<div class="FTQUOTE"><begin quote><i>Originally posted by: <b>NoExcuses</b></i>
<div class="FTQUOTE"><begin quote><i>Originally posted by: <b>Solo</b></i>
<div class="FTQUOTE"><begin quote>Antibiotics suppress your immune system </end quote></div>
No, bacteria do not suppress your immune system. Are you kidding? I'm shocked you are making such blatantly false statements.
</end quote></div>
Really? Amy, you are one of the most educated people I know when it comes to drugs and their usage. But please, tell me you are not so immersed in the pharma culture that you can at least not admit this?
Actually, antibiotics do suppress your immune system. There is a ton of research being done right now that suggests that immune modulation by antibiotic therapy/chemotherapy actually shifts Th1 response of immune response to Th2 immune response. By killing intestinal microflora, antibiotics put us on a crash course for allergies and acqusition of more pathogenic bacteria. Because most of the immune system is based in the microflora of the gut (recent studies suggest 80%), when we kill off this bacteria with antibiotic therapy, we actually change our immune response to Th2 (which by the way is what cfers who culture PA consistently have). Th2 response in the body is associated with allergies, inflammation with no purpose (bc the chemicals that are associated with a fighting Th1 response to infection fall and are replaced with chemicals that only induce heightened inflammation) and this leads us to the possibility of culturing bugs that never would have been an issue.
I spoke with a researcher recently who was spoke at the European cf conference this year. He said that studies now show that almost all strains of Pseudo in the cf lung are genetically related....they are all mutations of each other and this is proven by DNA analysis. I asked why would this happen. Simply put, over-use of antibiotics to control pseudomonas infection. I am sure you know Amy that if you don't kill all of the bugs they mutate and form stronger more resilient and virulent strains. That they are all genetically the same should not surprise us at all. Furthermore, studies from the latest European cf conference suggest a growing number of clinics with pan resistant strains of pseudo and many more just resistant to tobra. Tobi is creating a culture of resistant strains that gets passed not just to other cystics but even more immuno-compromised patients.
Having said that, do I believe their use in CF is important and essential. Absolutely. Do I believe that researchers are starting to realize they over-prescribe antibiotic therapy in Cf and should focus more on maintaining immune response..? The evidence for that is everywhere. NAC, glutathione, studies with gamma interferon, studies with probiotics....which by the way, are all associated with a functioning Th1 immune response. In cf, we are not focusing enough on (you know I am gonna say it) food as a driving force in immune modulation.
As far as milk goes, it does affect immune response. Now, some people are going to experience more or less symptomology from its use in diet. Do you know that the highest rate of Type 1 diabetes is in Finland where the most cows milk is consumed? It is 28 in 100,000 and is growing every year. Researchers are looking into the the correlation between genetic disease susceptibility and dietary exposures in the development diabetes. Do I experience more inflammation when I eat dairy? yes. Do I produce more mucus? NO.
Do I believe my food allergies are a direct result of my gut flora being killed off by cf disease pathology and antibiotics usage? Yes, yes 100% yes. And, if you believe that antibiotics do not suppress your immune system, you will in a few years when your antibiotics no longer work on your bugs and you begin to lose lung function. At this point you will start researching other avenues and you will be STUNNED by the research out there that shows the drugs are just creating more problems and many can be alleviated by what we eat or don't eat.
The following is research study on mice. as you know mice are the most closely related to humans in their airway disease. That is why they are used in cf research as they follow similar lung pathology as humans. Keep in mind this study is translated from Chinese. Only 10% of journal articles from China, Japan etc are translated into English. Their scientists are very progressive when it comes to studying immune response and unfortunately we NEVER hear about it and when we do, we tend to take it with a grain of salt because the western world does not manage disease the same way.
Zhonghua Er Ke Za Zhi. 2007 Jun;45(6):450-4.Links
[Allergic airway response associated with the intestinal microflora disruption induced by antibiotic therapy]
[Article in Chinese]
Liu CH, Yang XQ, Liu CH, He Y, Wang LJ.
Department of Immunology, Children's Hospital, Chongqing Medical University, Chongqing 400014, China.
