An illness to a single bacteria is a standard medical practice. Helicobacter pylori for ulcer, or one of several E. Coli (E. coli O157:H7 and other STECs like E. coli O145 and E. coli O121:H19) for food poisoning.

If we expand our eyes and ask “What if the condition is caused by over or under production of some metabolite?”

For CFS over production of d-lactic acid has been proposed, see this post

• Approaches to D-Lactic Acidosis
• D-lactic Acidosis -Sauerkraut is not good for you if you have CFS!

Let us assume that this is part of it. So which bacteria produces it?

Our old friend DataPunk lists:

PRODUCED AS ENDPRODUCT BY: 

1. Aerococcus
2. Allobaculum
3. Anaerostipes
4. Atopobium
5. Bacillus coagulans
6. Bifidobacterium
7. Cardiobacteriales
8. Cardiobacterium
9. Carnobacterium
10. Catenibacterium
11. Enterococcus
12. Faecalibaculum
13. Faecalibaculum rodentium
14. Gemella
15. Haemophilus
16. Holdemania
17. Lachnobacterium
18. Lactobacillales
19. Lactobacillus
20. Lactobacillus acidophilus
21. Lactobacillus casei
22. Lactobacillus delbrueckii
23. Lactobacillus helveticus
24. Lactobacillus rhamnosus
25. Lactococcus
26. Leptotrichia
27. Leuconostoc
28. Microbacterium
29. Moryella
30. Oenococcus
31. Pediococcus
32. Rothia
33. Ruminococcus faecis
34. Scardovia
35. Serratia marcescens
36. Streptococcus
37. Tetragenococcus
38. Vagococcus

Let us suppose that we also have low or no butyrate – again datapunk lists:

PRODUCED AS ENDPRODUCT BY:

1. Agathobacter rectalis
2. Allobaculum
3. Anaerostipes
4. Anaerostipes hadrus
5. Anaerotruncus
6. Butyricicoccus
7. Butyricicoccus pullicaecorum
8. Butyricicoccus sp. ORNL_6EZ5-Gt_4_Pl1-35
9. Butyricicoccus sp. ORNL_6EZ5-Gt_6_Pl2-147
10. Butyricicoccus sp. ORNL_V42_E05
11. Butyricicoccus sp. ORNL_W42_C10
12. Butyricimonas
13. Catenibacterium
14. Christensenella
15. Cloacibacillus
16. Cloacibacillus porcorum
17. Clostridia
18. Clostridiales
19. Clostridium
20. Clostridium butyricum
21. Coprococcus
22. Defluviitalea
23. Eubacteriaceae
24. Eubacterium limosum
25. Eubacterium oxidoreducens
26. Faecalibacterium
27. Faecalibacterium prausnitzii
28. Flavonifractor
29. Flavonifractor plautii
30. Fusibacter
31. Fusobacterium
32. Lachnobacterium
33. Lachnospiraceae
34. Moryella
35. Moryella indoligenes
36. Oscillospira
37. Peptoniphilus
38. Roseburia
39. Roseburia faecis
40. Roseburia hominis
41. Roseburia intestinalis
42. Roseburia inulinivorans
43. Ruminococcus torques
44. Subdoligranulum

So how many possible “too much and not enough” pairs are there if we just pick just one from each list…  38 x 44 = 1,672!!! 

My current gut feeling is that taking the % of each taxonomy in each group –> producing a fuzzy measure of a 0.23% Lactic acid and 0.01% butyrate, may reveal clearer patterns for symptoms than the individual bacteria taxonomy. This is a fuzzy measure because the production of lactic acid and butyrate vary greatly from genus to genus.

Other options for stepping away from pine needles of individual bacteria to looking at tree as a whole include KEGG pathways,

KEGG pathways produce some tentative correlation for D-Arginine and D-ornithine metabolism in CFS/IBS in my earlier post.

Bottom Line

The same change of metabolites in the body can happen in many many different ways. Looking at the metabolites (even with fuzzy ‘punted’ data base on what is available) may produce better predictive results than just looking at individual bacteria.

The page will update as shown below

In a few minutes an email should be delivered

Click on the link, and this will appear

Enter password (please try to make them strong …) You will next be sent to the login screen

You will land on a page like below (unless you also have ubiome samples already uploaded under your email – in which case they will be listed)

Please check your upload file, the first line should be:

“taxon_id”,”rank”,”name”,”parent”,”count”

If it is not, please email it to me at ken /at/ lassesen /dot/ com so I may adjust the code.

Select your file, the name of who it is (in case you are handling several people) and when the sample was taken.

Bottom Line

This is still in Alpha–  there were a lot of side-effects and refactoring required to support these imports — but changes would make it easier to support other uploads.

Email me if you encounter any bugs  Ken /at/ lassesen /dot/ com

This describes how ubiome and other gut bacteria work… And more important, what they totally miss.

”

“

From A huge number of mystery microbes are living on your skin https://www.newscientist.com/article/2172076-a-huge-number-of-mystery-microbes-are-living-on-your-skin/

A reader wrote about this year being very bad for allergies/hay fever for her. DAO, REAL sudafed, etc only made a small dent in it. She tried niacin (the flushing type) and fibrinolytics (bromelain, serrapetase, lumbrokinease, nattokinease) which made a much bigger improvement …. what gives?

