Firstly, let me apologize for not forewarning you that I wouldn’t be posting last week. I did this absolutely K-RAAAAZY thing last week – I took a vacation. I am not sure that in the almost 5 year history of this blog, such insanity has ever happened.
As my regular readers know, while all biome research interests me, there are several subjects that I particularly obsess over: autism, Parkinson’s, Alzheimer’s, phages, the obesity epidemic, to name just a few. Today’s research is about that latter one: obesity. I have written many, many times before about the staggering numbers involved: see here and here, as just two of (at the moment) 71 examples. Remember that obesity is defined as a BMI of 30 and over, and according to the CDC, in the USA alone, 42.2% of the population was obese between 2017 and 2018. Obesity related conditions like heart disease, stroke, type 2 diabetes, some kinds of cancer are among the leading causes of death in the country.[i] The numbers, worldwide, are equally terrifying: according to the World Health Organization in 2016, 2 billion adults are overweight, with 650 million being classified as clinically obese. That is about 39% of the world’s adult population.[ii]
Today’s research is not directly involved with the inhabitants of the gut, but it involves the digestive system, and is just so interesting that I feel compelled to tell you about it. It was published in the eminent journal, Nature, and really blew me away. Remember my posts about the adverse biome-effects of processed sugars – mainly high fructose corn syrup? (Here are two examples of many: here and here.) The exact causes of the growing obesity epidemic are not as yet known, but more and more research suggests that increased consumption of these is at least one of the major causes: “Fructose consumption is linked to the rising incidence of obesity and cancer, which are two of the leading causes of morbidity and mortality globally.”[iii]
It turns out that there is evidence that the small intestine acts as a gatekeeper, preventing the excess accumulation of fat in the liver (fatty liver) that can be causes by excess consumption of fructose. Moderate amounts like you’d find in fruit, are broken down by the intestinal cells. However, excess amounts such as you’d find in sugar-laden sodas, overwhelm the intestine’s ability to absorb the fructose, which then leaks into the bloodstream (making its way to the liver, still intact) or it makes its way down to the colon.
Fructose in the colon is broken down by our gut bacteria, which produce molecules that can fuel lipid synthesis (creation of fat) in the liver. To boot, fructose in the intestines compromises the epithelial lining, leading to leaky gut, “…a condition in which loose connections between gut cells enable ingested nutrients, and toxins from bacteria in the colon, to escape to the liver, where they activate inflammatory signals from immune cells…”[iv] Thus, excess fructose is known to harm the liver both directly and indirectly through changes in the intestines.
But wait – there’s more. It gets way worse. In the research I’m reporting to you today, scientists have found that excess fructose has a previously unknown effect on the actual structure of the intestine. Knowing that high-fructose corn syrup (HFCS) “…promotes metabolic pathways that support the formation of colon tumours…,” they wondered what it might do to non-cancer cells. What they found is astounding: mice fed HFCS had longer villi (the microscopic, finger-like projections of the small intestine, which absorb nutrients) and thus, the small intestines of the mice absorbed more dietary nutrients from food compared to controls. What does that mean? It means that they got much, much fatter. And if the scientists added large amounts of fat to the HFCS diet, the mice gained even more weight. That is, increased fructose consumption also led to increased fat consumption.
I’m going to go into the explanation of why this happens but yes, the scientists did figure it out. Very simply: fructose prevented the normal death of old cells in the villi. And, by the way, they also discovered that the same mechanism that makes the villi longer also causes increased tumor size. Thus, they conclude that, “The ability of fructose to promote cell survival through an allosteric metabolite thus provides additional insights into the excess adiposity generated by a Western diet, and a compelling explanation for the promotion of tumour growth by high-fructose corn syrup.”