OBJECTIVE: Over the past several decades, there has been a significant increase in allergy and asthma in the world, which correlates with alterations in microflora and widespread use of antibiotics. The authors have developed a mouse model of antibiotics-induced microbiota disruption. In that model, mice were challenged by intranasal exposure to Aspergillus fumigatus allergens to explore the relation of allergic airway response and intestinal microflora disruption. METHODS: Sixty female BALB/c mice were divided at random into 6 groups with 10 mice in each. (1) First antibiotic therapy group: the mice were given oral cefoperazone for 7 days, on day 7, mice were inoculated with Candida albicans (10(9)/ml, 50 microl) orally. (2) First control group: the mice were treated as first antibiotic therapy group, but cefoperazone and Candida albicans were replaced by saline. The mice in groups (1) and (2) were sacrificed on day 8, and cecal contents were collected for quantitative analysis of the intestinal bacterial flora. (3) Antibiotic therapy and challenge group: the mice were treated as the first antibiotic therapy group, then challenged (day 9 and 16) by intranasal exposure to Aspergillus fumigatus allergen. (4) Second antibiotic therapy group: the mice were treated as the first antibiotic therapy group, then challenged (day 9 and 16) by intranasal exposure to saline. (5) Challenge group: the mice were treated as the first control group, then challenged (day 9 and 16) by intranasal exposure to Aspergillus fumigatus allergen. (6) Second control group: the mice were treated as the first control group, then challenged (day 9 and 16) by intranasal exposure to saline. The mice in (3) - (6) group were killed for analysis of allergic airway response on day 19. RESULTS:<b> The quantity of Enterobacteriaceae, Enterococcus, Bifidobacterium and Lactobacillus in first antibiotic therapy group was significantly lower than that in the first control group, the quantity of Candida albicans increased in the first antibiotic therapy group as compared with the first control group. Mice intestinal microflora were disrupted with weight reduction and increased moisture in feces. After challenging with Aspergillus fumigatus allergens via intranasal inhalation, the total cell count, eosinophils, lymphocytes and neutrophils increased in BALF, especially in bronchoalveolar lavage fluid (BALF) from the mice in antibiotic therapy and challenge groups</b>. IL-4 level in BALF from antibiotic therapy and challenge group (45.35 +/- 2.36) pg/ml was higher than that in the second control group (35.32 +/- 2.53) pg/ml. The expression of GATA-3 mRNA in the mice lung tissue (0.569 +/- 0.023) was higher than that in the second control group (0.410 +/- 0.020), and the ratios of T-bet/GATA-3 (0.578 +/- 0.021) decreased as compared with that in the second control group (0.804 +/- 0.035). IFN-gamma level in BALF from any group was not significantly different. <b>In the absence of antibiotics, mice exposed to Aspergillus fumigatus allergen did not develop an allergic response in the airways.</b> CONCLUSIONS: <b>The allergic (Th2) immune response can be induced by airway challenge with Aspergillus fumigatus allergen in the mice in which the intestinal microflora disruption resulted from antibiotic therapy, this result suggests that the intestinal microflora disruption resulted from antibiotic therapy is a risk factor for allergy and asthma.
</b>
SORRY I HIJACKED THE THREAD<img src=""> I SHOULD HAVE CREATED A NEW THREAD FOR THIS INFO.
<div class="FTQUOTE"><begin quote><i>Originally posted by: <b>Solo</b></i>
<div class="FTQUOTE"><begin quote>Antibiotics suppress your immune system </end quote></div>
No, bacteria do not suppress your immune system. Are you kidding? I'm shocked you are making such blatantly false statements.
</end quote></div>
Really? Amy, you are one of the most educated people I know when it comes to drugs and their usage. But please, tell me you are not so immersed in the pharma culture that you can at least not admit this?
Actually, antibiotics do suppress your immune system. There is a ton of research being done right now that suggests that immune modulation by antibiotic therapy/chemotherapy actually shifts Th1 response of immune response to Th2 immune response. By killing intestinal microflora, antibiotics put us on a crash course for allergies and acqusition of more pathogenic bacteria. Because most of the immune system is based in the microflora of the gut (recent studies suggest 80%), when we kill off this bacteria with antibiotic therapy, we actually change our immune response to Th2 (which by the way is what cfers who culture PA consistently have). Th2 response in the body is associated with allergies, inflammation with no purpose (bc the chemicals that are associated with a fighting Th1 response to infection fall and are replaced with chemicals that only induce heightened inflammation) and this leads us to the possibility of culturing bugs that never would have been an issue.
I spoke with a researcher recently who was spoke at the European cf conference this year. He said that studies now show that almost all strains of Pseudo in the cf lung are genetically related....they are all mutations of each other and this is proven by DNA analysis. I asked why would this happen. Simply put, over-use of antibiotics to control pseudomonas infection. I am sure you know Amy that if you don't kill all of the bugs they mutate and form stronger more resilient and virulent strains. That they are all genetically the same should not surprise us at all. Furthermore, studies from the latest European cf conference suggest a growing number of clinics with pan resistant strains of pseudo and many more just resistant to tobra. Tobi is creating a culture of resistant strains that gets passed not just to other cystics but even more immuno-compromised patients.
Having said that, do I believe their use in CF is important and essential. Absolutely. Do I believe that researchers are starting to realize they over-prescribe antibiotic therapy in Cf and should focus more on maintaining immune response..? The evidence for that is everywhere. NAC, glutathione, studies with gamma interferon, studies with probiotics....which by the way, are all associated with a functioning Th1 immune response. In cf, we are not focusing enough on (you know I am gonna say it) food as a driving force in immune modulation.
