March 18, 2012
Bacterial Infection Boosts Insulin-Resistant Diabetes Risk?

Helicobacter pylori (H. pylori) bacteria causes stomach ulcers and also may increase the risks of some types of cancers while possibly lowering the risks of other cancers. It isn't clear (at least to me) whether killing the H. pylori that might be in your stomach will lower or raise all cause mortality risk. However, a new study finds evidence that H. pylori could contribute to development of insulin-resistant (type 2) diabetes.

NEW YORK, March 14, 2012 – A new study by researchers at NYU Langone Medical Center reveals that the presence of Helicobacter pylori (H. pylori) bacteria is associated with elevated levels of glycosylated hemoglobin (HbA1c), an important biomarker for blood glucose levels and diabetes. The association was even stronger in obese individuals with a higher Body Mass Index (BMI). The results, which suggest the bacteria may play a role in the development of diabetes in adults, are available online in The Journal of Infectious Diseases.

There have been several studies evaluating the effect of the presence of H. pylori on diabetes outcomes, but this is the first to examine the effect on HbA1c, an important, objective biomarker for long-term blood sugar levels, explained Yu Chen, PhD, MPH, associate professor of epidemiology at NYU School of Medicine, part of NYU Langone Medical Center.

"The prevalence of obesity and diabetes is growing at a rapid rate, so the more we know about what factors impact these conditions, the better chance we have for doing something about it," Dr. Chen said. Looking at the effects of H. pylori on HbA1c, and whether the association differs according to BMI status, provided what could be a key piece of information for future treatment of diabetes, she explained.

Too high blood sugar accelerates aging. So it is worth the effort to avoid the risk of insulin-insensitive diabetes.

Getting tested for H. pylori might be worth the trouble, especially if you had the test done as part of a larger set of tests to check for other risk factors such as bad blood lipid profile and high blood sugar.

Share |      Randall Parker, 2012 March 18 10:16 PM  Health Risks


Comments
Wolf-Dog said at March 19, 2012 12:51 PM:

The chronic gastritis that H. Pylori indirectly puts pressure on the adrenal glands, increasing the cortisol levels. High cortisol leads to high insulin, which causes resistance to insulin. But this might be reversible with treatment of H. Pylori. However, it is also claimed by some doctors that H. Pylori is part of the natural ecosystem of the digestive system and that it should not be eliminated, but that some people mysteriously have more intolerance to H. Pylori. In any case, it is known that most stomach cancers and ulcers are due to H. Pylori. There is drug resistant H. Plori in the world, and this strain is becoming an epidemic. In many poor countries, especially in agricultural countries 80 % of the population carry H. Pylori. In the industrialized western countries 30% of the people have H. Pylori.

PacRim Jim said at March 20, 2012 1:35 AM:

Scientists seem to be researching in circles, because they are generalizing their results across the entire species of Homo sapience.
Only when personal medicine is adopted will it become possible to fully understand what the hell goes on within these marvelous, yet short-lived, bodies that we inhabit.

Robert Roy said at March 21, 2012 7:10 PM:

I hate how many studies I see lately that don't distinguish between cause and effect. I mean, isn't it possible that H. Pylori levels are elevated because of a high-carb diet which also happens to cause metabolic syndrome and diabetes?? Personally, my gastrointestinal issues were starting to get pretty severe until I went on a low carb diet, and now I've not even touched an antacid since.

anon said at March 21, 2012 7:11 PM:

we've known for years that almost any infection effects insulin resistance.

Julian Lieb,M.D said at April 4, 2012 5:23 PM:

HIV-sites

HOPE

Julian Lieb, M.D

drjulianlieb@gmail.com

STIMULATING IMMUNE FUNCTION TO DEFEAT THE HUMAN IMMUNODEFICIENCY VIRUS, RESISTANT BACTERIA, THE TUBERCULOSIS MICROORGANISM, AND OTHER PATHOGENS: A SUPPRESSED INNOVATION


Stimulating defective immune function to perform efficiently is a desirable approach to defeating pathogens. Such stimulation is represented as unavailable, while in truth the immunostimulating properties of lithium and antidepressants were documented many years ago.1-4 A therapeutic claim is reinforced when the mechanism is known. Prostaglandins, when produced excessively, depress every component of immune function, and induce microbial replication. Wherever HIV comes into contact with arachidonic acid, an envelope glycoprotein powerfully converts this precursor to prostaglandin E2, depressing immune function and promoting viral replication, excessive prostaglandin E2 a leading candidate for the immunosuppression that is the hallmark of AIDS.5-7 Antidepressants inhibit the synthesis of prostaglandin E2, antagonize its actions, and stimulate the primary prostaglandin-degrading enzyme.8-10

