..Eve; because she was the mother of all living.
Genesis 3:20
"A Chinese famine was so severe that 35 million lives perished between 1958 and 1962 due to the state's agricultural mistakes. Interestingly, this tragedy highlights an unseen biological relationship between organisms and their environment over multiple generations.
A large study recently published in the American Journal of Clinical Nutrition focuses on one Chinese city immersed in the famine. It compared the adult health status of residents between those who had prenatal (before birth) exposure to famine and those who were not exposed. Researchers wanted to see if famine exposure in parents correlated to the development of a high blood sugar concentration (hyperglycemia) and type 2 diabetes in their children and grandchildren.
Prenatal exposures in offspring were classified as having 1) no parent exposed to famine, 2) only a mother exposed to famine, 3) only a father exposed to famine, or 4) both parents exposed to famine.
The researchers used standard diagnostic criteria for hyperglycemia and type 2 diabetes.
Results
After statistical analysis, which controlled for other disease risk factors, prenatal exposure to famine was associated with an increased risk of type 2 diabetes and hyperglycemia in the children of starved parents. The odds of developing hyperglycemia were about 2:1 in both children and grandchildren, while there was about a 75% increased risk of type 2 diabetes in the children of starved parents. The risk of developing a disease was higher if both parents were starved.
Proper Epidemiological Procedures Pinpoint "Process Causation"
Epidemiologists employ several procedural checks to guard against the mistake of deducing that an observed exposure "caused" a subsequent biological outcome in an organism.
This mistake can be depicted as: (+) exposure —> outcome.
This relationship is depicted as: (+) famine (exposure) |— parent's innate systems response (exposure) |— offspring's innate systems —> offspring (+/-) hyperglycemia or diabetes (outcome)
So, this study actually compares two different womb environments: one within a starving mother and one in a more normally fed mother.
Not all external exposures are a "stimulus" to an organism. Internal programming within anything designed by humans—or within an organism—specifies a condition to be a "stimulus." In addition, most entities also have a detector on one of their boundary surfaces which corresponds to the specified stimulus.
Human-engineered sensors and those in organisms share several key elements. A sensor's purpose is to discover or identify the presence of specific environmental events or changes, and then provide a corresponding output signal into a system as a response.
Humans don't have any known "famine detector," but the body does detect the changes when it is being starved and responds accordingly. If humans were intelligently designed, then it would make good engineering sense for the developing baby to be able to also detect those same physiologic changes in its parent, or for the mother to send some internal signals her baby can detect. If the mother is in a nutrition-deprived environment, one purpose of design-based systems would be to prepare the baby during development to cope with that same environment.
The famine researchers do speculate that "genetic, epigenetic reprogramming, and subsequent gene-diet interaction are all possible explanations." This mechanism would be consistent with other epigenetic changes that have been detected in the offspring of starved parents.
A Duke University study on the tiny worm C. elegans appeared on October 26 in PLOS Genetics. It described "a genetic network that mediates effects of a mother's diet on the size and starvation resistance of her offspring" that worked by "signaling through [an] insulin-like receptor" which "function[s] in the mother to transmit information about her diet to her offspring." They add that since this "genetic network" is likely not limited to worms, it could influence "such effects of diet across generations" and this "is likely relevant to human diseases related to nutrient sensing and storage."
Creationist theory also enables predictions of findings. While parents may "program" offspring through persistent epigenetic markers, another mechanism is more likely. Offspring will be shown to be able to detect signals from a parent during development (and afterward) and make self-adjustments to their own traits per internal algorithms. All these sophisticated designs point to a Designer." ICR
Genesis 3:20
"A Chinese famine was so severe that 35 million lives perished between 1958 and 1962 due to the state's agricultural mistakes. Interestingly, this tragedy highlights an unseen biological relationship between organisms and their environment over multiple generations.
A large study recently published in the American Journal of Clinical Nutrition focuses on one Chinese city immersed in the famine. It compared the adult health status of residents between those who had prenatal (before birth) exposure to famine and those who were not exposed. Researchers wanted to see if famine exposure in parents correlated to the development of a high blood sugar concentration (hyperglycemia) and type 2 diabetes in their children and grandchildren.
Prenatal exposures in offspring were classified as having 1) no parent exposed to famine, 2) only a mother exposed to famine, 3) only a father exposed to famine, or 4) both parents exposed to famine.
Results
After statistical analysis, which controlled for other disease risk factors, prenatal exposure to famine was associated with an increased risk of type 2 diabetes and hyperglycemia in the children of starved parents. The odds of developing hyperglycemia were about 2:1 in both children and grandchildren, while there was about a 75% increased risk of type 2 diabetes in the children of starved parents. The risk of developing a disease was higher if both parents were starved.
Proper Epidemiological Procedures Pinpoint "Process Causation"
Epidemiologists employ several procedural checks to guard against the mistake of deducing that an observed exposure "caused" a subsequent biological outcome in an organism.
This mistake can be depicted as: (+) exposure —> outcome.
This relationship is depicted as: (+) famine (exposure) |— parent's innate systems response (exposure) |— offspring's innate systems —> offspring (+/-) hyperglycemia or diabetes (outcome)
So, this study actually compares two different womb environments: one within a starving mother and one in a more normally fed mother.
Not all external exposures are a "stimulus" to an organism. Internal programming within anything designed by humans—or within an organism—specifies a condition to be a "stimulus." In addition, most entities also have a detector on one of their boundary surfaces which corresponds to the specified stimulus.
Human-engineered sensors and those in organisms share several key elements. A sensor's purpose is to discover or identify the presence of specific environmental events or changes, and then provide a corresponding output signal into a system as a response.
Humans don't have any known "famine detector," but the body does detect the changes when it is being starved and responds accordingly. If humans were intelligently designed, then it would make good engineering sense for the developing baby to be able to also detect those same physiologic changes in its parent, or for the mother to send some internal signals her baby can detect. If the mother is in a nutrition-deprived environment, one purpose of design-based systems would be to prepare the baby during development to cope with that same environment.
The famine researchers do speculate that "genetic, epigenetic reprogramming, and subsequent gene-diet interaction are all possible explanations." This mechanism would be consistent with other epigenetic changes that have been detected in the offspring of starved parents.
A Duke University study on the tiny worm C. elegans appeared on October 26 in PLOS Genetics. It described "a genetic network that mediates effects of a mother's diet on the size and starvation resistance of her offspring" that worked by "signaling through [an] insulin-like receptor" which "function[s] in the mother to transmit information about her diet to her offspring." They add that since this "genetic network" is likely not limited to worms, it could influence "such effects of diet across generations" and this "is likely relevant to human diseases related to nutrient sensing and storage."
Creationist theory also enables predictions of findings. While parents may "program" offspring through persistent epigenetic markers, another mechanism is more likely. Offspring will be shown to be able to detect signals from a parent during development (and afterward) and make self-adjustments to their own traits per internal algorithms. All these sophisticated designs point to a Designer." ICR
