczak, and Daniele Jörg, "Evidence for Rapid Speciation Following a Founder Event in the Laboratory," Evolution 46 (1992): 1214–1220.
(8) Francisco Rodriquez-Trelles, James R. Weinberg, and Francisco J. Ayala, "Presumptive Rapid Speciation After a Founder Event in a Laboratory Population of Nereis: Allozyme Electrophoretic Evidence Does Not Support the Hypothesis," Evolution 50 (1996): 457–461.
(9) E. Paterniani, "Selection for Reproductive Isolation Between Two Populations of Maize, Zea mays L.," Evolution 23 (1969): 534–547.
(10) William R. Rice and George W. Salt, "Speciation via Disruptive Selection on Habitat Preference: Experimental Evidence," The American Naturalist 131 (1988): 911–917. See also Coyne and Orr, Speciation, 138–141.
(11) Darwin, Origin of Species, 111.
(12) Alan Linton, "Scant Search for the Maker," The Times Higher Education Supplement (April 20, 2001), Book Section, 29, available online with registration (last accessed January 9, 2007).
(13) Lynn Margulis and Dorion Sagan, Acquiring Genomes: A Theory of the Origins of Species (New York: Basic Books, 2002), 32.
Why the geekocracy will not save us.
Science, Knowledge, and the "Epistemic Horizon"
David Klinghoffer
National Review Online's Kevin Williamson has sometimes rubbed me the wrong way, but in the 24 hours or so since Neil deGrasse Tyson shot off his "#Rationalia" tweet, Williamson composed an essay in response that can only be called profound. Tyson, the "dumbest smart person on Twitter," proposed a "virtual country," with a "one-line Constitution: All policy shall be based on the weight of evidence." In reply, Williamson offers the image of a limit to knowledge, an "epistemtic horizon" like the "event horizon" of a black hole.
Read it all for yourself, but this is the conclusion and upshot:
The epistemic horizon is not very broad. We do not, in fact, know what the results of various kinds of economic policies or social policies will be, and there isn't any evidence that can tell us with any degree of certainty. The housing projects that mar our cities weren't supposed to turn out like that; neither was the federal push to encourage home-ownership or to encourage the substitution of carbohydrates for fats and proteins in our diets. A truly rational policy of the sort that Tyson imagines must take into account not only how little we know about the future but how little we can know about the future, even if we consult the smartest, saintliest, and most disinterested experts among us.
That is part of the case for limited government and free markets. Government can do some things, such as guard borders (though ours chooses not to) and fight off foreign invaders. There are things that it cannot do, even in principle, such as impose a "rational" order on the nation's energy markets, deciding that x share of our electricity supply shall come from solar, y share from wind, z share from natural gas, all calculated to economic and environmental ideals. That is simply beyond its ken, even if all the best people -- including Tyson, from time to time -- pretend that it is otherwise. Free markets go about solving social problems in the opposite way: Dozens, or thousands, or millions, or even billions of people, firms, organizations, investors, and business managers trying dozens or thousands of approaches to solving social problems....
There isn't a road to Rationalia. There are billions of them, negotiated by individuals and institutions dozens or hundreds of times a day, every time they make a significant choice. Government programs are, by their nature, centralized, unitary, and static attempts to impose a rational order on complexity beyond the understanding of the people who would claim to manage it....
It isn't ideology that imposes a relatively narrow circle on what government planners can do. And, with all due respect to the genius of F. A. Hayek ("The curious task of economics is to demonstrate to men how little they really know about what they imagine they can design"), it isn't only economics, either. The limitations on human knowledge are real, and they are consequential. As men like him have done for ages, Tyson dreams of a world of self-evident choices, overseen by men of reason such as himself who occupy a position that we cannot help but notice is godlike. It's nice to imagine ruling from an Olympus of Reason, with men and nations arrayed before one as on a chessboard.
Down here on Earth, the view is rather different, and the lines of sight inside the epistemic horizon are not nearly so long as our would-be rulers imagine.
I would add -- and this he doesn't say -- that the idea of a limit or horizon to knowledge goes far beyond politics, economics, urban planning, the issues that seem to animate Kevin Williamson. It includes faith, notwithstanding the certainty of the New Atheists and some religious spokesmen as well. In this context, I think of the Talmud's interesting gnomic statement warning of four boundaries of reality beyond which we are better off not seeking to gaze -- "what is above, what is below, what was before, and what will be after."
