There are many reasons why I advise against taking antibiotics.
For one, they harm your microbiome, the colonies of healthy bacteria living in your GI tract. This effect, in turn, causes digestion problems and can even harm your body’s ability to absorb nutrients.
Second, the overuse of antibiotics has also led to the creation of antibiotic-resistant “super bugs.” Yet doctors still prescribe them inappropriately to treat viral infections, such as colds and flus, where they can’t do any good. (Yesterday, I told you what you can do to prevent colds and flus, beyond the ineffective government vaccines.)
Plus, according to a report published in the Science Translational Medicine Journal, antibiotics may even lead to DNA damage, if you take them long enough. This disturbing chain of events actually begins in your mitochondria, your cells’ energy factories.
Your cells’ energy factories date back millions of years
Some of the oldest cells on Earth are single-cell bacteria that could breathe oxygen.
Over time, larger cells “engulfed” single-cell bacteria and used them as breathing apparatuses. (Think of the single-cell bacteria as little scuba tanks attached to the host cells’ bodies.) The bacteria also helped the host cells produce energy and stay hydrated.
Eventually, the host cells’ genetic coding changed to incorporate the bacteria permanently into its DNA.
Human mitochondria are actually the direct descendants of this ancient, single-celled bacteria, which could live and breathe on their own. And mitochondria still function in much the same way as the bacteria did millions of year ago, producing energy and hydration for the cell.
Furthermore, it makes sense that antibiotics harm mitochondria, since these ancient structures originated from bacteria! It’s a wonder to me that it’s taken researchers this long to figure it out.
Antibiotics harm our cell’s energy centers
To study the effect of antibiotics on mitochondria, researchers with Boston University treated human cells and mice with three different types of common antibiotics.
As a result, they observed how antibiotic treatment ignited a chain of events…
First, the antibiotics clearly disrupted normal mitochondrial function in the human tissues, depriving cells of energy and hydration.
And when something damages your mitochondria, it doesn’t just affect your energy. It actually speeds aging.
In fact, mitochondrial damage plays a role in a wide array of common diseases, including chronic fatigue, dementia, diabetes, liver disease, Parkinson’s, and heart disease.
Second, the cells experienced a “surge” in the production of unstable molecules called reactive oxygen species (ROS). ROS can damage human cells. And build-up of ROS can even damage DNA and cause cell death.
Third, the cells began to exhibit oxidative stress. Your body experiences oxidative stress when there is an imbalance between unstable free radicals like ROS and antioxidants. It damages DNA and can also lead to bigger problems like cancer.
Of course, antibiotics aren’t the only drugs shown to harm mitochondria…
Cholesterol-lowering statin drugs also harm your cells’ energy factories. And doctors have long observed that prolonged antibiotic treatment can cause many of the same side effects as statin drugs, including damage to hearing, kidneys and even muscle tendons.
Houston we have a problem
These findings worry Ronald DePinho, a researcher with the prestigious MD Anderson Cancer Center in Houston. DePinho makes clear that the average person who takes a short course of antibiotics probably doesn’t have much to worry about. “We have very robust DNA damage repair mechanisms [for short-term].” “However,” he added, “It could be different in the context of chronic administration of antibiotics.”
But I think Ronald has his head in the sand.
The researchers used “clinical levels” of these antibiotics. And even that limited amount caused a surge in ROS and oxidative stress, which can lead to DNA damage.
Plus, if one treatment of common antibiotics at clinical levels can cause those problems…could a long course of antibiotics (or multiple courses) cause cancer?
Antioxidants lessen the harm caused by antibiotics
For the last part of the study’s research, Boston University researchers treated the human cells and mice with an antioxidant called N-acetyl-L-cysteine (NAC).
As it turns out, NAC helped alleviate the harmful effects of antibiotics. And it didn’t interfere with the antibiotics’ ability to treat the bacterial infection. The researchers even recommended taking NAC as a supplement to lessen the harm of antibiotics.
I was surprised — and impressed — by this suggestion. Oncologists could learn a thing or two about this approach…
As you probably know, many supplements have been shown to alleviate the side effects of chemotherapy without interfering with the drugs’ anti-cancer actions. Yet most oncologists won’t recommend supplementation to patients.
Just as I was finishing up this Dispatch, I came across an article published in Nature Microbiology about yet another danger of taking antibiotics. For this lab study, researchers transplanted either normal gut bacteria, or bacteria that had been exposed to antibiotics, into healthy, pregnant mice.
The mice that received the bacteria that had been exposed to antibiotics experienced changes to their microbiome (the probiotic environment in their gut). And the newborn mice also exhibited those same harmful microbiome changes. While we already knew that antibiotics harm the microbiome, now we know those changes are even passed down to the next generation!
The bottom line?
Avoid taking antibiotics whenever you can. Instead, focus on prevention and building a strong immune system, as I explained in yesterday’s Daily Dispatch. As I often say, prescriptions should be a last resort for treatment — natural approaches and remedies should always be the first place you start.
“Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells,” Sci. Transl. Med 2013, Jul 3: 5(192): 192ra85
“Intergenerational transfer of antibiotic-perturbed microbiota enhances colitis in susceptible mice,” Nature Microbiology (2017) doi:10.1038/s41564-017-0075-5