PTSD And Gene expression: The MicroRNA Connectiom

Here is a fascinating article suggesting that post-traumatic stress disorder is associated with varying levels of certain microRNAs, which can affect gene expression.  Abstract:

Posttraumatic stress disorder (PTSD) affects many returning combat veterans, but underlying biological mechanisms remain unclear. In order to compare circulating micro RNA (miRNA) of combat veterans with and without PTSD, peripheral blood from 24 subjects was collected following deployment, and isolated miRNA was sequenced. PTSD was associated with 8 differentially expressed miRNA. Pathway analysis shows that PTSD is related to the axon guidance and Wnt signaling pathways, which work together to support neuronal development through regulation of growth cones. PTSD is associated with miRNAs that regulate biological functions including neuronal activities, suggesting that they play a role in PTSD symptomatology.

This altered gene expression may be linked to the mechanism of the disorder, both underscoring the seriousness of it and possibly pointing in the direction of therapy.  This article was from several years ago; we will be looking for any updates.

Rare Variants For Human Height

At left, genetics of height. By The original uploader was Pete.Hurd at English Wikipedia - Transferred from en.wikipedia to Commons by MichaelSchoenitzer using CommonsHelper., Public Domain, 

https://commons.wikimedia.org/w/index.php?curid=19496489

Interesting paper, abstract:

Height is a highly heritable, classic polygenic trait with approximately 700 common associated variants identified through genome-wide association studies so far. Here, we report 83 height-associated coding variants with lower minor-allele frequencies (in the range of 0.1-4.8%) and effects of up to 2 centimetres per allele (such as those in IHH, STC2, AR and CRISPLD2), greater than ten times the average effect of common variants. In functional follow-up studies, rare height-increasing alleles of STC2 (giving an increase of 1-2 centimetres per allele) compromised proteolytic inhibition of PAPP-A and increased cleavage of IGFBP-4 in vitro, resulting in higher bioavailability of insulin-like growth factors. These 83 height-associated variants overlap genes that are mutated in monogenic growth disorders and highlight new biological candidates (such as ADAMTS3, IL11RA and NOX4) and pathways (such as proteoglycan and glycosaminoglycan synthesis) involved in growth. Our results demonstrate that sufficiently large sample sizes can uncover rare and low-frequency variants of moderate-to-large effect associated with polygenic human phenotypes, and that these variants implicate relevant genes and pathways.

Obviously, there's nothing you can do about what gene variants you inherited and nothing you can do about height as an adult, but genetic height potential can be maximized by having adequate nutrition while growing, which is why people in given populations tend to be taller today than in centuries past.

Tea Genetics

Understanding the tea genome; abstract

Tea, one of the world's most important beverage crops, provides numerous secondary metabolites that account for its rich taste and health benefits. Here we present a high-quality sequence of the genome of tea, Camellia sinensis var. sinensis (CSS), using both Illumina and PacBio sequencing technologies. At least 64% of the 3.1-Gb genome assembly consists of repetitive sequences, and the rest yields 33,932 high-confidence predictions of encoded proteins. Divergence between two major lineages, CSS and Camellia sinensis var. assamica (CSA), is calculated to ∼0.38 to 1.54 million years ago (Mya). Analysis of genic collinearity reveals that the tea genome is the product of two rounds of whole-genome duplications (WGDs) that occurred ∼30 to 40 and ∼90 to 100 Mya. We provide evidence that these WGD events, and subsequent paralogous duplications, had major impacts on the copy numbers of secondary metabolite genes, particularly genes critical to producing three key quality compounds: catechins, theanine, and caffeine. Analyses of transcriptome and phytochemistry data show that amplification and transcriptional divergence of genes encoding a large acyltransferase family and leucoanthocyanidin reductases are associated with the characteristic young leaf accumulation of monomeric galloylated catechins in tea, while functional divergence of a single member of the glutamine synthetase gene family yielded theanine synthetase. This genome sequence will facilitate understanding of tea genome evolution and tea metabolite pathways, and will promote germplasm utilization for breeding improved tea varieties.