The idea of an epistemic horizon definitely includes science, especially historical scientific theories that seek to lay bare biological origins. Everyone who speaks about science in public should be reminded of this.
I don't mean we can never have an informed opinion on how life arose, became complex and diverse. That's exactly what we talk about when we talk about intelligent design. But the horizon should be kept in view when we hear Darwinian evolution asserted as "fact" -- "as much a fact as gravity or erosion," in a typical formulation. No, that is wrong.
ID advocates don't talk that way -- ID as "fact," rather than a tentative inference. And good for them. That modesty is a point in favor of the design argument.
David Klinghoffer
National Review Online's Kevin Williamson has sometimes rubbed me the wrong way, but in the 24 hours or so since Neil deGrasse Tyson shot off his "#Rationalia" tweet, Williamson composed an essay in response that can only be called profound. Tyson, the "dumbest smart person on Twitter," proposed a "virtual country," with a "one-line Constitution: All policy shall be based on the weight of evidence." In reply, Williamson offers the image of a limit to knowledge, an "epistemtic horizon" like the "event horizon" of a black hole.
Read it all for yourself, but this is the conclusion and upshot:
The epistemic horizon is not very broad. We do not, in fact, know what the results of various kinds of economic policies or social policies will be, and there isn't any evidence that can tell us with any degree of certainty. The housing projects that mar our cities weren't supposed to turn out like that; neither was the federal push to encourage home-ownership or to encourage the substitution of carbohydrates for fats and proteins in our diets. A truly rational policy of the sort that Tyson imagines must take into account not only how little we know about the future but how little we can know about the future, even if we consult the smartest, saintliest, and most disinterested experts among us.
That is part of the case for limited government and free markets. Government can do some things, such as guard borders (though ours chooses not to) and fight off foreign invaders. There are things that it cannot do, even in principle, such as impose a "rational" order on the nation's energy markets, deciding that x share of our electricity supply shall come from solar, y share from wind, z share from natural gas, all calculated to economic and environmental ideals. That is simply beyond its ken, even if all the best people -- including Tyson, from time to time -- pretend that it is otherwise. Free markets go about solving social problems in the opposite way: Dozens, or thousands, or millions, or even billions of people, firms, organizations, investors, and business managers trying dozens or thousands of approaches to solving social problems....
There isn't a road to Rationalia. There are billions of them, negotiated by individuals and institutions dozens or hundreds of times a day, every time they make a significant choice. Government programs are, by their nature, centralized, unitary, and static attempts to impose a rational order on complexity beyond the understanding of the people who would claim to manage it....
It isn't ideology that imposes a relatively narrow circle on what government planners can do. And, with all due respect to the genius of F. A. Hayek ("The curious task of economics is to demonstrate to men how little they really know about what they imagine they can design"), it isn't only economics, either. The limitations on human knowledge are real, and they are consequential. As men like him have done for ages, Tyson dreams of a world of self-evident choices, overseen by men of reason such as himself who occupy a position that we cannot help but notice is godlike. It's nice to imagine ruling from an Olympus of Reason, with men and nations arrayed before one as on a chessboard.
Down here on Earth, the view is rather different, and the lines of sight inside the epistemic horizon are not nearly so long as our would-be rulers imagine.
I would add -- and this he doesn't say -- that the idea of a limit or horizon to knowledge goes far beyond politics, economics, urban planning, the issues that seem to animate Kevin Williamson. It includes faith, notwithstanding the certainty of the New Atheists and some religious spokesmen as well. In this context, I think of the Talmud's interesting gnomic statement warning of four boundaries of reality beyond which we are better off not seeking to gaze -- "what is above, what is below, what was before, and what will be after."
The idea of an epistemic horizon definitely includes science, especially historical scientific theories that seek to lay bare biological origins. Everyone who speaks about science in public should be reminded of this.
I don't mean we can never have an informed opinion on how life arose, became complex and diverse. That's exactly what we talk about when we talk about intelligent design. But the horizon should be kept in view when we hear Darwinian evolution asserted as "fact" -- "as much a fact as gravity or erosion," in a typical formulation. No, that is wrong.
ID advocates don't talk that way -- ID as "fact," rather than a tentative inference. And good for them. That modesty is a point in favor of the design argument.
