Are Antibiotics Making You and Your Child Fat?

Farmers intentionally feed chicken and other livestock antibiotics to increase their size. But antibiotics may be doing the same thing to you posits Dr. Oz in a new episode of The Dr. Oz Show that takes a look at why antibiotics may be making you fat and could be the cause of your obesity.

“Today I’ve got breaking news. Experts are uncovering the hidden reason behind America’s obesity problem: Could you be gaining weight because of antibiotics that you take every day for problems like sore throats and earaches? Or from antibiotics found in our food? It’s an alarming finding, but it raises a simple question—are antibiotics making you fat?” asks Dr. Oz, who previously has discussed how certain natural cereals cause weight gain as well as medications that can make you fat.

With Dr. Oz is special guest Dr. Martin Blaser, Director of the Human Microbiome Program at New York University who has spent years researching what he considers a suspicious association between weight gain and antibiotic use.

“Farmers have been using antibiotics to fatten up all of their livestock for decades now. And one day, I thought, if that’s working on the farm, what are we doing to our children? What are the antibiotics we are giving them, doing?”

One of Dr. Blaser’s first tests toward answering these questions was to see what would happen if antibiotics were fed to laboratory mice that are typically used as animal models for studying human disease. In his research, Dr. Blaser found that when comparing two groups of mice of which all were given the same amount and type of food but one group with added antibiotics and the other group without antibiotics, that the antibiotic fed mice gained 50% more fat.

Furthermore, when he extended his experiments to include mice being fed a high-fat diet, both groups became fat. However, those mice that were on a high-fat diet with antibiotics became even significantly fatter.

“Interestingly, for the women out there—this problem was more pronounced in female mice. The male mice didn’t have as big of a problem. They actually got more muscle as well as fat. Which may explain some of the differences we are seeing between the genders,” says Dr. Oz.

Dr. Blaser explains that not only does feeding antibiotics to these animals result in increased body fat, but that it also changes the bacteria in the gut—an important finding that could explain how antibiotics may cause weight gain.

Dr. Oz tells viewers that antibiotics could be affecting how much and how easily some of us gain weight due to 3 possible ways antibiotics may be changing our bodies:

Antibiotic-induced change #1: Antibiotics make you metabolize food differently

According to Dr. Oz, taking antibiotics may be selecting for certain bacteria that actually causes your body to retain more calories from eating a specific amount of food in comparison to normal gut bacteria that will cause your body to retain less calories from the same amount of food. In other words, your metabolism may be determined by the type of bacteria in your gut. And, being exposed to antibiotics may be selecting for the wrong type of bacteria that then causes increased calorie retention.

Dr. Oz tells viewers that new research is finding that the type of bacteria you have in your gut may be responsible for feelings for cravings of certain high-calorie foods. Therefore, again, if antibiotics wipe out normal bacteria that do not induce cravings, antibiotics may then be selecting for bad bacteria that induce food cravings that lead to weight gain.

“It turns out that antibiotics actually changes the number of fat cells in your body,” says Dr. Oz who explains that this is significant when you are young and your body is developing into one that has more fat cells in it than the body of someone who is young and not being exposed to antibiotics.

This point is supported by Dr. Blaser’s research that associates childhood antibiotic exposure with the potential for growing up into a fat adult.

“We studied a big group of kids, and some of them had antibiotics early in life and some of them didn’t. We looked at them when they were three, and then when they were seven. The kids who got antibiotics the first six months of life had higher indices of fat in both of those ages,” says Dr. Blaser. “What a kid’s weight is when they are five years old is a big determinant of what they are going to be like when they are fourteen. And fourteen is a big determinant of what they are going to be like when they are an adult.”

Dr. Blaser also points out that when it comes to antibiotic exposure from eating chicken that has been fed antibiotics, the previously held belief that the antibiotics are gone by the time you cook and eat the meat is not always true. He tells viewers that currently it is not known if antibiotic fed livestock have the same effect on us as antibiotics given to us directly during childhood.

Dr. Oz closes the episode by telling viewers that antibiotics are a necessary part of medicine when they are needed, but that too often they are over-prescribed. Dr. Oz recommends two things we can do for now about antibiotic exposure:

1. Stop demanding antibiotics from your doctor when you have a cold—they do not help.

2. Eat probiotics for two weeks beginning the first day of taking any antibiotic—to replenish the good bacteria in your gut.

“We don’t know if this is going to work, but for now that is a step [eating probiotic supplements] I would take prophylactically,” recommends Dr. Oz, who also discussed the importance of probiotics for weight loss in his new magazine.

There might be a way to reverse this. This is a long piece, but it has a lot of useful data in it, so if you don’t read it now, it might be good to save it as text to read later.

