A Chinese famine was so severe that 35 million lives perished between 1958 and 1962 due to the state's agricultural mistakes.1 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.2 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.
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.
Mistakes in Process Description Yield Faulty Conclusions
The famine researchers did not identify a causal mechanism in their paper. So, the headline about this research at medicalexpress.com is erroneous. It reads, "Famine alters metabolism for successive generations."3 But for many people—including scientists—that headline is logical, therefore true. The headline is more of an analytical blunder since it claims that the famine causes altered metabolism. However, the research only identified an association between them. But, just as importantly, there is a basic mistake in process description. The headline links the simple exposure of famine directly to the outcome of altered metabolism as cause and effect. It ignores the vital role of a person's biological systems—which are directly responsible for all metabolic outcomes—though exactly which ones and how it happens is still poorly understood.
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.
The first safeguard is contingent on a valid study finding a valid statistical correlation between an exposure and an outcome. Second, there must be biological mechanisms to explain how the presence of an exposure could have a plausible biochemical link to the outcome. The biological mechanism always involves the organism itself.
This correct relationship is depicted as: (+) exposure |—> organism's innate systems outcome.
The symbol |— represents an organism's boundary. This boundary will always have traits with features that exclude many elements of the external environment, but other qualities to detect, actively transfer, or allow elements into the organism for further processing.
Even scientists may miss looking for the organism's innate mechanisms which link an exposure to an outcome. Anyone studying technical reports must check to see if the researchers attempted to find a mechanism, or, rather, if they mistakenly report an (+) exposure —> outcome conclusion.
These Chinese cases more easily highlight medicalexpress.com's (+) exposure —> outcome mistake, since the outcome is two steps removed from exposure rather than one. This study differs from many cohort studies where the person with the disease is directly exposed to an "external" condition. In these cases, "prenatal exposure" to famine of the people assessed for disease means that their parents were starved. The parent's external exposure was the famine itself—while the baby's external environmental exposure is the womb. The womb isolates the baby from the parent's environment of oral deprivation of nutrition.
Mistakes in process description happen when researchers fail to report key steps; perhaps, in this case, by thinking that a parent's exposure to malnutrition is essentially the same exposure for a baby in-utero. But these exposures are clearly not equivalent. Malnutrition for a baby in the womb does not start at the same time—or even necessarily happen at all—as malnutrition for the mother. For example, in pregnant women with severe iron-deficiency anemia, the baby's iron and hematocrit may actually be normal.4 Algorithm-based programming within the placenta regulates the selective uptake and distribution of circulating nutritional elements in mother's blood. These "rules" tend to work so that the baby's needs are met first—then the mother's.
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.
Do Parents Detect a Famine "Stimulus" and "Signal" Developing Offspring?
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."5 This mechanism would be consistent with other epigenetic changes that have been detected in the offspring of starved parents.6
Recent experimental results support maternal-to-offspring signals about a nutrition-deprived environment. 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."7 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."
Lead researcher L. Ryan Baugh commented on the capabilities of offspring born to diet-restricted mothers saying, "these animals are able to anticipate adverse conditions based on their mothers' experience."8 The report acknowledges that though "the molecular mechanisms behind the buffering effects of maternal diet are still unclear," Baugh believes that "mom somehow provisions the embryo, or programs it."
These findings tend to confirm design-based creationist theory that emphasizes active, problem-solving organisms capable of self-adjusting to fill dynamic environments. The wisdom of the Lord Jesus to design parents to be sensors of the environment for their offspring is profound.
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.
- Jisheng, Y. 2013. Tombstone: The Great Chinese Famine, 1958-1962. New York: Farrar, Straus and Giroux.
- Li, J. et al. 2016. Prenatal exposure to famine and the development of hyperglycemia and type 2 diabetes in adulthood across consecutive generations: a population-based cohort study of families in Suihua, China. American Journal of Clinical Nutrition. DOI: 10.3945/ajcn.116.138792
- Orenstein, D. Famine alters metabolism for successive generations. Posted on medicalexpress.com December 12, 2016, accessed December 15, 2016.
- Cunningham, F. G. et al. 2005. Williams Obstetrics, 22nd Edition. New York: McGraw-Hill, 130.
- Orenstein, D. Famine alters metabolism for successive generations.
- Guliuzza, R. A Response to "Does Natural Selection Exist?": Creatures' Adaptation Explained by the Design-based, Organism-driven Approach: Part 3. Posted on answersingenesis.org November 5, 2014, accessed December 15, 2016.
Hibshman, J. D., A. Hung, and L. R. Baugh. 2016. Maternal Diet and Insulin-Like Signaling Control Intergenerational Plasticity of Progeny Size and Starvation Resistance. PLOS Genetics. 12(10): e1006396. doi:10.1371/journal.pgen.1006396
- Smith, R. A. Underfed Worms Program Their Babies to Cope With Famine. Posted on today.duke.edu October 27, 2016, accessed December 16, 2016.
* Dr. Guliuzza is ICR's National Representative. He earned his M.D. from the University of Minnesota, his Master of Public Health from Harvard University, and served in the U.S. Air Force as 28th Bomb Wing Flight Surgeon and Chief of Aerospace Medicine. Dr. Guliuzza is also a registered Professional Engineer.
Article posted on January 23, 2017.