People with acne skin are protected against aging

Dermatologists have long noted that the skin of acne sufferers appears to age more slowly than the skin of those with no history of acne. Signs of aging such as wrinkles and skin thinning often appear much later in people who have experienced acne in their lifetime. It has been suggested that this is due to increased oil production but there are likely to be other factors involved. Previous studies have shown that white blood cell telomere length can be predictive of biological aging and is linked with telomere length in other cells in the body.

Telomeres are repetitive nucleotide sequences found at the end of chromosomes which protect them from deteriorating during the process of replication. Telomeres gradually break down and shrink as cells age, eventually leading to cell death which is a normal part of human growth and aging. Researchers suggest that the cause could be linked to the length of telomeres which appears to be different in acne sufferers and means their cells may be protected against aging. Longer telomeres are likely to be one factor explaining the protection against premature skin aging in individuals who previously suffered from acne. Another important pathway, related to the p53 gene (a protector of the genome), is also relevant when we looked at gene expression in the skin of acne.

Ref: S. Ribero et al.,  (2016) Acne and telomere length. A new spectrum between senescence and apoptosis pathways. Journal of Investigative Dermatology.

DOI: 10.1016/j.jid.2016.09.014

Tooth enamel originated in skin and colonized teeth later

When did the enamel that covers our teeth evolve? And where in the body did this tissue first appear? In a new study, researchers combined data from two very different research fields - paleontology and genomics  to arrive at a clear but unexpected answer to this question: enamel originated in the skin and colonized the teeth much later.

A research group found that in most of the fossil bony fishes along with few archaic living ones such as the gar (Lepisosteus) from North America, the scales are made up with an enamel-like tissue called “ganoine”. They found that it contains genes for two of our three enamel matrix proteins: the first to be identified from a ray-finned bony fish. Furthermore, these genes are expressed in the skin, strongly suggesting that ganoine is a form of enamel. The hardest substance produced by the body is this enamel and this is made mostly of the mineral apatite (calcium phosphate) deposited on a substrate of three unique enamel matrix proteins.

Ref: Qingming Qu, Tatjana Haitina, Min Zhu, Per Erik Ahlberg. New genomic and fossil data illuminate the origin of enamel. Nature, 2015.

DOI: 10.1038/nature15259

Smoking and alcohol use are linked to premature aging

Cigarette smoking and heavy alcohol use cause epigenetic changes to DNA that reflect accelerated biological aging in distinct, measurable ways. Patterns of DNA methylation, a molecular modification to DNA that affects when and how strongly a gene is expressed. Methylation patterns change in predictable ways as people age, as well as in response to environmental exposures, such as cigarette smoke and alcohol. Dr. Philibert's laboratory identified two specific locations in the genome, base pairs cg05575921 on the AHRR gene and cg23193759 on chromosome 10, at which methylation levels were highly associated with smoking and alcohol consumption, respectively. They estimated each person's biological age using a previously validated epigenetic "clock" based on methylation levels at 71 locations in the genome, as measured by the widely used Infinium HumanMethylation450 BeadChip. Then, they calculated the difference between biological age and chronological age, and assessed the relationship between tobacco and alcohol use and premature aging. Interestingly, moderate alcohol use about one to two drinks per day was correlated with the healthiest aging, while very low and high consumption were linked to accelerated aging.

Source: American Society of Human Genetics

Why elephants rarely get cancer?

Elephants have 38 additional modified copies (alleles) of a gene that encodes p53, a well-defined tumor suppressor, as compared to humans, who have only two. Further, elephants may have a more robust mechanism for killing damaged cells that are at risk for becoming cancerous. In isolated elephant cells, this activity is doubled compared to healthy human cells, and five times that of cells from patients with Li-Fraumeni Syndrome, who have only one working copy of p53 and more than a 90 percent lifetime cancer risk in children and adults. The results suggest extra p53 could explain elephants' enhanced resistance to cancer. The scientists combed through the African elephant genome and found at least 40 copies of genes that code for p53, a protein well known for its cancer-inhibiting properties. DNA analysis provides clues as to why elephants have so many copies, a substantial increase over the two found in humans. The vast majority, 38 of them, are so-called retrogenes, modified duplicates that have been churned out over evolutionary time.

hey extracted white blood cells from blood drawn from the animals during routine wellness checks and subjected the cells to treatments that damage DNA, a cancer trigger. In response, the cells reacted to damage with a characteristic p53-mediated response: they committed suicide. Schiffman says, "If you kill the damaged cell, it's gone, and it can't turn into cancer. This may be more effective of an approach to cancer prevention than trying to stop a mutated cell from dividing and not being able to completely repair itself."

To test this, the researchers did a side-by-side comparison with cells isolated from elephants (n=8), healthy humans (n=10), and from patients with Li-Fraumeni Syndrome (n=10). They found that elephant cells exposed to radiation self-destruct at twice the rate of healthy human cells and more than five times the rate of Li-Fraumeni cells (14.6%, 7.2%, and 2.7%, respectively). These findings support the idea that more p53 offers additional protection against cancer.

Ref: Joshua D. Schiffman, MD et al. (2015) Potential mechanisms for cancer resistance in elephants and comparative cellular response to DNA damage in humans. JAMA.

DOI: 10.1001/jama.2015.13134