Akkermansia muciniphila

A. muciniphila resides in the mucus layer of the ileum and colon and comprises about 3% to 5% of the gut flora found there. It is a mucin-degrading bacteria that thrives in this environment. Leptin deficient obese mice have a 3,300-fold lower abundance of this bacteria in their intestines in contrast to their lean counterparts. And in mice fed high-fat food, the numbers of A. muciniphila are 100-times lower.

(Conversely, at least one Phylum, the Firmicutes, and 26 species of bacteria in the human gut microbiota, along with the entire genus of Enterobacter, appear to be linked to obesity, even causing obesity directly, as well as related metabolic complications, with obese people having flora that instead of having hundreds of dominant strains as is normal, only have a limited number of these strains that take up most of the space.)

To determine whether A. muciniphila would impact weight regulation, obese-prone mice were supplemented with this bacteria after being fed a control diet for sixteen weeks. For all measurements of fat accumulation–subcutaneous, mesenteric, and epididymal–amounts were lower in the high-fat group that also received A. muciniphila in contrast to the mice who were fed just the high-fat food. In this group, body weight also normalized to levels matching those seen in the control group.

Serum lipopolysaccharide (LPS) are derived from gram-negative bacteria. The high-fat mice had the highest levels, but once supplemented with A. muciniphila, levels approached those seen in the control group. Stress and the cortisol secretion that results from this, including cortisol secretion due to metabolic endotoxemia, will tend to increase appetite while decreasing metabolic rate. Decrease endotoxemia and both appetite and metabolism tends to normalize.

These results, according to the researchers, were due to a 40% reduction in the hepatic enzyme glucose-6-phosphatase, an enzyme necessary for the new production of glucose by the liver. Other interesting observations were that the supplementation of this microbe reduced inflammation in fat tissue, affected the differentiation of adipose cells, and led to increases in fat burning.

The endocannabinoid system is involved in memory, appetite, energy balance and metabolism, stress response, social behavior, anxiety, pain sensation, immunity, fertility, pain control, body temperature, and sleep. The expression of at least one of its receptors, CB1, can be affected by both beneficial and pathogenic bacteria. Aclyglycerols are chemical compounds containing both glycerol and fatty acids. The increase in A. muciniphila elevated levels of these endocannabinoid compounds and would be expected to have impacts on CB1 receptors throughout the body as well as decrease intestinal permeability.

Many of the observed improvements in weight and glucose control can be explained by a strengthening of gut-barrier function due to an increase in the thickness of the mucus layer. The thicker this layer, the less likely it is that endotoxins breach the gut wall, provoke an inflammatory response, and cause other metabolic problems.

There is an association of obesity with a decrease in mucus thickness, which supports an additional mechanism of increased gut permeability that is characteristic of obesity and associated disorders. Furthermore, A. muciniphila restores this mucus layer, which suggests that this mechanism contributes to the reduction in metabolic endotoxemia that was observed during A. muciniphila treatment.

These effects are also seen in mice who are fed prebiotics. They too experience reductions in serum endotoxins, improvements in weight control, and increases in A. muciniphila populations. Prebiotic (oligofructose) treatment restored A. muciniphila abundance and improved gut barrier and metabolic parameters. However, the mechanisms that were responsible for the bloom in A. muciniphila caused by prebiotic administration are not clear.

A. muciniphila does not grow on oligofructose-enriched media (in vitro), which suggests that complex cross-feeding interactions contributed to this effect. However, it has been previously shown in rats that oligofructose feeding increases the number of goblet cells and mucus layer thickness. Thus, whether oligofructose feeding increases A. muciniphila by providing the main source of energy for this bacterium and thereby favoring its growth or whether the increase of A. muciniphila increases mucus production and degradation (i.e., turnover) remain to be demonstrated.

Bifidobacteria thrives on prebiotics, producing the short-chain fatty acids propionate, acetate and butyrate when fermenting them. One or more of these short-chain fatty acids may encourage the growth of A. muciniphila directly or by increasing the production of the mucins these bacteria feed on.

Another explanation for these results may have to do with gut hormones. Prebiotics stimulate the secretion of two gut peptides: glucagon peptide 1 (GLP-1) and glucagon peptide 2 (GLP-2). Glucagon-like peptides (GLPs) are also released by healthy L-cells of the small intestine and colon, and the alpha cells of the pancreas. These hormones influence insulin and glucagon secretion and their dysregulation may be a contributing factor in insulin resistance.

The abundance of A. muciniphila is associated with increased L-cell activity. By increasing L-cell activity, this is yet another way prebiotics may encourage the growth of this bacteria.

A. muciniphila sends a signal that appears to alter production of anti-microbial molecules, while also increasing production of mucus. It has been proposed that the bacterium establishes a mutually beneficial relationship with the host: in exchange for more food, it will deal with any invading harmful microbes.

(Added note: oligosaccharides, but not inulin, are fermented in the right side of the large intestine, so only inulin is fermented in the left side, so optimally both are needed as prebiotics. Inulin and oligosaccharides are available as OTC supplements.)

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