Data collected from the Dutch famine and similar events, such as the one at Leningrad, provided a reliable source of information to scientists studying DOHaD.
[6][9][10] These studies in turn led to greater interest in the roles of developmental plasticity and early life environmental exposures in adult disease.
[1] Between 1944 and 1945, in the western regions of the Netherlands and in Amsterdam, a famine broke out due to a railway strike and German control limiting supplies.
Further studies indicated that older people had a resilience to the effects of malnutrition on physical health in late life, but a higher vulnerability to socioeconomic stunting.
[12] Results concluded that the women with low caloric and nutritional intake during pregnancy had children that had greater rates of obesity as opposed to those who were not exposed to famine.
[13] This hypothesis suggested that poor growth during the fetal and infant stages can cause a development of type 2 diabetes later in life.
Since this is occurring during the plastic stage of development, this can cause the foetus to be "programmed" to conserve energy and store fat, thus leading to a lower metabolism.
For pregnant women who are living in this type of circumstance the foetuses which are in utero are more likely to sense a low-protein condition and alter their development to survive.
The embryo will develop insulin resistance and enzyme levels will convert the food that is not being used into fat, which in later life can lead to obesity and diabetes.
DNA methylation, histone modifications and non-coding RNAs are altered by the environment in the womb and potentially go on to produce higher rates of adult disease later in life.
The methylation of chief regulatory cytosines changes the DNA's hydrophobicity and begins to inhibit interactions with transcription factors responsible for the expression of the gene.
[17] Unbalanced diets increase the thioredoxin-interacting protein expressions causing blastocysts to form incorrectly because of altered histone methylation.
[17] High-fat diets are shown to alter histone methylation and acetylation and potentially lead to changes in gene expression within fetal adipose, liver, and skeletal muscle tissues.
[17] Recent studies have shown the importance in non-coding RNA's ability to regulate cell differentiation and organismal development.
[17] In a study done by Barker, he found a strong connection between poor prenatal environments and increased possibilities of cardiovascular diseases in adults.
[7] Studies on rats found that maternal nutrient restriction resulted in damage to the cardiac renin-angiotensin system (which regulates blood pressure and volume).
[24] During the Dutch famine doctors found that under-nutrition during the gestation period related to reduced glucose tolerance and raised insulin concentrations between the ages 50 and 58.
[14] The effect could be explained due to the lower birth rates of babies that were born during the famine and the low weight gain of their mothers.
It is a developmental disorder that impairs the brain's ability to develop the typical social and communication skills that are necessary for everyday life.
People with ASD may experience difficulties with social interactions, verbal and nonverbal communication, and repetitive or restricted behaviors.
The degree to which ASD affects an individual can vary widely, with some people experiencing mild symptoms while others may face more significant challenges.
For instance, some scientists believe that damage to a specific region of the brain, the amygdala, may be linked to ASD, while others are examining the possibility that a viral infection may trigger the disorder.
Treatment for ASD involves a highly structured schedule of constructive activities that build on the child's interests and various techniques.
A team led by Mingqing Xu investigated this possible connection between prenatal malnutrition and schizophrenia by analyzing medical records of people born between 1960 and 1961 during the Great Chinese Famine.
[29][30] Folate jumps out as a key candidate as the occurrence of neural tube defects raised alongside schizophrenia during the Dutch famine.
Protein-calorie malnutrition has been associated with increased dopamine and serotonin release and malfunctions in the hippocampus such as reduced dendritic branching and a lower cell count, which are also found in people with schizophrenia.
Human and animal studies did show that infants from stressed pregnancies have a poor immune function and are more likely to contract childhood illnesses as well as mental disorders.
[34] There was a study published in the Journal of Pediatrics of August 19, 2020, which looked at how maternal recognition and stress can affect infant health after or during pregnancy.