For back references:

• moderating-histamines-more-herbs Post
• Reflections on the Treatment of Histamine Over-sensitivity Post
• Histamines and Anticoagulants – a review

Allergy and Coagulation

• Role of the coagulation system in allergic inflammation in the upper airways. [2008]
  • ” The results of this study suggest that activation of the coagulation system occurs during the allergic response and that thrombin plays a crucial role in the regulation of mucin production in the upper airways.”
• [Coagulation and anticoagulation systems of the blood in allergic diseases]. 1988
• Platelets and allergic inflammation. 2014
• The Mast Cell, Contact, and Coagulation System Connection in Anaphylaxis. 2017
• “The pathogenesis of mast cell degranulation and CSU was also shown to be associated with the activation of hemostatic factors such as fibrinogen and FXIIa. ” [2018]
• “These three cases illustrate the potential role platelets may have in anaphylaxis and possible increased secondary risk for the development of thrombosis. Larger studies are required to determine incidence and risk factors for bloodclots following anaphylaxis in order to provide management or screening recommendations.” [2018]

Different Allergy Mechanisms

• “The immune-mediated adverse reaction to food is defined as food allergy (FA) which is roughly divided into IgE mediated or non-IgE mediated FA (NFA)… there is far less of an understanding of NFA than IgE-mediated FA and its clinical relevance is likely under-estimated in most cases…The lack of easily accessible diagnostic measures also contributes to the problem.  ” [2008]
  • This also applies to Hay Fever and other allergies
• “Although pathogenesis of NFA is still not well understood, recent studies indicate widely variable clinical manifestations of NFA…This review discusses recent progress in our understanding of the regulatory mechanisms of gut immune homeostasis and recently revealed widely variable clinical presentations of NFA with respect to it pathogenesis.” [2012]
• Inhibition of IgE- and non-IgE-mediated histamine release from human basophil leukocytes in vitro by a histamine H1-antagonist, desethoxycarbonyl-loratadine. 1994
• “Nonallergic rhinitis represents a non-IgE-mediated group of disorders that share the symptoms of nasal congestion, rhinorrhea, sneezing, and/or postnasal discharge but not pruritus that characterizes allergic rhinitis…. skin testing for aeroallergens is negative.” [2012]

Of special interest (especially for MCS folks)
“The classic symptoms of idiopathic nonallergic rhinitis are nasal congestion, postnasal drip, and sneezing triggered by irritant odors, perfumes, wine, and weather changes.” [2012]

“: Idiopathic nonallergic rhinitis (iNAR) has been difficult to define because of the long differential diagnosis of rhinopathy in the absence of allergic rhinitis. iNAR has traditionally been a diagnosis of exclusion with no clear unifying pathophysiology. Increased sensitivity to triggers such has climate changes, cold air, tobacco smoke, strong odors, and perfumes have been thought to be characteristic, but recent studies do not support this hypersensitivity hypothesis. New investigations of the local nasal environment and systemic “functional” syndromes have offered new insights into this condition. iNAR may be a heterogenous disorder that includes (1) anatomic abnormalities requiring nasal endoscopy for diagnosis, (2) incipient, local atopy (entopy), (3) dysfunction of nociceptive nerve sensor and ion channel proteins, and (4) autonomic dysfunction as found in chronic fatigue syndrome and other functional disorders.” [2009]

Bottom Line

If you are having bad hay fever and the “standard popular knowledge” is not doing it for you, you may wish to discuss coagulation as being part of it with your medical professional.

A reader forwarded their report from NutraHacker (https://www.nutrahacker.com/). They offer free reports and more advanced paid reports.  Their reports also contain Encourage and Avoid items.

What is interesting is when you combine recommendations from http://microbiomeprescription.com/ with their recommendations. In some cases they corresponds and in other cases disagree. DNA says one thing, existing microbiome says another thing.

Simple Example for Vitamin E

So this person with AG should NOT be supplementing with Vitamin E because it will increase inflammation. What about the case of a high Vitamin E take by diet?

Looking at a list of foods that are HIGH in vitamin E, we see:

• Almonds
• Hazelnuts
• Sunflower Seeds
• Avocado
• Mango
• Abalone
• Salmon
• Wheat Germ Oil

Looking at this person’s suggestions from the Microbiome, we see Almonds listed.

This suggests that almonds should be excluded (mainly because there are lots of other suggestions) because of DNA and not microbiome.

Bottom Line

DNA and microbiome interacts.

• “Using multiple methods, we have demonstrated that some aspects of the human oral microbiome are heritable and that with a relatively small sample we were able to identify two previously unidentified loci that may be involved.” [2017]

• Host Genome Influence on Gut Microbial Composition and Microbial Prediction of Complex Traits in Pigs.

• The effect of host genetics on the gut microbiome.[2016] “provide evidence of a gene-diet interaction in the regulation of Bifidobacterium abundance.”

• The effect of heritability and host genetics on the gut microbiota and metabolic syndrome[2017].  “Our results suggest that an altered microbiota composition mediated by a specific host genotype can contribute to the development of Metabolic Syndrome.”