Must be lots of ABs in bacon...
when they first were giving out penicillin, doctors would also give the patients probiotics.
got lost along the way b/c you don’t make a lot of money on probiotics.
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.)
And whatever you do, don’t exercise.
[Little irony and sarcasm there.]
Are antibiotics making people fat?
Don’t know if they are or not, but I’m pretty sure all the crappy fast food we eat is certainly a contributing factor.
Eating children is making me fat.
If this was true, acidophilus would be a best selling weight loss drug.