Friday 1 July 2016
On the challenge of protecting our children:a commentary by the Watchtower Society
How to Protect Your Children
FEW of us want to dwell on the subject of sexual abuse of children. Parents shudder at the very thought of it! Such abuse, however, is a frightening and unpleasant reality in today’s world, and its effects on children can be devastating. Is the matter worth considering? Well, what would you be willing to give for the sake of your child’s safety? Learning about the unpleasant realities of abuse is surely a small price to pay. Such knowledge can really make a difference.
Do not let the plague of abuse rob you of your courage. At the very least, you have power that your child does not have—strengths that it will take years, even decades, for your child to gain. The passing years have brought you a fund of knowledge, experience, and wisdom. The key is to enhance those strengths and put them to use in protecting your child. We will discuss three basic steps that every parent can take. They are as follows: (1) Become your child’s first line of defense against abuse, (2) give your child some needed background education, and (3) equip your child with some basic protective tools.
Are You the First Line of Defense?
The primary responsibility for protecting children against abuse belongs to parents, not to children. So educating parents comes before educating children. If you are a parent, there are a few things you need to know about child abuse. You need to know who abuse children and how they go about it. Parents often think of molesters as strangers who lurk in the shadows, seeking ways to kidnap and rape children. Such monsters certainly do exist. The news media bring them to our attention very often. However, they are relatively rare. In about 90 percent of the cases of sexual abuse of a child, the perpetrator is someone the child already knows and trusts.
Naturally, you do not want to believe that an affable neighbor, teacher, health-care worker, coach, or relative could lust after your child. In truth, most people are not like that. There is no need to become suspicious of everybody around you. Still, you can protect your child by learning how the typical abuser operates.—See the box on page 6.
Knowing such tactics can make you, the parent, better prepared to act as the first line of defense. For instance, if someone who appears more interested in children than in adults singles out your child for special attention and gifts or offers free babysitting or private excursions with your child, what will you do? Decide that the person must be a molester? No. Do not be quick to jump to conclusions. Such behavior may be quite innocent. Nonetheless, it can put you on the alert. The Bible says: “Anyone inexperienced puts faith in every word, but the shrewd one considers his steps.”—Proverbs 14:15.
Remember, any offer that sounds too good to be true may be just that. Carefully screen anyone who volunteers to spend time alone with your child. Let such an individual know that you are likely to check on your child at any time. Melissa and Brad, young parents of three boys, are cautious about leaving a child alone with an adult. When one son had music lessons at home, Melissa told the instructor: “I’ll be in and out of the room while you’re here.” Such vigilance may sound extreme, but these parents would rather be safe than sorry.
Be actively involved in your child’s activities, friendships, and schoolwork. Learn all the details about any planned excursion. One mental-health professional who spent 33 years working with cases of sexual abuse notes that he has seen countless cases that could have been prevented by simple vigilance on the parents’ part. He quotes one convicted molester as saying: “Parents literally give us their children. . . . They sure made it easy for me.” Remember, most molesters prefer easy targets. Parents who are actively involved in their children’s lives make their children difficult targets.
Another way to act as your child’s first line of defense is to be a good listener. Children will rarely disclose abuse directly; they are too ashamed and worried about the reaction. So listen carefully, even for subtle clues.* If your child says something that concerns you, calmly use questions to draw him out.* If he says that he does not want a certain babysitter to come back, ask why. If he says that an adult plays funny games with him, ask him: “What kind of game? What does he do?” If he complains that someone tickled him, ask him, “Where did he tickle you?” Do not be quick to dismiss a child’s answers. Abusers tell a child that no one will believe him; all too often, that is true. And if a child has been abused, being believed and supported by a parent is a big step toward recovery.
Be your child’s first line of defense
Give Your Child Background Education
One reference work on the subject of child abuse quotes a convicted molester as saying: “Give me a kid who knows nothing about sex, and you’ve given me my next victim.” Those chilling words are a useful reminder to parents. Children who are ignorant about sex are much easier for molesters to fool. The Bible says that knowledge and wisdom can deliver us “from the man speaking perverse things.” (Proverbs 2:10-12) Is that not what you want for your child? Then, as your second basic step in protecting him, do not hold back from teaching him about this important subject.
How, though, do you go about it? More than a few parents find the subject of sex a bit awkward to discuss with children. Your child may find the subject even more awkward, and he is not likely to bring it up with you. So take the initiative. Melissa says: “We started early, with naming the body parts. We used real words, not baby words, to show them that there is nothing funny or shameful about any part of their body.” Instruction about abuse follows naturally. Many parents simply tell their children that the parts of their body that a bathing suit covers are private and special.