Prognostic Genes For Colon Cancer

Determining prognostic genes for colon cancer; abstract:

PROPOSE:

We aimed to explore the potential molecular mechanism and independent prognostic genes for colon cancer (CC).

METHODS:

Microarray datasets GSE17536 and GSE39582 were downloaded from Gene Expression Omnibus. Meanwhile, the whole CC-related dataset were downloaded from The Cancer Genome Atlas (TCGA) database. Differentially expressed mRNA (DEMs) were identified between cancer tissue samples and para-carcinoma tissue samples in TCGA dataset, followed by the KEGG pathway and GO function analyses. Furthermore, the clinical prognostic analysis including overall survival (OS) and disease-free survival (DFS) were performed in all three datasets.

RESULTS:

A total of 633 up- and 321 down-regulated mRNAs were revealed in TCGA dataset. The up-regulated mRNAs were mainly assembled in functions including extracellular matrix and pathways including Wnt signaling. The down-regulated mRNAs were mainly assembled in functions like Digestion and pathways like Drug metabolism. Furthermore, up-regulation of UL16-binding protein 2 (ULBP2) was associated with OS in CC patients. A total of 12 DEMs including Surfactant Associated 2 (SFTA2) were potential DFS prognostic genes in CC patients. Meanwhile, the GRP and Transmembrane Protein 37 (TMEM37) were two outstanding independent DFS prognostic genes in CC.

CONCLUSIONS:

ULBP2 might be a potential novel OS prognostic biomarker in CC, while GRP and TMEM37 could be served as the independent DFS prognostic genes in CC. Furthermore, functions including extracellular matrix and digestion, as well as pathways including Wnt signaling and drug metabolism might play important roles in the process of CC.

Genetic Variation And Immune Checkpoint Therapy

Patient response to immune checkpoint therapy is influenced by patient genotype.  It may be necessary to determine individual genetic variation before applying this therapy; alternatively, is it possible to adjust therapy to make it more effective even for patients with less optimal (for therapy) immune genotypes.  Abstract:

CD8+ T cell-dependent killing of cancer cells requires efficient presentation of tumor antigens by human leukocyte antigen class I (HLA-I) molecules. However, the extent to which patient-specific HLA-I genotype influences response to anti-PD-1 or anti-CTLA-4 is currently unknown. We determined the HLA-I genotype of 1,535 advanced cancer patients treated with immune checkpoint blockade (ICB). Maximal heterozygosity at HLA-I loci (A, B, and C) improved overall survival after ICB compared to patients who were homozygous for at least one HLA locus. In two independent melanoma cohorts, patients with the HLA-B44 supertype had extended survival, whereas the HLA-B62 supertype (including HLA-B*15:01) or somatic loss of heterozygosity at HLA-I, was associated with poor outcome. Molecular dynamics simulations of HLA-B*15:01 revealed unique elements that may impair CD8+ T cell recognition of neoantigens. Our results have important implications for predicting response to ICB and for the design of neoantigen-based therapeutic vaccines.

Genetics Of Indian Camel Breeds

Of purely academic interest for animal lovers and those interested in genetic studies, we see this paper about the genetic history of Indian camel breeds.  The same genetic techniques can - and have been - used to discern the genetic history of human populations as well.  Abstract:

The genetic and demographic bottleneck analysis of Indian camel breeds was carried out utilizing 40 microsatellite markers. Allelic polymorphism was observed at 20 loci in the Indian dromedary breeds. A total of 66 alleles were scored. The average number of alleles, expected heterozygosity and polymorphic information content were, respectively, 3.25 ± 0.27, 0.56 ± 0.04 and 0.49 ± 0.04 in Bikaneri; 3.25 ± 0.25, 0.53 ± 0.03 and 0.46 ± 0.03 in Jaisalmeri; 3.0 ± 0.21, 0.53 ± 0.04 and 0.45 ± 0.03 in Kachchhi and 3.1 ± 0.19, 0.51 ± 0.03 and 0.44 ± 0.03 in Mewari breed. Higher genetic variation was observed in most numerous Bikaneri breed. Genetic distances were least between the breed pair Bikaneri and Jaisalmeri which was closely placed with the Kachchhi breed. The Mewari camels had relatively higher genetic distance from the other three Indian dromedary breeds. The bottleneck analysis revealed the presence of genetic bottleneck in all four breeds of Indian dromedary. However, the qualitative graphical method resulted in normal L-shaped distribution of allele frequencies in Jaisalmeri breeds and shifted mode in Bikaneri, Kachchhi and Mewari breeds. The demographic bottleneck analysis revealed minimum reduction (-9.65 %) in the population of camels in Jaisalmeri breeding tract as compared to that of Bikaneri (-14.18 %), Kachchhi (-27.78 %) and Mewari (-32 %) breeding tracts. Conclusively, the genetic bottleneck analysis could explain the demographic bottleneck in the Indian dromedary populations. Therefore, appropriate conservation and improvement efforts are needed in all four dromedary breeds with immediate attention on Mewari and Kachchhi breeds. The present study is the first report in demonstrating the genetic basis of demographic bottleneck in the Indian dromedary populations.

Genetics of X Inactivation

By Michael Bodega - I (Michael Bodega) created this work entirely by myself., Public Domain, https://commons.wikimedia.org/w/index.php?curid=16831523

X inactivation shuts off many (but not all!) genes of one of the X chromosomes in the cells of female mammals, to balance gene expression with cells of males that have only one X chromosome.  The inactivation tends to be random (as to which of the pair of X chromosomes experiences inactivation in each cell), and has phenotypic consequences for health and disease  and also affects fur color in female cats.  The set of inactivated X chromosome genes in female human cells has been analyzed, which may help in understanding X-linked disorders in females.  Abstract:

X chromosome inactivation (XCI) silences transcription from one of the two X chromosomes in female mammalian cells to balance expression dosage between XX females and XY males. XCI is, however, incomplete in humans: up to one-third of X-chromosomal genes are expressed from both the active and inactive X chromosomes (Xa and Xi, respectively) in female cells, with the degree of 'escape' from inactivation varying between genes and individuals. The extent to which XCI is shared between cells and tissues remains poorly characterized, as does the degree to which incomplete XCI manifests as detectable sex differences in gene expression and phenotypic traits. Here we describe a systematic survey of XCI, integrating over 5,500 transcriptomes from 449 individuals spanning 29 tissues from GTEx (v6p release) and 940 single-cell transcriptomes, combined with genomic sequence data. We show that XCI at 683 X-chromosomal genes is generally uniform across human tissues, but identify examples of heterogeneity between tissues, individuals and cells. We show that incomplete XCI affects at least 23% of X-chromosomal genes, identify seven genes that escape XCI with support from multiple lines of evidence and demonstrate that escape from XCI results in sex biases in gene expression, establishing incomplete XCI as a mechanism that is likely to introduce phenotypic diversity. Overall, this updated catalogue of XCI across human tissues helps to increase our understanding of the extent and impact of the incompleteness in the maintenance of XCI.

Genetic Structure Affected By Maternal Care (In Mice)

Early life experiences, such as maternal care, alters the genetic structure in neurons in mice, with mobile genetic elements seemingly responsible.  Does the same apply to humans?  Abstract:

The brain is a genomic mosaic owing to somatic mutations that arise throughout development. Mobile genetic elements, including retrotransposons, are one source of somatic mosaicism in the brain. Retrotransposition may represent a form of plasticity in response to experience. Here, we use droplet digital polymerase chain reaction to show that natural variations in maternal care mediate the mobilization of long interspersed nuclear element-1 (LINE-1 or L1) retrotransposons in the hippocampus of the mouse brain. Increasing the amount of maternal care blocks the accumulation of L1. Maternal care also alters DNA methylation at YY1 binding sites implicated in L1 activation and affects expression of the de novo methyltransferase DNMT3a. Our observations indicate that early life experience drives somatic variation in the genome via L1 retrotransposons.

