• Rhythmus – prescribing clarity

    Rhythmus is a new app that makes prescribing natural agents simpler than before when using the Opus23 database of natural agent effects on genes.

    Taking an overview of all SNPs for the client, the main Rhythmus screen shows a list of genes sorted by combined SNP effect power factor, with the color scheme of orange for overall downregulated and green for overall upregulated genes. With over 7,800 individual associations of genes and natural agents in the database, all based on and hyperlinked to PubMed published studies, Opus23 makes visualisation simple for the genes with the highest editor-defined power factor and with associated natural agents that affect the gene function.

    Rhythmus Prescribing App

    Taking the Agency app one step further, Rhythmus also includes the gene visualising ability of Powerspot to help the practitioner choose the best agents for the clientThe AI Pre fills the option of upregulating or downregulating the gene function and the effect required from the agents (although these can be changed manually if required). The numbers of agents associated with the gene function is also listed.

    Rhythmus can be used by checking some genes and other options, then click the Run Rhythmus button. The result is a network map of the genes in the query along with the natural agents that influence their function.

    Rhythmus network map

    The relative size of the agent indicates the confidence of the effect on the gene, and as with other network maps on Opus23, clicking on the gene or agent opens a popup for that element, from where it can be curated to the Client Report or the Protocol Report.

    The AI saves time in selecting the best options according to the available data, but this can alway be overridden by the practitioner, who may have other information about the client. Opus23 subscribes to the philosophy of ‘TMTOWTDI’ (There’s more than one way to do it, pronounced ‘Tim Toady’.) The program was designed with this idea in mind, in that it ‘doesn’t try to tell the practitioner how to parse the data.’ Rather, it presents many different frameworks and cross-sections of the available client data, using a myriad of infographic treatments. Therefore Rhythmus also offers the practitioner a user-defined alternative visualisation of up to five manually entered genes, again with an up- or downregulatory effect and the required effect size. The user-defined visualisation gives a Manhattan map of the combined effect of the possible agents, similar to one side of the Psychic app.

    Result of the user-defined selection in Rhythmus

    As before, clicking on the agent opens the agent popup, where it can be curated. Rhythmus takes Opus23 to another level of utility for data mining and analysing its huge database of PubMed-based gene-agent interactions.

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  • Opus23 Onsite Training, May 19-20, 2018

    Most patients improve through committing themselves to lifestyle, diet, mindset and environmental changes. When they don’t, additional history and sleuthing is needed. As our patients get more complex, the need for quickly evaluating thousands ofgenes is needed. Peter’s Opus23 allows one to do exactly this. I highly recommend using Opus23 for those patients who have ‘tried everything’ and are still stuck. It could very well find the answers to your patient’s riddle.” — Dr. Ben Lynch

    There will be an in-person training at the Center of Excellence in Generative Medicine (University of Bridgeport, Connecticut) for the weekend of May 19-20.

    This weekend training hosted by the Center of Excellence in Generative Medicine at the University of Bridgeport, Bridgeport CT, USA. A rare opportunity to receive hands-on training in Opus23 from Peter D’Adamo and key developers of the platform.

    SEMINAR DESIGN

    The seminar is a mix of some lecture and extensive hands-on learning. During experiential sessions, attendees will break up into 4-5 person workgroups. Each workgroup will have its own teaching assistant (TA), a GM/COE clinician with extensive experience with Opus. Attendees will work directly in Opus on a series of different clients.

    Successful completion of the onsite training allows you full access to the Opus23 software, with the ability to upload and analyze raw data from 23andMe, Ancestry, Genos and uBiome, and produce notes and patient reports.

    SEMINAR SCHEDULE

    The seminar will run from 9AM-5PM Saturday, May 19 and 9AM-12PM Sunday, May 20. Classes will take  place on the University of Bridgeport campus, at the Center of Excellence in Generative Medicine, 115 Broad Street Bridgeport CT 06604. Lunch will be provided on Saturday at the COEGM as well as dinner at a local restaurant.