Says Heather, mentioned in the preceding article: “Scott and I told our son that his penis is private, personal, and not a toy. It’s not for anyone to play with—not for Mommy, not for Daddy, not even for a doctor. When we take him to the doctor, I explain that he’s only going to make sure everything is OK, and that’s why he may touch there.” Both parents take part in these little talks from time to time, and they assure the child that he can always come to them and tell them if anyone touches him in a way that’s wrong or makes him feel uncomfortable. Experts in child care and abuse prevention recommend that all parents have similar talks with their children.
Many have found the book Learn From the Great Teacher* to be a real help in teaching this subject. Chapter 32, “How Jesus Was Protected,” has a direct yet comforting message for children on the dangers of abuse and the importance of staying safe. “The book has given us a perfect way to reinforce what we have told our children personally,” says Melissa.
In today’s world children need to know that there are some people who want to touch children or get children to touch them in ways that are wrong. These warnings need not fill children with fear or make them distrust all adults. “It’s just a safety message,” says Heather. “And it’s one message among many others, most of them having nothing to do with abuse. It hasn’t made my son fearful at all.”
Your child’s education should include a balanced view of obedience. Teaching a child to obey is an important and difficult lesson. (Colossians 3:20) However, such lessons can go too far. If a child is taught that he must always obey any adult, regardless of the circumstances, he is vulnerable to abuse. Molesters are quick to notice when children are overly compliant. Wise parents teach their children that obedience is relative. For Christians, that is not as complicated as it may sound. It simply means saying to them: “If anybody tells you to do something that Jehovah God says is wrong, you don’t have to do it. Even Mommy or Daddy should never tell you to do something that Jehovah says is wrong. And you can always tell either Mommy or Daddy if someone tries to get you to do something wrong.”
Finally, let your child know that no one should ask him to keep a secret from you. Tell him that if anyone asks him to keep any kind of secret from you, he should always come and let you know. No matter what he is told—even if scary threats are made or he has done something wrong himself—it is always OK to come to Mommy or Daddy and tell them all about it. Such instruction need not scare your child. You can reassure him that most people would never do such things—touch him where they shouldn’t, ask him to disobey God, or ask him to keep a secret. Like a planned escape route in case of fire, these are just-in-case messages and will probably never be needed.
Give your child background education
Equip Your Child With Some Basic Protective Tools
The third step we will discuss is to give your child some simple actions to take in case someone tries to take advantage of him when you are not there. One method that is often recommended is like a game. Parents ask “What if . . . ?” and the child answers. You might say, “What if we were at the store together and we got separated? How would you find me?” The child’s answer may not be exactly what you would hope for, but you can guide him along with further questions, such as “Can you think of anything you could do that would be safer?”
You can use similar questions to ask a child what the safest response would be if someone tried to touch him in a wrong way. If the child is easily alarmed by such questions, you might try telling a story about another child. For example: “A little girl is with a relative she likes, but then he tries to touch her where he shouldn’t. What do you think she should do to stay safe?”
Equip your child with basic protective tools
What should you teach your child to do in situations like the one above? Notes one author: “A firm ‘No!’ or ‘Don’t do that!’ or ‘Leave me alone!’ does wonders to frighten the seductive offender into retreat and into rethinking his or her choice of victim.” Help your child act out brief scenarios so that he feels confident to refuse loudly, get away quickly, and report to you whatever has happened. A child who seems to understand the training thoroughly may easily forget it within a few weeks or months. So repeat this training regularly.
All the child’s direct caregivers, including the males—whether father, stepfather, or other male relatives—should be part of these discussions. Why? Because all involved in such teaching are, in effect, promising the child that they will never commit such acts of abuse. Sadly, much sexual abuse occurs right within the confines of the family. The following article will discuss how you can make your family a safe haven in an abusive world.
Experts note that many abused children give nonverbal clues that something is wrong. For example, if a child suddenly regresses to behavior he had outgrown some time earlier, such as bed-wetting, clinginess, or fear of being alone, he may be sending a signal that something serious is upsetting him. Such symptoms should not be taken as definite proof of abuse. Calmly draw out your child to learn the cause of the distress so that you can offer comfort, reassurance, and protection.
For the sake of simplicity, both the abuser and the victim are referred to here as males. Regardless of gender, though, the same principles apply.
Published by Jehovah’s Witnesses.