Collective evidence shows that lithium has acute immunostimulating, anti-viral, and anti-bacterial properties, 11 antidepressants chronic immunostimulating, anti-viral, anti-bacterial,1-4 anti-parasite, and fungicidal properties.12-15 Tuberculosis, now the #1 killer of the HIV infected, is developing resistance to standard treatment. In the late nineteen forties, physicians working in tuberculosis sanitaria observed patients with elevations of mood and energy. Their charts revealed that all were taking the monoamine oxidase inhibitors isoniazid or iproniazid, an observation from which antidepressant therapy developed. If anti-tuberculosis agents double as antidepressants, surely antidepressants must double as anti-tuberculosis agents? The antimalarial properties of antidepressants in vitro are supported by many studies.12 When added to anti-retrovirals, antidepressants can reduce HIV viral loads to undetectable.16 The authors of this study attribute this to adherence, seemingly unaware of the antiviral properties of antidepressants. The advantage of immunostimulation is its non-specificity, a stimulated immune system indifferent to antigenicity.

People with intact immune function are relatively invulnerable to pathogens, compared to those with defective function. Depression is a seldom mentioned cause of defective immunity, although indices of immune function indicate that it does so.17 In a study of 405 HIV-positive gay and bisexual men, those who reported being depressed throughout the eight-year study period, were two-thirds more likely to die than those who were never significantly depressed.18,

Forty years ago, prostaglandins were shown to regulate immune function, and lithium and antidepressants to inhibit prostaglandins. Gradually, prostaglandins were found to regulate every aspect of HIV replication, and HIV to stimulate prostaglandin E2 production, to a greater degree than other viruses. This prostaglandin, when produced excessively, is thought to be responsible for the immune depression that is the hallmark of AIDS. Initially, I suspected that lithium and antidepressants could be used as heavy artillery against HIV, but when lithium failed to improve patients with HIV in two small clinical trials, came to favor antidepressants for this purpose. 19,20,21
Tragically, vested interests worldwide have suppressed the innovation.

1. Lieb J. Remission of herpes virus infection and immunopotentiation with lithium carbonate: inhibition of prostaglandin E1 synthesis by lithium may explain its antiviral, immunopotentiating, and antimanic properties. Biol Psychiatry 1981; 695-698.

2. Lieb J. Remission of rheumatoid arthritis and other disorders of immunity in patients taking monoamine oxidase inhibitors. Int J Immunopharmacol 1983; 5(4): 353-357.

3. Rosenthal S, Fitch W. The antiherpetic effects of phenelzine. J Clin Psychopharmacol 1987; 7(2):119.

4. Murphy D, Donnelly C, Moskowitz J. Inhibition by lithium of prostaglandin E1 and norepinephrine effects on cyclic adenosine monophosphate production in human platelets. Clin Pharmacol Ther 1973; 14(5):810-814.

5. Lee R. The influence of psychotropic drugs on prostaglandin biosynthesis. Prostaglandins 1974; 5(1):63-68.

6. Manku MS, Horrobin DF. Chloroquine, quinine, procaine, quinidine and clomipramine are prostaglandin agonists and antagonists. Prostaglandins 1976; 12: 789-801.

7. Mak O, Chen S. Effects of two antidepressant drugs imipramine and amitriptyline on the enzyme activity of 15-hydroxyprostaglandin dehydrogenase purified from brain, lung, liver and kidney of mouse. Prog Lipid Res 1986; 25: 153-155.

8. Fernandez-Cruz E, Gelpi E, Longo N, Gonzalez B, de la Morena, MT, Montes, MG,
Rosello , J, Ramis I,Suarez A, Fernandez, A. Increased synthesis and production of prostaglandin E2 by monocytes from drug addicts with AIDS. AIDS 1989; 3: 93-96.

9. Wahl L, Corcoran M, Pyle S, Pyle SW, Arthur LO, Harel-Bellan A, Farrar WL. Human immunodeficiency virus glycoprotein (gp120) induction of monocyte arachidonic acid metabolites and interleukin 1. Proc. Natl Acad. Sci. USA 1989; 86:621-625.