    HOTEL/LODGING

    Bridgeport Holiday Inn
    1070 Main Street
    Bridgeport CT 06604
    Phone: 203 334-1234
    Fax: 203 696-1985

    http://www.ihg.com/holidayinn/hotels/us/en/bridgeport/bgdct/hoteldetail

    REGISTRATION

    Cost of the seminar is $800. Registration is available at the below secure PayPal checkout and will be limited to 15 individuals.





    Please email Dr. Robert Boyd at dr.boyd@datapunk.net if you are interested.

     

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  • Vitamin B12, Secretor Status and Ancestry Raw Data

    The Opus 23 genetic interpretation software [1] checks for ABH secretor status as part of the hereditary genetics algorithms. Knowing whether your client is a secretor or non-secretor is important for many reasons, one being that non-secretors have increased levels of serum vitamin B12. This is a well known association: at least five GWAS studies found SNPs in FUT2 show the strongest statistical association with circulating vitamin B12 [2-6]. Two of these studies also report a 10-25% increase in circulating total vitamin B12 concentration in homozygotes for the common non-secretor alleles, as determined by the FUT2 genotype of the nonsense stop-gain mutation W143X, rs601338. The mechanism for this is however unclear.

    Previously theories have included the influence of H. pylori infection, which has been associated with vitamin B12 deficiency. [7,8] Some authors have proposed that FUT2 genotype can influence the extent to which H. pylori attaches to gastric mucosa and influences vitamin B12 absorption. [9, 10] This was refuted by a subsequent study in 2012, which found that secretor status as determined by FUT2 variation correlates with plasma vitamin B12 concentrations, but is independent of H. pylori serotype. [11]

    Chery et. al. Proposed that FUT2 genotype could affect the glycosylation status of another vitamin B12 transporter, gastric intrinsic factor (GIF) [12]. This was a small study however, and although a potential effect was observed on GIF secretion and glycosylation according to FUT2 rs601338 genotype, the GIF phenotypes of the FUT2 rs601338 GA heterozygotes more closely aligned with those of the non-secretor genotype (AA) than those with the secretor genotype (GG). It is currently unclear to what extent FUT2 genotype influences GIF secretion and thereby alters vitamin B12 concentration in the general population.

    It is important to note that all the above mentioned studies measured only total circulating vitamin B12, which does not distinguish the proportion of B12 bound to its two separate carrier proteins, transcobalamin and haptocorrin. Haptocorrin, also known as transcobalamin-1 (TCN1), is a glycoprotein produced by the salivary glands of the oral cavity in response to ingestion of food. This protein binds strongly to vitamin B12 in the mouth to protect it from the acidic environment of the stomach. Haptocorrin also circulates and binds approximately 80% of circulating B12, rendering it unavailable for cellular delivery by transcobalamin II. These carrier proteins carry significantly different quantities of vitamin B12 in blood, and have different biological properties: transcobalamin II delivers vitamin B12 to all tissues, while vitamin B12 carried by haptocorrin is ultimately returned to the gut. In a recent paper on a GWAS study by Velkova et. al. using The Trinity Student Study population of 2,524 subjects in Ireland, the authors hypothesized that the expression of functional FUT2 enzyme could influence total circulating vitamin B12 concentration by altering the glycosylation of haptocorrin. This is the first study to assess the relationship between ‘active’ B12, total B12 and the FUT2 secretor status variant. [13]

    The authors reported that FUT2 genotype influences the concentration of haptocorrin-bound vitamin B12 to a far greater extent than transcobalamin-bound vitamin B12. This is consistent with FUT2 exerting influence via its fucosylation function, as haptocorrin is a glycosylated protein and transcobalamin is not. They also suggest that FUT2 activity impacts the intra-organismal recycling of vitamin B12, not the absorption and assimilation of the vitamin from the diet.