SEXUAL ABUSE—A GLOBAL PROBLEM
In 2006 the secretary-general of the United Nations transmitted to the UN General Assembly a world report on violence against children that had been compiled by an independent expert for the UN. During a recent year, according to the report, an estimated 150 million girls and 73 million boys under 18 years of age experienced “forced sexual intercourse or other forms of sexual violence.” Those numbers are staggering, but the report notes: “This is certainly an underestimate.” A review of studies from 21 countries suggested that in some places as many as 36 percent of women and 29 percent of men had been subjected to some form of sexual victimization in childhood. The majority of the perpetrators were relatives!
A PATTERN OF SEDUCTION
An abuser is likely to be too clever to use force on his victims. Rather, he may prefer to seduce children gradually. He begins by selecting a target, often a child who seems vulnerable and trusting, thus relatively easy to control. Next, he singles out that child for special attention. He may also try to win the trust of the child’s parents. Molesters are often expert at pretending to be sincerely interested in the child and the family.
In time, the molester will begin grooming the child for abuse. He gradually becomes more physical with the child through innocent-looking displays of affection, playful wrestling, and tickling. He may give generous gifts and begin to separate the child from friends, siblings, and parents, in order to spend time alone with the child. At some point he may ask the child to keep some minor secret from the parents—perhaps a gift or plans for some future excursion. Such tactics set the stage for seduction. When the abuser has won the child’s trust and that of the parents, he is ready to make his move.
Again, he is likely to be subtle about it rather than violent or forceful. He may exploit the child’s natural curiosity about sex, offering to act as a “teacher,” or he may suggest that they play a “special game” together that only they will know about. He may try exposing the child to pornography in order to make such behavior seem normal.
If he succeeds in molesting the child, he is now eager to ensure that the child does not tell anyone about it. He may use a variety of tactics, including threats, blackmail, and blame, or perhaps a combination of these. For example, he may say: “It’s your fault. You didn’t tell me to stop.” He may add: “If you tell your parents, they’ll call the police and send me to jail forever.” Or he may say: “It’s our secret. If you tell, no one will believe you. If your parents ever do find out, I will hurt them.” There is no end to the devious and malicious tactics such individuals will try.
FEW of us want to dwell on the subject of sexual abuse of children. Parents shudder at the very thought of it! Such abuse, however, is a frightening and unpleasant reality in today’s world, and its effects on children can be devastating. Is the matter worth considering? Well, what would you be willing to give for the sake of your child’s safety? Learning about the unpleasant realities of abuse is surely a small price to pay. Such knowledge can really make a difference.
Do not let the plague of abuse rob you of your courage. At the very least, you have power that your child does not have—strengths that it will take years, even decades, for your child to gain. The passing years have brought you a fund of knowledge, experience, and wisdom. The key is to enhance those strengths and put them to use in protecting your child. We will discuss three basic steps that every parent can take. They are as follows: (1) Become your child’s first line of defense against abuse, (2) give your child some needed background education, and (3) equip your child with some basic protective tools.
Are You the First Line of Defense?
The primary responsibility for protecting children against abuse belongs to parents, not to children. So educating parents comes before educating children. If you are a parent, there are a few things you need to know about child abuse. You need to know who abuse children and how they go about it. Parents often think of molesters as strangers who lurk in the shadows, seeking ways to kidnap and rape children. Such monsters certainly do exist. The news media bring them to our attention very often. However, they are relatively rare. In about 90 percent of the cases of sexual abuse of a child, the perpetrator is someone the child already knows and trusts.
Naturally, you do not want to believe that an affable neighbor, teacher, health-care worker, coach, or relative could lust after your child. In truth, most people are not like that. There is no need to become suspicious of everybody around you. Still, you can protect your child by learning how the typical abuser operates.—See the box on page 6.
Knowing such tactics can make you, the parent, better prepared to act as the first line of defense. For instance, if someone who appears more interested in children than in adults singles out your child for special attention and gifts or offers free babysitting or private excursions with your child, what will you do? Decide that the person must be a molester? No. Do not be quick to jump to conclusions. Such behavior may be quite innocent. Nonetheless, it can put you on the alert. The Bible says: “Anyone inexperienced puts faith in every word, but the shrewd one considers his steps.”—Proverbs 14:15.