The Rose Genome

The rose genome; abstract

Roses have high cultural and economic importance as ornamental plants and in the perfume industry. We report the rose whole-genome sequencing and assembly and resequencing of major genotypes that contributed to rose domestication. We generated a homozygous genotype from a heterozygous diploid modern rose progenitor, Rosa chinensis 'Old Blush'. Using single-molecule real-time sequencing and a meta-assembly approach, we obtained one of the most comprehensive plant genomes to date. Diversity analyses highlighted the mosaic origin of 'La France', one of the first hybrids combining the growth vigor of European species and the recurrent blooming of Chinese species. Genomic segments of Chinese ancestry identified new candidate genes for recurrent blooming. Reconstructing regulatory and secondary metabolism pathways allowed us to propose a model of interconnected regulation of scent and flower color. This genome provides a foundation for understanding the mechanisms governing rose traits and should accelerate improvement in roses, Rosaceae and ornamentals.

The Genetic Architecture Of Osteoarthritis

Genetic links between higher BMI and osteoarthritis exist. Abstract:

Osteoarthritis is a common complex disease imposing a large public-health burden. Here, we performed a genome-wide association study for osteoarthritis, using data across 16.5 million variants from the UK Biobank resource. After performing replication and meta-analysis in up to 30,727 cases and 297,191 controls, we identified nine new osteoarthritis loci, in all of which the most likely causal variant was noncoding. For three loci, we detected association with biologically relevant radiographic endophenotypes, and in five signals we identified genes that were differentially expressed in degraded compared with intact articular cartilage from patients with osteoarthritis. We established causal effects on osteoarthritis for higher body mass index but not for triglyceride levels or genetic predisposition to type 2 diabetes.

New ALS Gene Discovered

A novel gene that influences ALS has been identified; this may eventually have therapeutic implications. Abstract:

To identify novel genes associated with ALS, we undertook two lines of investigation. We carried out a genome-wide association study comparing 20,806 ALS cases and 59,804 controls. Independently, we performed a rare variant burden analysis comparing 1,138 index familial ALS cases and 19,494 controls. Through both approaches, we identified kinesin family member 5A (KIF5A) as a novel gene associated with ALS. Interestingly, mutations predominantly in the N-terminal motor domain of KIF5A are causative for two neurodegenerative diseases: hereditary spastic paraplegia (SPG10) and Charcot-Marie-Tooth type 2 (CMT2). In contrast, ALS-associated mutations are primarily located at the C-terminal cargo-binding tail domain and patients harboring loss-of-function mutations displayed an extended survival relative to typical ALS cases. Taken together, these results broaden the phenotype spectrum resulting from mutations in KIF5A and strengthen the role of cytoskeletal defects in the pathogenesis of ALS.

The Taste Of Fats

There does not seem to be a significant genetic component to fat taste sensitivity in humans; abstract:

BACKGROUND:

Individuals with impaired fat taste (FT) sensitivity have reduced satiety responses after consuming fatty foods, leading to increased dietary fat intake. Habitual consumption of dietary fat may modulate sensitivity to FT, with high consumption decreasing sensitivity [increasing fatty acid taste threshold (FATT)] and low consumption increasing sensitivity (decreasing FATT). However, some individuals may be less susceptible to diet-mediated changes in FATT due to variations in gene expression.

OBJECTIVE:

The objective of this study was to determine the effect of an 8-wk low-fat or high-fat diet on FATT while maintaining baseline weight (<2.0 kg variation) to assess heritability and to explore the effect of genetics on diet-mediated changes in FATT.

DESIGN:

A co-twin randomized controlled trial including 44 pairs (mean ± SD age: 43.7 ± 15.4 y; 34 monozygotic, 10 dizygotic; 33 women, 10 men, 1 gender-discordant) was conducted. Twins within a pair were randomly allocated to an 8-wk low-fat (<20% of energy from fat) or high-fat (>35% of energy from fat) diet. FATT was assessed by a 3-alternate forced choice methodology and transformed to an ordinal scale (FT rank) at baseline and at 4 and 8 wk. Linear mixed models were fit to assess diet effect on FT rank and diet effect modification due to zygosity. A variance components model was fit to calculate baseline heritability.