    In both the H. pylori and the GIF models described above, FUT2 genotype would alter the pool of vitamin B12 absorbed from the gut. As vitamin B12 transported from the gut binds to transcobalamin in plasma, these models are not consistent with the data from Velkova et. al., which shows that FUT2 genotype influences the concentration of haptocorrin-bound vitamin B12 to a far greater extent than transcobalamin-bound vitamin B12.

    The connection between secretor status and B12 levels is consistent with FUT2 exerting influence via its fucosylation function on B12 carriers, as haptocorrin is a glycosylated protein and transcobalamin is not. It also suggests that FUT2 activity impacts the intra-organismal recycling of vitamin B12, not the absorption and assimilation of the vitamin from the diet. This could be the reason why the standard test for vitamin B12 has significant false positive and false negative rates: only ~20% of circulating vitamin B12 (holoTC) represents the “active” bioavailable form, meaning that the most commonly ordered clinical test for vitamin B12 mainly measures the holoHC, which could mask an existing vitamin B12 deficiency. When evaluating or confirming vitamin B12 deficiency, additional markers of vitamin B12-dependent enzyme activity such as methylmalonic acid (MMA) and total homocysteine are also problematic. FUT2 secretor status may therefore be useful when considering the overall B12 status of an individual, and non-secretors may appear to have falsely elevated serum total B12 when compared with active B12.

    Opus 23 handles a range of raw data files, however Ancestry.com and Genos data files do not include the rs601338 SNP, which denotes the non-secretor mutation when homozygous. When only these data files are loaded Opus 23 looks for another SNP on FUT2 that is reported in Ancestry.com and Genos raw data files, and which is in perfect linkage disequilibrium with rs601338. This will give you the client’s imputed secretor status, and therefore indications for interpreting serum vitamin B12 tests. Opus 23 also checks for another FUT2 non-secretor SNP found only in Asians and not in Caucasians when looking for secretor status.

    References: 

    1. Opus 23 Pro genetic analysis and reporting software by Dr P. D’Adamo www.opus23.com.

    2 .Hazra, A., Kraft, P., Selhub, J., Giovannucci, E.L., Thomas, G., Hoover, R.N., Chanock, S.J. and Hunter, D.J. (2008) Common variants of FUT2 are associated with plasma vitamin B12 levels. Nat Genet, 40, 1160-1162. PMID 18776911.

    3. Lin, X., Lu, D., Gao, Y., Tao, S., Yang, X., Feng, J., Tan, A., Zhang, H., Hu, Y., Qin, X. et al. (2012) Genome-wide association study identifies novel loci associated with serum level of vitamin B12 in Chinese men. Hum Mol Genet, 21, 2610-2617. PMID 22367966.

    4. Tanaka, T., Scheet, P., Giusti, B., Bandinelli, S., Piras, M.G., Usala, G., Lai, S., Mulas, A., Corsi, A.M., Vestrini, A. et al. (2009) Genome-wide association study of vitamin B6, vitamin B12, folate, and homocysteine blood concentrations. Am J Hum Genet, 84, 477-482. PMID 19303062.

    5. Grarup, N., Sulem, P., Sandholt, C.H., Thorleifsson, G., Ahluwalia, T.S., Steinthorsdottir, V., Bjarnason, H., Gudbjartsson, D.F., Magnusson, O.T., Sparso, T. et al. (2013) Genetic architecture of vitamin B12 and folate levels uncovered applying deeply sequenced large datasets. PLoS Genet, 9, e1003530. PMID 23754956.

    6. Hazra, A., Kraft, P., Lazarus, R., Chen, C., Chanock, S.J., Jacques, P., Selhub, J. and Hunter, D.J. (2009) Genome-wide significant predictors of metabolites in the one-carbon metabolism pathway. Hum Mol Genet, 18, 4677-4687. PMID 19744961

    7. Kaptan, K., Beyan, C., Ural, A.U., Cetin, T., Avcu, F., Gulsen, M., Finci, R. and Yalcin, A. (2000) Helicobacter pylori–is it a novel causative agent in Vitamin B12 deficiency? Arch Intern Med, 160, 1349-1353. PMID 10809040.