Remember, any offer that sounds too good to be true may be just that. Carefully screen anyone who volunteers to spend time alone with your child. Let such an individual know that you are likely to check on your child at any time. Melissa and Brad, young parents of three boys, are cautious about leaving a child alone with an adult. When one son had music lessons at home, Melissa told the instructor: “I’ll be in and out of the room while you’re here.” Such vigilance may sound extreme, but these parents would rather be safe than sorry.
Be actively involved in your child’s activities, friendships, and schoolwork. Learn all the details about any planned excursion. One mental-health professional who spent 33 years working with cases of sexual abuse notes that he has seen countless cases that could have been prevented by simple vigilance on the parents’ part. He quotes one convicted molester as saying: “Parents literally give us their children. . . . They sure made it easy for me.” Remember, most molesters prefer easy targets. Parents who are actively involved in their children’s lives make their children difficult targets.
Another way to act as your child’s first line of defense is to be a good listener. Children will rarely disclose abuse directly; they are too ashamed and worried about the reaction. So listen carefully, even for subtle clues.* If your child says something that concerns you, calmly use questions to draw him out.* If he says that he does not want a certain babysitter to come back, ask why. If he says that an adult plays funny games with him, ask him: “What kind of game? What does he do?” If he complains that someone tickled him, ask him, “Where did he tickle you?” Do not be quick to dismiss a child’s answers. Abusers tell a child that no one will believe him; all too often, that is true. And if a child has been abused, being believed and supported by a parent is a big step toward recovery.
Be your child’s first line of defense
Give Your Child Background Education
One reference work on the subject of child abuse quotes a convicted molester as saying: “Give me a kid who knows nothing about sex, and you’ve given me my next victim.” Those chilling words are a useful reminder to parents. Children who are ignorant about sex are much easier for molesters to fool. The Bible says that knowledge and wisdom can deliver us “from the man speaking perverse things.” (Proverbs 2:10-12) Is that not what you want for your child? Then, as your second basic step in protecting him, do not hold back from teaching him about this important subject.
How, though, do you go about it? More than a few parents find the subject of sex a bit awkward to discuss with children. Your child may find the subject even more awkward, and he is not likely to bring it up with you. So take the initiative. Melissa says: “We started early, with naming the body parts. We used real words, not baby words, to show them that there is nothing funny or shameful about any part of their body.” Instruction about abuse follows naturally. Many parents simply tell their children that the parts of their body that a bathing suit covers are private and special.
Says Heather, mentioned in the preceding article: “Scott and I told our son that his penis is private, personal, and not a toy. It’s not for anyone to play with—not for Mommy, not for Daddy, not even for a doctor. When we take him to the doctor, I explain that he’s only going to make sure everything is OK, and that’s why he may touch there.” Both parents take part in these little talks from time to time, and they assure the child that he can always come to them and tell them if anyone touches him in a way that’s wrong or makes him feel uncomfortable. Experts in child care and abuse prevention recommend that all parents have similar talks with their children.
Many have found the book Learn From the Great Teacher* to be a real help in teaching this subject. Chapter 32, “How Jesus Was Protected,” has a direct yet comforting message for children on the dangers of abuse and the importance of staying safe. “The book has given us a perfect way to reinforce what we have told our children personally,” says Melissa.
In today’s world children need to know that there are some people who want to touch children or get children to touch them in ways that are wrong. These warnings need not fill children with fear or make them distrust all adults. “It’s just a safety message,” says Heather. “And it’s one message among many others, most of them having nothing to do with abuse. It hasn’t made my son fearful at all.”
Your child’s education should include a balanced view of obedience. Teaching a child to obey is an important and difficult lesson. (Colossians 3:20) However, such lessons can go too far. If a child is taught that he must always obey any adult, regardless of the circumstances, he is vulnerable to abuse. Molesters are quick to notice when children are overly compliant. Wise parents teach their children that obedience is relative. For Christians, that is not as complicated as it may sound. It simply means saying to them: “If anybody tells you to do something that Jehovah God says is wrong, you don’t have to do it. Even Mommy or Daddy should never tell you to do something that Jehovah says is wrong. And you can always tell either Mommy or Daddy if someone tries to get you to do something wrong.”
Finally, let your child know that no one should ask him to keep a secret from you. Tell him that if anyone asks him to keep any kind of secret from you, he should always come and let you know. No matter what he is told—even if scary threats are made or he has done something wrong himself—it is always OK to come to Mommy or Daddy and tell them all about it. Such instruction need not scare your child. You can reassure him that most people would never do such things—touch him where they shouldn’t, ask him to disobey God, or ask him to keep a secret. Like a planned escape route in case of fire, these are just-in-case messages and will probably never be needed.
