Have you considered getting your DNA sequenced? Wonder what kind of information you could expect out of it?
I recently got my DNA sequenced at Self Decode and the results are in! Let’s take a look at whats in there and how I might be able to use it to improve my health and lifespan.
The introductory report shows me a high level overview of things I may want to dig deeper into.
Now, what does this mean and what can I do about it?
Typical risk of vit. k deficiency so, not much needed to be done hereMostly typical ability to convert beta-carotene to Vit. A. Nothing to see here.Seemingly normal ability to process B12. Good news.I know I have one of two MTFHR gene mutations so no surprises here on Folate. I supplement with MTHF or Methyl-Folate to make up for this. Now, I don’t drink Coffee, nor do I drink and caffeinated drinks so, nothing to worry about here. Basically I can process caffeine more readily. Need to keep an eye on food intake. I have recently started intermittent fasting and have reduce my sugar and dairy intake (see our post about miRNA’s in milk expressing mTOR and suppressing AMPK).Mix results here meaning no real action needed except that I should possibly target power training. Typical Lipid levels. Not better or worse, just your regular ability to process lipids.I never considered that DNA may influence something like my levels of empathy. I guess this explains why I’ve started Health Hacker to help people live healthier and longer lives. Look out Black Friday and Cyber Monday, here comes an impulse shopper!Anxiety is something I’ve struggled with for most of my life. I employ multiple strategies to help with it including CBD and B3, along with Omega-3.
Along with the report are sources to NIH publications to back the assertions. You also get deeper reports on each of those subject areas including MTFHR, APOE, Mood, Cognitive, Essential Minerals, Vitamins, Sleep, Cardiovascular, Inflammation and Fitness. You also get a personalised blog that shows you articles related to SNPs in your results.
I’m not saying that this is the best DNA service but it’s the one I chose and this is what I got. It seems quite comprehensive and does a good job at explaining what it all means and how I can adjust my diet and lifestyle to account for deficiencies caused by gene mutations. If this is something you are interested in then it might be an option for you.
“Fundamental cellular mechanisms such as nutrient sensing, DNA damage response pathways, and cell cycle regulation influence the aging process. Studies have shown that the nutrient sensory kinase, mTOR (TOR in yeast), regulates lifespan in response to nutrient availability. The mTOR kinase forms two distinct protein complexes: TORC1 and TORC2. TORC1, which is inhibited by rapamycin, regulates cell growth, proliferation, and metabolism. It is well established that TORC1 promotes protein translation via phosphorylation of ribosomal protein S6 kinase and the eIF4Eâ€binding protein (BP; Zoncu, Efeyan, & Sabatini,2011). The TORC2 branch is less studied; however, TORC2 also plays important roles in metabolism, cell survival, and proliferation (Zoncu et al.,2011). Although the involvement of the TORC1 pathway in lifespan regulation is conserved among many species (i.e., TORC1 inhibition extends lifespan), it is still unclear how this pathway affects multiple downstream stress and damage response mechanisms.”
“The global population of individuals over the age of 65 is growing at an unprecedented rate and is expected to reach 1.6 billion by 2050. Most older individuals are affected by multiple chronic diseases, leading to complex drug treatments and increased risk of physical and cognitive disability. Improving or preserving the health and quality of life of these individuals is challenging due to a lack of wellâ€established clinical guidelines. Physicians are often forced to engage in cycles of “trial and error†that are centered on palliative treatment of symptoms rather than the root cause, often resulting in dubious outcomes. Recently, geroscience challenged this view, proposing that the underlying biological mechanisms of aging are central to the global increase in susceptibility to disease and disability that occurs with aging. In fact, strong correlations have recently been revealed between health dimensions and phenotypes that are typical of aging, especially with autophagy, mitochondrial function, cellular senescence, and DNA methylation. Current research focuses on measuring the pace of aging to identify individuals who are “aging faster†to test and develop interventions that could prevent or delay the progression of multimorbidity and disability with aging. Understanding how the underlying biological mechanisms of aging connect to and impact longitudinal changes in health trajectories offers a unique opportunity to identify resilience mechanisms, their dynamic changes, and their impact on stress responses. Harnessing how to evoke and control resilience mechanisms in individuals with successful aging could lead to writing a new chapter in human medicine.”