    8. Carmel, R., Perez-Perez, G.I. and Blaser, M.J. (1994) Helicobacter pylori infection and food-cobalamin malabsorption. Dig Dis Sci, 39, 309-314. PMID 8313813.

    9 Ikehara, Y., Nishihara, S., Yasutomi, H., Kitamura, T., Matsuo, K., Shimizu, N., Inada, K., Kodera, Y., Yamamura, Y., Narimatsu, H. et al. (2001) Polymorphisms of two fucosyltransferase genes (Lewis and Secretor genes) involving type I Lewis antigens are associated with the presence of anti-Helicobacter pylori IgG antibody. Cancer Epidemiol Biomarkers Prev, 10, 971-977. PMID 11535550.

    10 Magalhaes, A., Rossez, Y., Robbe-Masselot, C., Maes, E., Gomes, J., Shevtsova, A., Bugaytsova, J., Boren, T. and Reis, C.A. (2016) Muc5ac gastric mucin glycosylation is shaped by FUT2 activity and functionally impacts Helicobacter pylori binding. Sci Rep, 6, 25575. PMID: 27161092.

    11. Oussalah, A., Besseau, C., Chery, C., Jeannesson, E., Gueant-Rodriguez, R.M., Anello, G., Bosco, P., Elia, M., Romano, A., Bronowicki, J.P. et al. (2012) Helicobacter pylori serologic status has no influence on the association between fucosyltransferase 2 polymorphism (FUT2 461 G->A) and vitamin B-12 in Europe and West Africa. Am J Clin Nutr, 95, 514-521. PMID 22237057.

    12. Chery, C., Hehn, A., Mrabet, N., Oussalah, A., Jeannesson, E., Besseau, C., Alberto, J.M., Gross, I., Josse, T., Gerard, P. et al. (2013) Gastric intrinsic factor deficiency with combined GIF heterozygous mutations and FUT2 secretor variant. Biochimie, 95, 995-1001. PMID 23402911.

    13. Velkova A, Diaz JEL, Pangilinan F, et. al; The FUT2 secretor variant p.Trp154Ter influences serum vitamin B12 concentration via holo-haptocorrin (holoHC), but not holo-transcobalamin (holoTC), and is associated with haptocorrin glycosylation, Hum Mol Genet, Volume 26, Issue 24, 15 December 2017, Pages 4975–4988. PMID 29040465.

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  • Meet and greet O23 webinars!

    Starting in January 2018, we will begin hosting monthly webinars to showcase the powerful tools of Opus23. These webinars are completely FREE and will cover the basics of Opus23, discuss what sets us apart from other genomic analysis programs and provide a live demo of both Opus23 and Utopia. The first webinar will be held on January 9th at 11:00AM ET.

    The webinars are hosted by Dr. Robert Boyd, one of developers of Opus23, and chief resident at the Center of Excellence in Generative Medicine.

    These introductory webinars are best suited for individuals who are interested in learning about Opus23, but have not yet taken the training webinar. They will also serve as a great refresher for any users who have completed the Opus training in the past.

    A special discount offer will be provided to all attendees for an upcoming training webinar or client upload.

    Click here to register here for the webinar!

    Please share this post to anyone you know who would benefit from using Opus23 in their practice!

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  • Opus 23 now supports multiple platforms

    The recent change in the reporting done by 23andMe from the V4 to V5 chip has thrown things into a bit of a dither. The earlier V4 SNP array was more robust, at least with SNPs of interest to those who work in nutrigenomics. For example, V4 reported over ten MAO SNPs of nutritional interest, whist V5 reports none. To circumvent the problem, I’ve recoded Opus 23 to allow the clinician to upload, singly or in combination, data files from 23andMe (V3, V4, V5), Ancestry DNA and the ‘Export to Promethease’ file available from Genos. To move Opus in this direction required a lot of recoding and I thank all our users for their support and patience.