Give your child background education
Equip Your Child With Some Basic Protective Tools
The third step we will discuss is to give your child some simple actions to take in case someone tries to take advantage of him when you are not there. One method that is often recommended is like a game. Parents ask “What if . . . ?” and the child answers. You might say, “What if we were at the store together and we got separated? How would you find me?” The child’s answer may not be exactly what you would hope for, but you can guide him along with further questions, such as “Can you think of anything you could do that would be safer?”
You can use similar questions to ask a child what the safest response would be if someone tried to touch him in a wrong way. If the child is easily alarmed by such questions, you might try telling a story about another child. For example: “A little girl is with a relative she likes, but then he tries to touch her where he shouldn’t. What do you think she should do to stay safe?”
Equip your child with basic protective tools
What should you teach your child to do in situations like the one above? Notes one author: “A firm ‘No!’ or ‘Don’t do that!’ or ‘Leave me alone!’ does wonders to frighten the seductive offender into retreat and into rethinking his or her choice of victim.” Help your child act out brief scenarios so that he feels confident to refuse loudly, get away quickly, and report to you whatever has happened. A child who seems to understand the training thoroughly may easily forget it within a few weeks or months. So repeat this training regularly.
All the child’s direct caregivers, including the males—whether father, stepfather, or other male relatives—should be part of these discussions. Why? Because all involved in such teaching are, in effect, promising the child that they will never commit such acts of abuse. Sadly, much sexual abuse occurs right within the confines of the family. The following article will discuss how you can make your family a safe haven in an abusive world.
Experts note that many abused children give nonverbal clues that something is wrong. For example, if a child suddenly regresses to behavior he had outgrown some time earlier, such as bed-wetting, clinginess, or fear of being alone, he may be sending a signal that something serious is upsetting him. Such symptoms should not be taken as definite proof of abuse. Calmly draw out your child to learn the cause of the distress so that you can offer comfort, reassurance, and protection.
For the sake of simplicity, both the abuser and the victim are referred to here as males. Regardless of gender, though, the same principles apply.
Published by Jehovah’s Witnesses.
SEXUAL ABUSE—A GLOBAL PROBLEM
In 2006 the secretary-general of the United Nations transmitted to the UN General Assembly a world report on violence against children that had been compiled by an independent expert for the UN. During a recent year, according to the report, an estimated 150 million girls and 73 million boys under 18 years of age experienced “forced sexual intercourse or other forms of sexual violence.” Those numbers are staggering, but the report notes: “This is certainly an underestimate.” A review of studies from 21 countries suggested that in some places as many as 36 percent of women and 29 percent of men had been subjected to some form of sexual victimization in childhood. The majority of the perpetrators were relatives!
A PATTERN OF SEDUCTION
An abuser is likely to be too clever to use force on his victims. Rather, he may prefer to seduce children gradually. He begins by selecting a target, often a child who seems vulnerable and trusting, thus relatively easy to control. Next, he singles out that child for special attention. He may also try to win the trust of the child’s parents. Molesters are often expert at pretending to be sincerely interested in the child and the family.
In time, the molester will begin grooming the child for abuse. He gradually becomes more physical with the child through innocent-looking displays of affection, playful wrestling, and tickling. He may give generous gifts and begin to separate the child from friends, siblings, and parents, in order to spend time alone with the child. At some point he may ask the child to keep some minor secret from the parents—perhaps a gift or plans for some future excursion. Such tactics set the stage for seduction. When the abuser has won the child’s trust and that of the parents, he is ready to make his move.
Again, he is likely to be subtle about it rather than violent or forceful. He may exploit the child’s natural curiosity about sex, offering to act as a “teacher,” or he may suggest that they play a “special game” together that only they will know about. He may try exposing the child to pornography in order to make such behavior seem normal.
If he succeeds in molesting the child, he is now eager to ensure that the child does not tell anyone about it. He may use a variety of tactics, including threats, blackmail, and blame, or perhaps a combination of these. For example, he may say: “It’s your fault. You didn’t tell me to stop.” He may add: “If you tell your parents, they’ll call the police and send me to jail forever.” Or he may say: “It’s our secret. If you tell, no one will believe you. If your parents ever do find out, I will hurt them.” There is no end to the devious and malicious tactics such individuals will try.
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