RESULTS:

There was a significant time × diet interaction for FT rank after the 8-wk trial (P < 0.001), with the same conclusions for the subset of participants maintaining baseline weight (low-fat; n = 32; high-fat: n = 35). There was no evidence of zygosity effect modification (interaction of time × diet × zygosity: P = 0.892). Heritability of baseline FT rank was 8%.

CONCLUSIONS:

There appears to be little to no genetic contribution on heritability of FATT or diet-mediated changes to FATT. Rather, environment, specifically dietary fat intake, is the main influencer of FT sensitivity, regardless of body weight. This trial was registered with the Australian New Zealand Clinical Trials Registry at http://www.anzctr.org.au/ as ACTRN12613000466741.

Related: salt promotes passive overconsumption of dietary fat in humans.

Take home point: eating more salt and fat will likely lead to even more fat consumption.

Childhood Cancer Genetic Landscapes

A bit of good news in the midst of an unfortunate topic: “nearly 50% of paediatric neoplasms harbour a potentially druggable event, which is highly relevant for the design of future clinical trials.” Abstract:

Pan-cancer analyses that examine commonalities and differences among various cancer types have emerged as a powerful way to obtain novel insights into cancer biology. Here we present a comprehensive analysis of genetic alterations in a pan-cancer cohort including 961 tumours from children, adolescents, and young adults, comprising 24 distinct molecular types of cancer. Using a standardized workflow, we identified marked differences in terms of mutation frequency and significantly mutated genes in comparison to previously analysed adult cancers. Genetic alterations in 149 putative cancer driver genes separate the tumours into two classes: small mutation and structural/copy-number variant (correlating with germline variants). Structural variants, hyperdiploidy, and chromothripsis are linked to TP53 mutation status and mutational signatures. Our data suggest that 7-8% of the children in this cohort carry an unambiguous predisposing germline variant and that nearly 50% of paediatric neoplasms harbour a potentially druggable event, which is highly relevant for the design of future clinical trials.

Don’t Blame Your Genes

It’s not your genes, it’s your appetite and eating habits.

But weight loss averaged about 13 pounds over a year, regardless of genes, insulin levels or diet type. Also, some people lost as much as 60 pounds and others gained 15 pounds — more evidence that genetic characteristics and diet type appeared to make no difference.

What seemed to make a difference was healthful eating. Participants on both diets who consumed the fewest processed foods, sugary drinks, unhealthy fats and ate the most vegetables lost the most weight.

The results suggest that "precision medicine is not as important as eating mindfully, getting rid of packaged, processed food" and avoiding unhealthy habits like eating while watching television, said lead author Christopher Gardner.

So, excuses about “it’s my genes” do not justify BMI realities, and fad diets are a waste of time, if key essentials are met: “Participants on both diets who consumed the fewest processed foods, sugary drinks, unhealthy fats and ate the most vegetables lost the most weight."

I for one cut out sugary drinks – including orange juice and other fruit juices – cut back on saturated fats, cut back on foods with lots of added sugar, eat a bit less “packaged food,” while increasing fruits, vegetables, and whole grain as opposed to white.

Type 2 Diabetes, SNPs, And Wnt Signaling

Identification of genetic variants (SNPs) found in humans associated with type 2 diabetes (T2D) has shown some associated with Wnt signaling, which has been previously identified as linked to changes in T2D metabolism   Abstract:

Clinical studies in type 2 diabetes (T2D) primarily focused on the single nucleotide polymorphisms (SNPs) located in protein-coding regions. Recently, the SNPs located in noncoding regions have also been recognized to play an important role in disease susceptibility. The super enhancer is a cluster of transcriptional enhancers located in noncoding regions. It plays a critical role in cell-type specific gene expression. However, the exact mechanism of the super enhancer SNPs for T2D remains unclear. In this study, we integrated genome-wide association studies (GWASs) and T2D cell/tissue-specific histone modification ChIP-seq data to identify T2D-associated SNPs in super enhancer, followed by comprehensive bioinformatics analyses to further explore the functional importance of these SNPs. We identified several interesting T2D super enhancer SNPs. Interesting, most of them were clustered within the same or neighboring super enhancers. A number of SNPs are involved in chromatin interactive regulation and/or potentially influence the binding affinity of transcription factors. Gene Ontology (GO) analysis showed a significant enrichment in several well-known signaling pathways and regulatory process, e.g. WNT signaling pathway, which plays a key role in T2D metabolism. Our results highlighted the potential functional importance of T2D super enhancer SNPs, which may yield novel insights into the pathogenesis of T2D.

New Breast Cancer Risk Gene Variants

Below we see some new studies in which new genetic variants that increase breast cancer risk have been discovered.  Such findings have multiple long-term benefits.  First, to identify at-risk patients, who can then have additional screenings, earlier screening, etc.  Second, to understand the mechanisms by which these variants, or the genes linked to them (if the variants themselves are just "markers" of risk), affect breast cancer, so as to devise new preventive and therapeutic approaches.  Third, to combine points one and two, to devise individualized screening and prevention (and therapy?) regimens for specific individuals.

Paper one; abstract:

Most common breast cancer susceptibility variants have been identified through genome-wide association studies (GWAS) of predominantly estrogen receptor (ER)-positive disease. We conducted a GWAS using 21,468 ER-negative cases and 100,594 controls combined with 18,908 BRCA1 mutation carriers (9,414 with breast cancer), all of European origin. We identified independent associations at P < 5 × 10-8 with ten variants at nine new loci. At P < 0.05, we replicated associations with 10 of 11 variants previously reported in ER-negative disease or BRCA1 mutation carrier GWAS and observed consistent associations with ER-negative disease for 105 susceptibility variants identified by other studies. These 125 variants explain approximately 16% of the familial risk of this breast cancer subtype. There was high genetic correlation (0.72) between risk of ER-negative breast cancer and breast cancer risk for BRCA1 mutation carriers. These findings may lead to improved risk prediction and inform further fine-mapping and functional work to better understand the biological basis of ER-negative breast cancer.

Paper two; abstract:

Breast cancer risk is influenced by rare coding variants in susceptibility genes, such as BRCA1, and many common, mostly non-coding variants. However, much of the genetic contribution to breast cancer risk remains unknown. Here we report the results of a genome-wide association study of breast cancer in 122,977 cases and 105,974 controls of European ancestry and 14,068 cases and 13,104 controls of East Asian ancestry. We identified 65 new loci that are associated with overall breast cancer risk at P < 5 × 10-8. The majority of credible risk single-nucleotide polymorphisms in these loci fall in distal regulatory elements, and by integrating in silico data to predict target genes in breast cells at each locus, we demonstrate a strong overlap between candidate target genes and somatic driver genes in breast tumours. We also find that heritability of breast cancer due to all single-nucleotide polymorphisms in regulatory features was 2-5-fold enriched relative to the genome-wide average, with strong enrichment for particular transcription factor binding sites. These results provide further insight into genetic susceptibility to breast cancer and will improve the use of genetic risk scores for individualized screening and prevention.

Physical Activity Can Affect Genetic Susceptibility To Weight Gain

By Javierlayus - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=15900701

One often hears the excuse that genes makes someone overweight (note of course that humans have not undergone some sort of rapid genetic change precipitating the obesity epidemic).  It is therefore useful to know that a study has shown that to the extent that genetic differences between people can influence weight gain, that the weight gain can be "diminished by increasing physical activity."  Of course, controlling diet is usually the greatest factor in weight control, even taking genetic differences into account.  Again, genetic differences influencing weight gain have always existed; the skyrocketing expansion of waistlines and BMIs cannot be attributed to genetics as the major factor. Excerpted from the abstract:

Whether change in physical activity over time modifies the genetic susceptibility to long-term weight gain is unknown…In the combined cohorts, 4-year BMI change per 10-risk allele increment was -0.02 kg/m2 among participants with greatest increase in physical activity and 0.24 kg/m2 among those with greatest decrease in physical activity (P[interaction]<0.001), corresponding to 0.01 kg versus 0.63 kg weight changes every 4 years (P[interaction]=0.001). Similar but marginal interactions were observed for the BMI-GRS (P[interaction]=0.045). Our data indicate that the genetic susceptibility to weight gain may be diminished by increasing physical activity.

