Harvard: Concerning Information About Antibiotics

Age of Antibiotics is Coming to an End

Harvard: Discovers Concerning Information About Antibiotics

Alexander Fleming discovered penicillin in the 1940s, and it has been used as a poster child for ‘safe’ antibiotics ever since. Fleming’s discovery heralded the ‘age of antibiotics,’ but new research from Harvard scientists reveals concerning information about antibiotics, confirming that the antibiotic age is coming to an end.

Penicillin has been called better than the ‘big gun’ antibiotics for treating pneumonia and other childhood diseases, but it that really true in a new age of antibiotic resistance created by their overuse? Even the corrupt FDA admits that antibiotic misuse and overuse is a problem.

According to the Harvard summary:

“One of the oldest and most widely used antibiotics, penicillin, attacks enzymes that build the bacterial cell wall. Researchers have now shown that penicillin and its variants also set in motion a toxic malfunctioning of the cell’s wall-building machinery, dooming the cell to a futile cycle of building and then immediately destroying that wall.”

This would be a simple microbial process that we could take for granted if it weren’t for the resistance to penicillin and other antibiotics that has emerged in the last few decades. The fact is that scientists still don’t really know how the original ‘age of antibiotics’ worked.

See also: 6 dangerous prescription drugs you should think twice before taking

Thomas Bernhardt, associate professor of microbiology and immunobiology at Harvard Medical School, are looking closer at this phenomenon.

Their findings, published in the journal Cell, explain how penicillin can be devastating to bacteria — which may lead to new ways to thwart drug resistance, but could also explain why ‘good’ bacteria is harmed by antibiotics. How do these drugs differentiate after all?

Bernhardt and his team have shown that antibiotic drugs do more than simply block cell-wall assembly. Penicillin and its variants also “set in motion a toxic malfunctioning of the cell’s wall-building machinery, which dooms the cell to a futile cycle of building and then immediately destroying that wall. This downstream death spiral depletes cells of the resources they need to survive.”

Bernhardt explains the ramifications concerning drug-resistance:

[quote_box_center]“It seems to be a common theme with some of the best antibiotics that we have: They don’t just inhibit the enzyme they are targeting; they actually convert that target so that whatever activity it has left becomes toxic.”[/quote_box_center]

Penicillin and some other antibiotic drugs are included in a class called beta-lactams, all of which are derived from natural antibiotics produced by fungi and have known bacteria-fighting capabilities.

If a drug prohibits a cell from synthesizing new strands by blocking the enzymes that build cross-links, weakening the cell walls (meaning the cell wall can’t hold together), how do we keep the healthy cells from dying? It’s a bit like treating cancer cells with chemotherapy. All the cells die, not just the cancerous ones.

Bernhardt and Hongbaek Cho, lead author of the Cell paper, used a specific derivative of penicillin that targets only one enzyme in cell-wall assembly. Their aim was to genetically manipulate their study subject, E. coli, to make this enzyme dispensable for the life of the cell.

See also: What Really Happens When You Take Antibiotics?

Surprisingly, the scientists noticed that targeting the nonessential enzyme with the penicillin still killed the cell. This finding was quite a conundrum. The enzyme could be removed from cells completely without harm. Yet, when it was present and bound by the drug, the cells would die.

The investigators discovered that the root cause of the problem was that the drug not only inhibited the enzyme, but it also caused it to malfunction in such a way that its activity became toxic.

Bernhardt stated:

[quote_box_center]“Now that we know more about beta-lactams being toxic, it gives us a hook to look for new molecules that target the cell wall, the more we understand how these processes like cell wall synthesis work in bacteria, the better position we’ll be in to find new ways to disrupt it.”[/quote_box_center]

The problem is that more and more unwanted bacteria are becoming resistant to antibiotics, and in many cases, disease-causing bacteria are actually influenced to grow more.

Antibacterials usually work in one of two ways:

  • A bactericidal antibiotic like penicillin hopefully kills the unwanted or ‘bad’ bacteria.
  • A bacteriostatic antibiotic stops bacteria from multiplying.

Simple. natural antibiotics like garlic and onions, basil, chamomile, aloe vera, astragalus and others; however, don’t cause side effects like antibiotic resistance, diarrhea, nausea, fungal infections, and the disruption of healthy gut flora that help to fight disease.

Furthermore, with many antibiotics, sensitive bacteria are killed, but resistant germs may be left to grow and multiply.

[quote_box_center]“Some bacteria develop the ability to neutralize the antibiotic before it can do harm, others can rapidly pump the antibiotic out, and still others can change the antibiotic attack site so it cannot affect the function of the bacteria.”[/quote_box_center]

Pharmaceutical antibiotics simply kill bacteria indiscriminately throughout the body. That is how they are manufactured. So, if you contract strep throat, for example, the antibiotic you take will kill the good bacteria, lactobacillus, which you need to crowd out Candida and other issues. This is why vaginal and intestinal yeast infections are so common after antibiotic use.

Natural antibiotics don’t seem to cause the phenomenon of antibiotic resistance, and many are simply foods you eat on a daily basis. Natural, non-pharmaceutical antibiotics even fight anti-biotic resistant diseases, like MRSA, and E Coli.

Why use Big Pharma drugs at all? It doesn’t take a room of Harvard scientists to figure out better options that are less expensive and still effective.

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The views and opinions expressed in this article are those of the authors/source and do not necessarily reflect the position of CSGLOBE or its staff.

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