Prevention of the metabolic syndrome insulin resistance and the atherosclerotic diseases in Africans infected by Helicobacter pylori infection and treated by antibiotics

Prevention of the metabolic syndrome insulin resistance and the atherosclerotic diseases in Africans infected by Helicobacter pylori infection and treated by antibiotics
Purchase

B. Longo-MbenzaCorresponding Author Contact Information, E-mail The Corresponding Author, J. Nkondi Nsengaa and D. Vangu Ngomab

aDepartment of Internal Medicine, University of Kinshasa, and Lomo Medical/ Limete, Kinshasa, DR Congo

bBiostatistics Unit, Ministry of Public Health, Kinshasa Gombe, DR Congo
Received 29 March 2006;
revised 19 November 2006;
accepted 11 December 2006.
Available online 27 March 2007.

Abstract
Aims

To report on the association between certain components of the metabolic syndrome/Insulin resistance, gender, cardiovascular diseases and Helicobacter (H.) pylori seropositivity/Infection and the response of these cardiovascular risk factors to Helicobacter pylori titers after an antibiotic course.
Methods

In 205 consecutive Africans referred to the cardiovascular Center of LOMO MEDICAL in Kinshasa for management of their cardiovascular diseases, the proportions of seropositives for H. pylori and H. pylori infection (H. pylori seropositivety and histologically proven H. pylori gastritis) were investigated. The association between traditional cardiovascular risk factors, certain components of the metabolic syndrome and each H. pylori disease group (seropositivity or infection) was evaluated. The response of the cardio-metabolic level to H. pylori antibody titers after an antibiotic course was also evaluated for patients with H. pylori infection. Baseline levels of H. pylori antibody titer and cardio-metabolic parameters were compared with those after the antibiotic treatment.
Results

A total of 62.4% of participants were tested positive for the H. pylori antibody. Out of all participants, 25% had H. pylori infection and chronic gastritis without H. pylori. Men were more (p < 0.01) H. pylori seropositive than women. Older age, higher triglycerides, higher weight, wider waist girth, higher fibrinogenemia, greater intima-mediathighness and higher rate of hypertension were significantly associated with H. pylori seropositivity. Lower HDL-cholesterol, higher levels of systolic blood pressure, triglycerides, uric acid, fibrinogen, hematocrit, glycemia, arterial hypertension hypercholesterolemia, diabetes mellitus hypo-HDL-cholesterolemia, hyperuricemia (Total), Overweight, overall obesity, abdominal obesity were significantly associated with H. pylori infection. Within the total population, there was a significant dose-response relationship between the rates of arterial hypertension, rate of overweight/overall obesity, and H. pylori antibody titers, respectively. After adjusting for age, and compared with H. pylori-seropositive women, H. pylori-seropositive men showed higher mean values for body weight, waist girth, waist-to-hip ration blood pressure, hematocrit, uric acid, triglycerides and total cholesterol. The levels of uric acid (p < 0.05), plasma glucose (p < 0.01), total cholesterol (p < 0.01), fibrinogen (p < 0.01), blood pressure (p < 0.05), after 3 weeks antibiotics duration were lower than their baseline levels; weight, waist girth and triglyceride levels did not change (p < 0.05) with the antibiotics course. The total population was characterized by lower levels of triglycerides, absence of cases with triglycerides > 50 mg/dL.
Conclusion

This study adds evidence for supporting the association of seropositivity to H. pylori with cardiovascular diseases and elevated number of components of metabolic syndrome. In these Africans with low triglyceride levels, H. pylori infection per se might generate atherosclerosis or metabolic syndrome, particularly in men with H. pylori-seropositive. H. pylori infection might be one of the risk factors of atherosclerosis thorough inflammation (fibrinogen) and modulation of glucose and lipid profiles, which may be prevented by low antibiotics in developing countries.

That's very interesting action, not new though for a few people here.

Using fibrinolytic enzymes (and or ecklonia cava), iodine, enough nutrients, ensuring gut health are some of the things that come to mind to deal with the effects of this particular infection.


Is MPB a result of the biofilm of a specific or multiple pathogens?

I wonder how important could fibronlytic enzymes could be to deal with extraintestinal biofilms...

I guess we'll just have to find out!

And yeah, nothing new to me either, just trying to steer the forum in a constructive direction.

aI guess we'll just have to find out!

And yeah, nothing new to me either, just trying to steer the forum in a constructive direction.

Thanks a lot for that. It came to my mind after reading your original post, that this forum needs to refocus and this certainly helps.

Just adding more fuel to the fire:

9. Atherosclerosis-Pathogenesis

What is Atherosclerosis?
Atherosclerosis from Greek athero (meaning gruel or
paste) and sclerosis (hardness).

Almost 100% of atherosclerotic patients have anti-
nanobacteria antibodies in their serum, whereas in
healthy blood donors antinanobacteria antibodies are
present in about 15%

Nanobacteria very very slow growing saprophytic
microbe that causes “hardening of the arteries”.

Atheromas are complex colonies of mobile
Nanobacteria that spin and maintain a peptidoglycan
biofilm around their colonies.

Supported but not proven hypothesis

In a Plaque:
1) Early-Plaques have Monocyte infiltration
2) Later-Plaques complex inflammation
a) Foam cells (dead/dying Monocytes) trapped
in the biofilm, a source of inflammation
b) PMN
3) Calcium apatite (calcium phosphate)
a) Nidus is nanobacteria
b) Early microcalcifications form
c) Later is macrocalcification
d) Remodeling by osteoclast forming calcified
vessels
4) Biofilms around atheroma “peptidoglycan”?
5) Fibrous or fibrocalcific plaques
6) Thrombotic cascade
a) Apatite exposed to blood activates a
thrombotic cascade. Platelet activation
7) Lipid pools (Oxidize LDL foam dead Foam cells)
a) Cellular debris is Inflammatory
Endothelial destruction

Atheroma Ossification not Calcification of
Vessels (1863)
ν Calcification in Atherosclerosis is
similar to calcification seen in Ghon
Complex of Tuberculosiis
ν Initial calcification leads to formal
lamellae bone with osteoclasts and
osteoblasts, even marrow appears!
ν Heavily Calcified Coronaries are
dense chronic Osteoclastic
remodeling. Virchow, 1863
remodeling

Infectious Agent

Kajander's nanobacteria
Nanobacteria, Nanobacterium
sanguineum, Phyllobacterium
mysinacearum
Pleuropneumonic-like organisms or
Mycoplasma species

Archaea symbiont that requires cell
contact or lipids from other cells for
growth.

Cell volume of about 0.01 µm3

Sphere structures from 30 to 150 nm
and finger-like rod structures have
been identified in calcified human
tissue

Monocytes under Endothelial
Cells

Blood test: NANO-SERO IgG ELISA

NO EFFECT OF ANTIBIOTICS x yrs
Gatifloxacin (PROVE-IT-TIMI 22-2004)
Zithromycin (WIZARD, JAMA 2003)


Calcification pops up a lot.

No surprise that antibiotics have little to no effect, biofilm issue.

Very, very interesting stuff ... where nanobacteria aren't actually bacteria, or living things for that matter, jdp and his sources supposition that their place in this is merely protective makes sense, follows along CS's belief (that I tend to follow) that Virus's are merely cleaning agents. Makes sense seeing as a fever is a measure of defense, and purging, why wouldn't the body make, or in cirumstances, be open to such a measure? In this case, the nanobacteria is the equivalent of a police blockade so that the other pathogens aren't going anywhere.