“Sequencing technologies have changed not only our approaches to classical genetics, but also the field of epigenetics. Specific methods allow scientists to identify novel genome-wide epigenetic patterns of DNA methylation down to single-nucleotide resolution. DNA methylation is the most researched epigenetic mark involved in various processes in the human cell, including gene regulation and development of diseases, such as cancer. Increasing numbers of DNA methylation sequencing datasets from human genome are produced using various platforms—from methylated DNA precipitation to the whole genome bisulfite sequencing. Many of those datasets are fully accessible for repeated analyses. Sequencing experiments have become routine in laboratories around the world, while analysis of outcoming data is still a challenge among the majority of scientists, since in many cases it requires advanced computational skills. Even though various tools are being created and published, guidelines for their selection are often not clear, especially to non-bioinformaticians with limited experience in computational analyses. Separate tools are often used for individual steps in the analysis, and these can be challenging to manage and integrate. However, in some instances, tools are combined into pipelines that are capable to complete all the essential steps to achieve the result. In the case of DNA methylation sequencing analysis, the goal of such pipeline is to map sequencing reads, calculate methylation levels, and distinguish differentially methylated positions and/or regions. The objective of this review is to describe basic principles and steps in the analysis of DNA methylation sequencing data that in particular have been used for mammalian genomes, and more importantly to present and discuss the most pronounced computational pipelines that can be used to analyze such data. We aim to provide a good starting point for scientists with limited experience in computational analyses of DNA methylation and hydroxymethylation data, and recommend a few tools that are powerful, but still easy enough to use for their own data analysis.”
“The AMP-activated protein kinase (AMPK) acts as a cellular energy sensor. Once switched on by increases in cellular AMP : ATP ratios, it acts to restore energy homeostasis by switching on catabolic pathways while switching off cell growth and proliferation. The canonical AMP-dependent mechanism of activation requires the upstream kinase LKB1, which was identified genetically to be a tumour suppressor. AMPK can also be switched on by increases in intracellular Ca2+, by glucose starvation and by DNA damage via non-canonical, AMP-independent pathways. Genetic studies of the role of AMPK in mouse cancer suggest that, before disease arises, AMPK acts as a tumour suppressor that protects against cancer, with this protection being further enhanced by AMPK activators such as the biguanide phenformin. However, once cancer has occurred, AMPK switches to being a tumour promoter instead, enhancing cancer cell survival by protecting against metabolic, oxidative and genotoxic stresses. Studies of genetic changes in human cancer also suggest diverging roles for genes encoding subunit isoforms, with some being frequently amplified, while others are mutated.”
“Obesity and being overweight have become a worldwide epidemic affecting more than 1.9 billion adults and 340 million children. Efforts to curb this global health burden by developing effective long-term non-surgical weight loss interventions continue to fail due to weight regain after weight loss. Weight cycling, often referred to as Yoyo dieting, is driven by physiological counter-regulatory mechanisms that aim at preserving energy, i.e. decreased energy expenditure, increased energy intake, and impaired brain-periphery communication. Models based on genetically determined set points explained some of the weight control mechanisms, but exact molecular underpinnings remained elusive. Today, gene–environment interactions begin to emerge as likely drivers for the obesogenic memory effect associated with weight cycling. Here, epigenetic mechanisms, including histone modifications and DNA methylation, appear as likely factors that underpin long-lasting deleterious adaptations or an imprinted obesogenic memory to prevent weight loss maintenance.”
a pilot study using gastric mucosa infected with Helicobacter pylori
” Aberrant DNA methylation is induced by aging and chronic inflammation in normal tissues. The induction by inflammation is widely recognized as acceleration of age-related methylation. However, few studies addressed target genomic regions and the responsible factors in a genome-wide manner. Here, we analyzed methylation targets by aging and inflammation, taking advantage of the potent methylation induction in human gastric mucosa by Helicobacter pylori infection-triggered inflammation. “
“Aging is an important risk factor for several human diseases such as cancer, cardiovascular disease and neurodegenerative disorders, resulting from a combination of genetic and environmental factors (e.g., diet, smoking, obesity and stress), which, at molecular level, cause changes in gene expression underlying the decline of physiological function. Epigenetics, which include mechanisms regulating gene expression independently of changes to DNA sequence, regulate gene expression by modulating the structure of chromatin or by regulating the binding of transcriptional machinery to DNA. Several studies showed that an impairment of epigenetic mechanisms promotes alteration of gene expression underlying several aging-related diseases. Alteration of these mechanisms is also linked with changes of gene expression that occurs during aging processes of different tissues. In this review, we will outline the potential role of epigenetics in the onset of two age-related pathologies, cancer and cardiovascular diseases.”
“The unprecedented resolution of genome-wide interaction maps shows functional consequences that extend the initial thought of an efficient DNA packaging mechanism: gene regulation, DNA repair, chromosomal translocations and evolutionary rearrangements seem to be only the peak of the iceberg. One key concept emerging from this research is the topologically associating domains (TADs) whose functional role in gene regulation and their association with disease is not fully untangled.”
