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The Developmental Origins of Health and Disease (DOHaD)
Open accessAbstract
For years many have believed that genetic heritage defined one’s destiny, if an individual would grow to be healthy, or if he or she would suffer from chronic illness or cancer. Recent scientific evidence and the field of epigenetics has proven this to be untrue. Certainly, the DNA sequence and the genetic code are fixed; but the field of epigenetics has shown how methylation and other chemical modifications of the genome directly influence the production of proteins that can alter the phenotype of an organism. This article will lay out the supporting research, the details on how the internal and external environments influence genetic function, and will allow the reader to develop an action plan necessary to influence the genetic code, with the goal of then moving the individual toward optimal health. These research details will enable health care professionals in every field of medicine to work with patients on positively influencing the genetic output in order to improve the quality of life and longevity.
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“At its locus, it leads to a change in chromatin structure (from heterochromatin to euchromatin), and methylation marks have also been replenished at this level mediated by the mixed lineage leukemia (MLL) enzyme.”
From Revisiting Epigenetics Fundamentals and Its Biomedical Implications (2024) · cites this paper as [87]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
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“The overexpression of TNF-α has been observed in a wide variety of inflammatory diseases, such as rheumatoid arthritis, Crohn’s disease, ulcerative colitis, and asthma [86,87].”
From Revisiting Epigenetics Fundamentals and Its Biomedical Implications (2024) · cites this paper as [87]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
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“To cite an example, during tumorigenic progression, the loss of the expression of tumor suppressors—such as RB1; breast cancer type 1, BRCA1; anaphase promoting complex, APC; DNA mismatch repair protein MLH1; and Von Hippel–Lindau tumor suppressor VHL—has been observed due to hypermethylation at the promoter level.”
From Revisiting Epigenetics Fundamentals and Its Biomedical Implications (2024) · cites this paper as [87]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
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“Likewise, it has been reported that there are miRNAs that target the BACE1 protein that regulates the production of amyloid beta platelets, Aβ, which, when accumulated, contribute to the neuroinflammation and progression of this disease [86,87,88].”
From Revisiting Epigenetics Fundamentals and Its Biomedical Implications (2024) · cites this paper as [87]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
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“On the other hand, in Alzheimer’s disease, for example, changes have been identified in the methylation status of proteins such as human clusterin CLU; ATP binding cassette subfamily A member 7 ABCA7; MS4A6A; and CD2AP, which have been reported to contribute to the development of the disease.”
From Revisiting Epigenetics Fundamentals and Its Biomedical Implications (2024) · cites this paper as [87]
Experimental — accuracy not yet measured
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“As an example of the above, it has been described that TNF-α undergoes epigenetic modifications at the level of DNA methylation in its promoter (hypermethylation and hypomethylation) to regulate its expression or at the level of histone modifications due to acetylation orchestrated by the enzymes activating transcription factor 2, ATF2, and the CREB binding protein (CBP).”
From Revisiting Epigenetics Fundamentals and Its Biomedical Implications (2024) · cites this paper as [87]
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Citations
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How Early-Life Programming During Embryogenesis Imprints Cellular Memory
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Metadata
- Authors
- Lacagnina, S.
- Affiliations
- Lee Memorial Hospital (US)
- Corresponding author
- Lacagnina, Salvatore
- Venue
- American Journal of Lifestyle Medicine
- Publisher
- SAGE Publications
- Published
- 2019-10-11
- Volume
- 14
- Issue
- 1
- Pages
- 47-50
- ISSN
- 1559-8276 (ISSN-L)
- 1559-8284
- PMC
- PMC6933571
- OpenAlex
- W2979300097
- Cited by
- 244
- References
- 23
- Citations by year
- 2026: 96 · 2025: 71 · 2024: 42 · 2023: 19 · 2022: 4 · 2021: 8 · 2020: 2
- FWCI
- 3.64
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Lifestyle Medicine (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Nutrition, Genetics, and Disease
- Keywords
- developmental origins of health and disease, epigenetics, DNA methylation, gene-environment interaction, phenotypic expression, lifestyle intervention, health promotion, longevity, chronic disease prevention
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