    The first time you load an existing client profile into Opus it will take a bit longer to process the file. This is because they are being upgraded to the new data storage system. After that they should load as usual. Manage->Profiles->Append Raw Data to Current Client will take you to the BLENDER app,which allows you to merge raw data files. This will only be important as people begin to use Ancestry DNA, perhaps in combination with 23andMe V5. Since almost everyone currently in Opus is 23andMe V4 you really don’t need to do anything.

    The ‘Upload New Client Raw Data’ script has been extensively re-written. You still upload a ZIP file, but the script will identify the platform (V3/V4, V5, Ancestry DNA) and let you know. It also now features and extra screen so that you can verify/validate your form input before doing the final upload. Hopefully this will cut down on people contacting us having uploaded the same client twice.

    Uploading and merging  V5 and Ancestry DNA client data have about 74% of Opus-curated snps, while the prior V4 has about 79% coverage.

    If you do upload Ancestry DNA data, be advised that Ancestry names its raw data files in a non-unique manner, usually something like ‘dna-data-2017-09-03.zip’. This blunts the ability of the program to warn you that you are using the same data file on two different clients. You should rename the client raw data ZIP file on your hard drive to something unique (we recommend replacing Ancestry DNA filename with the client’s first and last initials and date of birth; in this case ‘dna-data-2017-09-03.zip’ might become ‘MG-11-22-1956.zip.’ But you can use any system you wish as long as each uploaded filename is unique.

    It looks like the best short term solution will be to have the client do BOTH 23andme V5 and Ancestry.  Opus 23  now allows you to sequentially upload the raw data and merge it. We will eventually move towards a dedicated chip. However this change from v4 to v5 caught everyone (not just Opus/Datapunk) flat-footed as to the huge drop in clinically significant SNPs that are reported in v5. Even in the best of circumstances it will be weeks and months until a specialized chip will become available. However, in the meantime, piggybacking 23andMe v5 with Ancestry DNA appears to be not all that bad of a temporary fix. Many of these SNP panels are having significant price drops, so having the client do bot 23andMe V5 and Ancestry DNA should not be prohibitively expensive.

     

    In Other News

    You can now compare V5, V4, Genos Promethease export, and Ancestry data as compared to the core 2600 Opus snps. Just log in, click the ‘Informatics’ pull down, the select ‘Tools/ Extras’ and “Platform Comparisons’. Table is searchable, sortable and filterable.

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  • Basic and advanced in-person training seminar, May 20-21.

    Most patients improve through committing themselves to lifestyle, diet, mindset and environmental changes. When they don’t, additional history and sleuthing is needed. As our patients get more complex, the need for quickly evaluating thousands of genes is needed. Peter’s Opus23 allows one to do exactly this. I highly recommend using Opus23 for those patients who have ‘tried everything’ and are still stuck. It could very well find the answers to your patient’s riddle.” — Dr. Ben Lynch

    There will be an in-person training at the Center of Excellence in Generative Medicine (University of Bridgeport, Connecticut) for the weekend of May 20-21.

    A weekend training hosted by the Center of Excellence in Generative Medicine at the University of Bridgeport, Bridgeport CT, USA. A rare opportunity to receive hands-on training in Opus23 from Peter D’Adamo, Jacqueline Greenfield and Tom Greenfield, the key developers of the platform.

    SEMINAR DESIGN

    The seminar is a mix of some lecture and extensive hands-on learning. During experiential sessions, attendees will break up into 4-5 person workgroups. Each workgroup will have its own teaching assistant (TA) a GM/COE student with extensive experience with Opus. Attendees will work directly in Opus on a series of different clients.

    Choose between the Level I (basic certification) needed for access to Opus23 or Level II (advanced training) for those who have already completed a basic webinar or seminar.  

    Level I covers the  fundamentals of Opus23: The user interface and design philosophy; the key informatic  apps, and curating a client report.