As far as milk goes, it does affect immune response. Now, some people are going to experience more or less symptomology from its use in diet. Do you know that the highest rate of Type 1 diabetes is in Finland where the most cows milk is consumed? It is 28 in 100,000 and is growing every year. Researchers are looking into the the correlation between genetic disease susceptibility and dietary exposures in the development diabetes. Do I experience more inflammation when I eat dairy? yes. Do I produce more mucus? NO.
Do I believe my food allergies are a direct result of my gut flora being killed off by cf disease pathology and antibiotics usage? Yes, yes 100% yes. And, if you believe that antibiotics do not suppress your immune system, you will in a few years when your antibiotics no longer work on your bugs and you begin to lose lung function. At this point you will start researching other avenues and you will be STUNNED by the research out there that shows the drugs are just creating more problems and many can be alleviated by what we eat or don't eat.
The following is research study on mice. as you know mice are the most closely related to humans in their airway disease. That is why they are used in cf research as they follow similar lung pathology as humans. Keep in mind this study is translated from Chinese. Only 10% of journal articles from China, Japan etc are translated into English. Their scientists are very progressive when it comes to studying immune response and unfortunately we NEVER hear about it and when we do, we tend to take it with a grain of salt because the western world does not manage disease the same way.
Zhonghua Er Ke Za Zhi. 2007 Jun;45(6):450-4.Links
[Allergic airway response associated with the intestinal microflora disruption induced by antibiotic therapy]
[Article in Chinese]
Liu CH, Yang XQ, Liu CH, He Y, Wang LJ.
Department of Immunology, Children's Hospital, Chongqing Medical University, Chongqing 400014, China.
OBJECTIVE: Over the past several decades, there has been a significant increase in allergy and asthma in the world, which correlates with alterations in microflora and widespread use of antibiotics. The authors have developed a mouse model of antibiotics-induced microbiota disruption. In that model, mice were challenged by intranasal exposure to Aspergillus fumigatus allergens to explore the relation of allergic airway response and intestinal microflora disruption. METHODS: Sixty female BALB/c mice were divided at random into 6 groups with 10 mice in each. (1) First antibiotic therapy group: the mice were given oral cefoperazone for 7 days, on day 7, mice were inoculated with Candida albicans (10(9)/ml, 50 microl) orally. (2) First control group: the mice were treated as first antibiotic therapy group, but cefoperazone and Candida albicans were replaced by saline. The mice in groups (1) and (2) were sacrificed on day 8, and cecal contents were collected for quantitative analysis of the intestinal bacterial flora. (3) Antibiotic therapy and challenge group: the mice were treated as the first antibiotic therapy group, then challenged (day 9 and 16) by intranasal exposure to Aspergillus fumigatus allergen. (4) Second antibiotic therapy group: the mice were treated as the first antibiotic therapy group, then challenged (day 9 and 16) by intranasal exposure to saline. (5) Challenge group: the mice were treated as the first control group, then challenged (day 9 and 16) by intranasal exposure to Aspergillus fumigatus allergen. (6) Second control group: the mice were treated as the first control group, then challenged (day 9 and 16) by intranasal exposure to saline. The mice in (3) - (6) group were killed for analysis of allergic airway response on day 19. RESULTS:<b> The quantity of Enterobacteriaceae, Enterococcus, Bifidobacterium and Lactobacillus in first antibiotic therapy group was significantly lower than that in the first control group, the quantity of Candida albicans increased in the first antibiotic therapy group as compared with the first control group. Mice intestinal microflora were disrupted with weight reduction and increased moisture in feces. After challenging with Aspergillus fumigatus allergens via intranasal inhalation, the total cell count, eosinophils, lymphocytes and neutrophils increased in BALF, especially in bronchoalveolar lavage fluid (BALF) from the mice in antibiotic therapy and challenge groups</b>. IL-4 level in BALF from antibiotic therapy and challenge group (45.35 +/- 2.36) pg/ml was higher than that in the second control group (35.32 +/- 2.53) pg/ml. The expression of GATA-3 mRNA in the mice lung tissue (0.569 +/- 0.023) was higher than that in the second control group (0.410 +/- 0.020), and the ratios of T-bet/GATA-3 (0.578 +/- 0.021) decreased as compared with that in the second control group (0.804 +/- 0.035). IFN-gamma level in BALF from any group was not significantly different. <b>In the absence of antibiotics, mice exposed to Aspergillus fumigatus allergen did not develop an allergic response in the airways.</b> CONCLUSIONS: <b>The allergic (Th2) immune response can be induced by airway challenge with Aspergillus fumigatus allergen in the mice in which the intestinal microflora disruption resulted from antibiotic therapy, this result suggests that the intestinal microflora disruption resulted from antibiotic therapy is a risk factor for allergy and asthma.
</b>
SORRY I HIJACKED THE THREAD<img src=""> I SHOULD HAVE CREATED A NEW THREAD FOR THIS INFO.