Personalized Genetics For Deodorant Use

By No machine-readable author provided. Dickbauch~commonswiki assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims). Public Domain, https://commons.wikimedia.org/w/index.php?curid=500634

Personalized genetics can be used for all sorts of things; apparently now it can determine whether you need to use deodorant.  Axillary (armpit) odor seems to be predominantly determined by variants of the ABCC11 gene (which also determines wet vs. dry earwax).  A study has found that individuals (of those studied) with the non-odor genotype were over-represented in the group that never used deodorant, which makes sense - they don't need it.  However, a large majority of white Europeans with the non-odor phenotype did use deodorant, while a small fraction of those who do have axillary odor do not use deodorant.  Therefore, social and cultural factors are at play. One may assume that some of the non-odor people who use deodorant may have been using deodorant since adolescence and may be unaware that they do not need it (they assume the lack of smell is due to deodorant use and not their genetics) and/or they adopt a "better safe than sorry attitude") toward it. As to why those who need it don't use it, who knows?  Also, the non-odor genotype is more frequently found in east Asians, who therefore would be less likely to need to use deodorant.  Abstract:

Earwax type and axillary odor are genetically determined by rs17822931, a single-nucleotide polymorphism (SNP) located in the ABCC11 gene. The literature has been concerned with the Mendelian trait of earwax, although axillary odor is also Mendelian. Ethnic diversity in rs17822931 exists, with higher frequency of allele A in east Asians. Influence on deodorant usage has not been investigated. In this work, we present a detailed analysis of the rs17822931 effect on deodorant usage in a large (N∼17,000 individuals) population cohort (the Avon Longitudinal Study of Parents and Children (ALSPAC)). We found strong evidence (P=3.7 × 10−20) indicating differential deodorant usage according to the rs17822931 genotype. AA homozygotes were almost 5-fold overrepresented in categories of never using deodorant or using it infrequently. However, 77.8% of white European genotypically nonodorous individuals still used deodorant, and 4.7% genotypically odorous individuals did not. We provide evidence of a behavioral effect associated with rs17822931. This effect has a biological basis that can result in a change in the family's environment if an aerosol deodorant is used. It also indicates potential cost saving to the nonodorous and scope for personalized genetics usage in personal hygiene choices, with consequent reduction of inappropriate chemical exposures for some.

Genes For Intelligence Discovered

IQ distribution centered around a mean of 100 shown at left.  By Dmcq - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=29433851

Some genes associated with intelligence have been discovered. Abstract:

Intelligence is associated with important economic and health-related life outcomes. Despite intelligence having substantial heritability (0.54) and a confirmed polygenic nature, initial genetic studies were mostly underpowered. Here we report a meta-analysis for intelligence of 78,308 individuals. We identify 336 associated SNPs (METAL P < 5 × 10-8) in 18 genomic loci, of which 15 are new. Around half of the SNPs are located inside a gene, implicating 22 genes, of which 11 are new findings. Gene-based analyses identified an additional 30 genes (MAGMA P < 2.73 × 10-6), of which all but one had not been implicated previously. We show that the identified genes are predominantly expressed in brain tissue, and pathway analysis indicates the involvement of genes regulating cell development (MAGMA competitive P = 3.5 × 10-6). Despite the well-known difference in twin-based heratiblity for intelligence in childhood (0.45) and adulthood (0.80), we show substantial genetic correlation (rg = 0.89, LD score regression P = 5.4 × 10-29). These findings provide new insight into the genetic architecture of intelligence.

Not much you can do about this for your own life of course, other than making the most of what you have.  The mind needs to be exercised as much as the body, and as a middle-aged man I wish that the younger generation would do more reading of books and less social media.