    Level II covers advanced topics in Opus23:  Advanced informatics apps, microbiome integration, and advanced prescriptives and protocol generation.

    Successful completion of the level I training allows you full access to the Opus23 software, with the ability to upload and analyze raw data from 23andMe and uBiome, and produce notes and patient reports. 

    Cost of the seminar is $800 USD. Proceeds go to the Center of Excellence in Generative Medicine (COEGM) which provides advanced clinical and didactic postgraduate training for the College of Naturopathic Medicine (UBCNM). Because of the hands-on nature of this seminar, seating is limited to 18 attendees.

    Please visit this link to register for the conference via our secure PayPal link.

    SEMINAR SCHEDULE

    The seminar will run from 9AM-5PM Saturday May  20 and 9AM-12 NOON May 21. You should arrive at 8:30AM for registration and to meet your TA. Classes will take  place on the University of Bridgeport campus, at the Center of Excellence in Generative Medicine, 115 Broad Street Bridgeport CT 06604. Lunch will be provided on Saturday at the COEGM as well as dinner at a local restaurant.

    HOTEL/LODGING

    Bridgeport Holiday Inn
    1070 Main Street
    Bridgeport CT 06604
    Phone: 203 334-1234
    Fax: 203 696-1985

    http://www.ihg.com/holidayinn/hotels/us/en/bridgeport/bgdct/hoteldetail

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  • Three new interactive networks

    We’ve added new mapping networks to Opus 23 MAPPER app. The MAPPER app allows you to visualize your client’s genomic data directly in a number of hand-curated pathway maps. In addition to allowing for quick pattern recognition, MAPPER uses combinatorics and graph theory to ascertain certain functional characteristics of genes in the network, based on their position in a web of interconnections. All gene nodes in MAPPER trigger extensive information popup windows.

    TSH Signaling Network

    tsh

    Human thyroid stimulating hormone (TSH) is a glycoprotein secreted by the anterior part of the pituitary gland. TSH plays an important physiological role in the regulation of the hypothalamic-pituitary-thyroid axis by modulating the release of the thyroid hormones from the thyroid gland. TSH is mainly expressed in adenohypophysis , thyroid gland, leukocyte, pituitary gland, stratum basale, stratum corneum, stratum granulosum, stratum spinosum and keratinocyte. Impairment of TSH signal transduction pathway leads to thyroid disorders such as goitre, hypothyroidism and hyperthyroidism, with complex clinical manifestations. T

    Endoplasmic Reticulum Stress and Unfolded Protein Response

    upr

    The endoplasmic reticulum (ER) is a dynamic intracellular organelle with multiple functions essential for cellular homeostasis, development, and stress responsiveness. In response to cellular stress, a well-established signaling cascade, the unfolded protein response (UPR), is activated. This intricate mechanism is an important means of reestablishing cellular homeostasis and alleviating the inciting stress. Now, emerging evidence has demonstrated that the UPR influences cellular metabolism through diverse mechanisms, including calcium and lipid transfer, raising the prospect of involvement of these processes in the pathogenesis of disease, including neurodegeneration, cancer, diabetes mellitus and cardiovascular disease. [PMC3039444]

    AR Signaling Network

    ar

    Androgens, mainly testosterone and 5alpha-dihydrotestosterone (DHT) play significant role in the growth and development of the male reproductive organs. AR is found to be expressed in a number of tissues and cells including prostate, testis, seminal vescicle, epididymis, skin, skeletal muscle, cardiac muscle, liver and central nervous system. The androgen receptor is known to bind to many co-regulators at different time points and in different cell types. This DNA protein complex triggers the expression of various target genes that are associated with the male phenotype. Androgen receptors are known to induce apoptosis under certain conditions. Various regulators that regulate androgen induced apoptosis include BRCA1 and Smad3 and Akt. Mutation in AR are also known to be associated in a number of diseases including spinal and bulbar muscular atrophy (SBMA) or Kennedy’s disease and Androgen Insensitivity syndrome (AIS). Abnormal amplification of the androgen gene as well as deregulation of AR gene expression have been shown to be associated with prostate cancer.