10. Dumais N, Barbeau B, Olivier M, Tremblay MJ. Prostaglandin E2 up-regulates HIV-1 long terminal repeat-driven gene activity in T cells via NF-kappa B-dependent and–independent signaling pathways. J Biol Chem 1998; 273(42): 27306-27314

11. Dutta P, Pinto J, Rivlin R. Antimalarial properties of imipramine and amitriptyline. J Protozool 1990; 37(1): 54-58.

12. Lieb,J.”The immunostimulating and antimicrobial properties of lithium and antidepressants.” J Infection (2004) 49; 88-93

13. Lass-Florl C, Dierich MP, Fuchs D, Semenitz E, Ledochowski M. Antifungal activity against Candida sp. by the selective serotonin reuptake inhibitor sertraline. Clin Infect Dis 2001; 33(12):E135-136.

14. Munoz-Bellido J, Munoz-Criado S, Garcia-Rodriguez J. Antimicrobial activity of psychotropic drugs: selective serotonin reuptake inhibitors. Int J Antimicrob Agents 2000; 14(3): 177-180.


15. Tsai A, Weiser S, Petersen M, Ragland K, Bangsberg D. Effect of antidepressant medication treatment on ARV adherence and HIV-1 RNA viral load in HIV+ homeless and marginally housed individuals. In: Program and abstracts of the 16th Conference on Retroviruses and Opportunistic Infections; February 8-11, 2009; Montréal, Canada. Abstract 584

16. Frank M, Hendricks S, Johnson D, Wiesler J L, Burke WJ. Antidepressants augment natural killer cell activity: in vivo and in vitro. Neuropsychobiology 1999; 39(1):18-24.

17. Mayne TJ, Vittinghoff E, Chesney MA, Barrett DC, Coates TJ. Depressive affect and survival among gay and bisexual men infected with HIV. Arch Intern Med. 1996 Oct 28; 156(19):2233-8.

18. Lieb,J.”Stimulating immune function to kill viruses, bacteria, parasites and fungi.” 2012 Amazon
19. Evans DL, Ten Have TR, Douglas SD, Gettes DR, Morrison M, Chiappini MS, Brinker-Spence P, Job C, Mercer DE, Wang YL, Cruess D, Dube B, Dalen EA, Brown T, Bauer R, Petitto JMAssociation of depression with viral load, CD8 T lymphocytes, and natural killer cells in women with HIV infection. Am J Psychiatry. 2002 Oct; 159(10):1752-9.
20. Evans DL, Lynch KG, Benton T, Dube B, Gettes Tustin NB, Lai JP, Metsger D, Douglas SD Selective serotonin reuptake inhibitor and substance P antagonist enhancement of natural killer cell innate immunity in human immunodeficiency virus/ acquired immunodeficiency syndrome. Biol Psychiatry 2008 May 1:63(9):899-905. Epub 2007 Oct 22.
21. Benton T, Lynch K, Dube,B, Gettes DR, Tustin NB, Lai JP, Metsger DS, Blume J, Douglas SD, Evans DL. Selective Serotonin Reuptake Inhibitor Suppression of HIV Infectivity and Replication Psychosom Med 2010 Oct 14 {Epub ahead of print}
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For educational purposes only, all treatment decisions to be made with a physician.

Published by Hiv-sites on December 3, 2010

Retired Yale medical school professor
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Additional Studies

Action mechanisms of lithium chloride on cell infection by transmissible gastroenteritis coronavirus. Ren X, Meng F, Yin J, Li G, Li X, Wang C, Herrler G. PLoS One. 2011 May 6;6(5):e18669. PMID: 21573100 [PubMed - indexed for MEDLINE]
Antiviral effect of diammonium glycyrrhizinate and lithium chloride on cell infection by pseudorabies herpesvirus. Sui X, Yin J, Ren X. Antiviral Res. 2010 Feb;85(2):346-53. Epub 2009 Oct 30. PMID: 19879899 [PubMed - indexed for MEDLINE]
Comparative analysis of the effect of glycyrrhizin diammonium and lithium chloride on infectious bronchitis virus infection in vitro. Li J, Yin J, Sui X, Li G, Ren X. Avian Pathol. 2009 Jun;38(3):215-21. PMID: 19468938 [PubMed - indexed for MEDLINE]
.Enhancement of the antimicrobial performance of biocidal formulations used for the preservation of white mineral dispersions. Di Maiuta N, Schwarzentruber P, Dow CS. Appl Microbiol Biotechnol. 2011 Jan; 89(2):429-39. Epub 2010 Sep 28. PMID: 20878320 [PubMed - indexed for MEDLINE]

Highly reversible lithium storage in Bacillus subtilis -directed porous Co₃O₄ nanostructures. Shim HW, Jin YH, Seo SD, Lee SH, Kim DW. ACS Nano. 2011 Jan 25; 5(1):443-9. Epub 2010 Dec 14. PMID: 21155558 [PubMed - indexed for MEDLINE]

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