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 the TNF-α locus, epigenetic changes lead to a change in chromatin structure from heterochromatin to euchromatin, and methylation marks are replenished mediated by the MLL enzyme.
“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]
The Objectives section describes epigenetics as involving conformational changes in chromatin, and the paper’s opening section discusses methylation as a genomic modification; page numbers are unavailable in our copy. Neither passage establishes a heterochromatin-to-euchromatin transition at the TNF-α locus or says that MLL replenishes methylation marks (searched: TNF, heterochromatin, euchromatin, MLL). (LLM, conf=0.77)
Experimental — accuracy not yet measuredOverexpression of TNF-α has been observed in rheumatoid arthritis, Crohn's disease, ulcerative colitis, and asthma.
“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]
The 'What About the Father?' section mentions asthma risk in relation to delivery and the infant microbiome, but does not discuss TNF-α overexpression. Searches for TNF-α, tumor necrosis factor, and the named inflammatory diseases found no passage in our copy addressing the claimed association. Page numbers were not available. (LLM, conf=0.74)
Experimental — accuracy not yet measuredDuring tumorigenic progression, loss of expression of tumor suppressors RB1, BRCA1, APC, MLH1, and VHL has been observed due to hypermethylation at the promoter level.
“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]
The DOHaD section says that methylation can influence protein production, and the section on inheritance discusses gene expression in men with early prostate cancer. Neither addresses promoter hypermethylation during tumorigenic progression or loss of expression of RB1, BRCA1, APC, MLH1, or VHL. Searches for those genes and the claimed mechanism found no supporting passage in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measuredmiRNAs target the BACE1 protein that regulates the production of amyloid beta platelets, Aβ, which when accumulated contribute to neuroinflammation and progression of Alzheimer's disease.
“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]
The Objectives passages discuss early-life epigenetic changes and metabolic disease, not Alzheimer’s disease. Searches of our copy for BACE1, miRNAs, amyloid beta, and neuroinflammation returned no passage addressing the attributed mechanism. (LLM, conf=0.74)
Experimental — accuracy not yet measuredIn Alzheimer's disease, changes have been identified in the methylation status of CLU, ABCA7, MS4A6A, and CD2AP, which have been reported to contribute to the development of the disease.
“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]
The DOHaD section discusses methylation and gene expression generally, but does not address Alzheimer’s disease or methylation changes in CLU, ABCA7, MS4A6A, or CD2AP. Searches for those gene names and for Alzheimer’s disease with methylation found no passage supporting the attributed claim. (LLM, conf=0.74)
Experimental — accuracy not yet measured
TNF-α undergoes epigenetic modifications at DNA methylation in its promoter (hypermethylation and hypomethylation) to regulate its expression or at histone modifications due to acetylation orchestrated by ATF2 and CBP.
“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]
The DOHaD section discusses methylation and other genome modifications in general, but does not address TNF-α. Searches for TNF-α promoter methylation, histone acetylation, ATF2, and CBP found no passage supporting the specific mechanisms attributed to this paper; page numbers are unavailable in our copy. (LLM, conf=0.76)
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- 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 · 2016: 1
- 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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