    To learn more about Opus23 training webinars, click here.

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  • Utopia: Advice, Intelligent interface with Opus23

    Advice: Intelligent Interface with OPUS23

    ADVICE is an app in Utopia that gives algorithmic considerations of multiple bacterial strains in conjunction with the client’s own genome to provide true/false clinical outcomes. ADVICE automatically pulls the client’s Opus23 genetic data where relevant, and incorporates it into algorithmic calculations. (comparable to LUMEN in Opus23).

    Getting around ADVICE

    From the Utopia drop down menu, hover over ‘Algorithms’ until a second list appears, then select ‘Advice’. You are presented with a list of algorithms, those that are true are at the top and display the word ‘TRUE’ in a green box, followed by those that are false, which display the word ‘FALSE’ in an orange box. Each algorithm will display the repute (risk, benefit or neutral), and the magnitude. If an algorithm suggests prescriptive metabolites which enhance or reduce specific bacteria, they will be listed under Encourage or Discourage.

    The client’s relevant genes will be displayed beneath the listed ‘microbiota’ information in the same format found in the Opus23 LUMEN app. Clicking on the colored semicircle will open a pop-up window with a description of the gene and giving details of the client’s SNPs for the gene from their Opus23 data.

    Utopia Advice algorithm

    An ADVICE algorithm for gluten-induced immunopathology

    All metabolites and taxa are clickable. Clicking a metabolite opens a pop-up window with a list of bacteria affected by it. Clicking a bacterium opens a pop-up window as described in previous apps. To add an algorithm to the client report, click on the ‘Add/ Uncurated’ button.

    Individual genera may also be curated and added to the client report for the current dataset by selecting the taxon to open its pop-up information and then clicking the ‘Add/Uncurated’ button.

    Screen shot of Metabolomics pop-up window

    Pop-up window in ADVICE showing metabolomics information

    Using the Algorithm Aggregate Analysis

    At the bottom of the page is the Algorithm Aggregate Analysis. This is a summary of all advice for the client listed under either an ‘increase’ and ‘decrease’ section heading. Each section provides both the microbiota and beneficial/ harmful metabolites that are suggested to be increased or decreased by your client. The ‘result’ information can be a useful tool for streamlining complex treatment strategies. Each metabolite listed in the Algorithm Aggregate Analysis details whether or not the metabolite has mixed results (included as both encourage and discourage in ADVICE algorithms), and whether it is specific to an algorithm.

    Algorithm Aggregate Analysis screenshot

    Algorithm Aggregate Analysis for the ADVICE app

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  • Upcoming Opus 23 In-Person Seminar

    Because of media obligations associated with the re-release of Dr. D’Adamo’s first book, there is a schedule conflict with the January 7-8 seminar date. The seminar will be rescheduled for a later date.  Please check back for further news and details.


    If you are even thinking about doing this sign up.Opus 23 has been a game changer for my patients who have had ‘mysterious’ problems that, after seeing many integrative practitioners, still were not better until Opus 23 ‘sang’ the perfect healing words. –Robert Lang, MD

    Dr. D’Adamo periodically does these for those practitioners who prefer a more hands-on approach to learning Opus 23 (vs. the wonderful 5 hour webinars done by Drs. Greenfield).

    Dr. D’Adamo writes:

    ‘Attendees work in 2-3 person pods under the direct supervision of one of my COE wunderkids. You also get a healthy dose of me lecturing on stuff: In this case a heavy focus on the new ‘Utopia’ module that allows you to mash up client genomic and microbiome data. Attendance is purposely kept to 10-12, to insure an intimate learning environment. You get lunch and I typically spring for dinner at a nice restaurant.’

    If you are interested in this type of hands-on training, contact Carol Agostino at carol@dadamo.com (203 761-0042) for full details.

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