Age and Dietary Fat Result in Larger Inflammatory Populations of Gut Microbes
Age-related changes in gut microbe populations provide an important contribution to the chronic inflammation that is characteristic of old age. Beneficial species diminish in number, reducing the production of metabolites that aid in optimal cell and tissue function. Harmful species increase in number, interacting with tissue and the immune system in ways that promote chronic inflammation. Practical approaches to reverse the age-related changes observed in the gut microbiome could be realized quite soon, given the will and funding: some form of fecal microbiota transplant, or intense probiotic treatment, perhaps. The former has been demonstrated to work in animals, improving health and extending life, and is already practiced for human patients in the medical community in order to treat certain conditions in which pathological bacteria have contaminated the gut.
Numerous studies have suggested that the composition of the gut microbiota differs between obese and normal weight individuals. However, the cause-effect relationship between obesity and gut microbiota composition is not yet fully understood. This study investigated the short-term responses of the gut microbiota composition to diets with different fat contents. Experimental animals were fed either a a normal diet (ND) or a high-fat diet (HFD) for 20 weeks and the microbial composition was evaluated at 10 and 20 weeks. In agreement with previous studies, body weight and the expression of colonic cytokines increased with higher dietary fat content. The diversity of the gut microbiota was significantly influenced by both age and diet, and two variable showed significant interactions.
At the phylum level, the proportion of Actinobacteria was significantly associated with dietary fat content, while the proportions of Firmicutes and Bacteroidetes were strongly associated with age. In the present study, a HFD significantly elevated the proportions of the phylum Actinobacteria and the class Actinobacteria_c in a positive association with body weight, which have also been shown to be increased in obese subjects and patients with type 2 diabetes.
A growing body of evidence suggests that a HFD increases gut permeability and endotoxemia, resulting in low-grade inflammation and impairment of the gut barrier. Given that bacteria in the phylum Actinobacteria are known as mucin-degrading bacteria, abundant Actinobacteria might be associated with gut barrier impairment induced by a HFD. Indeed, we observed that Actinobacteria was inversely related with tight junction proteins such as E-cadherin and positively associated with proinflammatory cytokines. Therefore, the HFD-mediated increase in Actinobacteria and Actinobacteria_c may play a role in the HFD-induced impairment of the intestinal barrier, leading to colonic inflammation.
We also found that in the phylum Actinobacteria, the class Coriobacteriia and the family Coriobacteriaceae were positively correlated with body weight and proinflammatory cytokines, while the change in the proportions of these bacteria was significantly associated with age. Although the mechanistic effects of age on the Coriobacteriaceae are unknown, it is positively associated with both ROS and inflammatory cytokines, which contribute to metabolic dysfunction.
Well, I see this but I feel so much better since I've been on a Keto diet. The plan is, meet weight goals then move to some kind of low carb Mediterranean diet.
So maybe because we try to emphasize the healthier fats, like always cooking in avocado or olive oil, etc...?
Another terrible study based on mice and totally unnatural "diets", for these, and any other spieces. Can you really extrapolate anything meaningful from this paper other than mice lard corn oil and pretty much everything from this list, do not mix?
https://bmcmicrobiol.biomedcentral.com/articles/10.1186/s12866-019-1557-9/tables/2
Kefir, Kimchi, Sauerkraut, Apple Cider Vinegar... to the rescue.
I hate this diet stuff. There are only three categories, so a diet can either be balanced, or it is high fat, high carb, or high protien, or low on one of those three.
Over the years, we've noticed that low fat, high carb diets don't seem very effective in losing weight--they just jack up insulin production and help the body to accumulate fat. Now we hear a study about mice (which are obviously not humans) that fat is bad because it disturbs the gut bacteria and leads to blah blah blah. So if carbs make you fat, and eating fat makes your guts leak, the only thing left is a high protein diet. Unfortunately, I hear high protein diets can cause different kinds of problems. You just can't win.
So after a lifetime of reading this ever-changing nonsense, I've pretty much stopped listening. I know I feel better on a low carb diet and particuarly when I avoid sugar and junk food. That's pretty much all I need to know.
We ain't gonna diet or exercise ourselves to actuarial escape velocity. Moderate exercise and diet will carry you far. If we want to live much longer than our allotted threescore and ten, we are going to need dramatic changes to our biochemistry, and I think SENS is on the right track. Yet another diet study tells us little and wastes precious resources that could be allocated in more promising directions.
> Over the years, we've noticed that low fat, high carb diets don't seem very effective in losing weight--they just jack up insulin production and help the body to accumulate fat.
This is just the byline of non-expert posturing by Gary Taubes and keto-fanatics to sell books and appearances by selectively ignoring the evidence to tell their own story.
The only way that the low fat diet advice failed is in that people never actually followed it by eating actual fruits and vegetables, and they increased their intake of processed foods (marketed as healthy low-fat snacks perhaps!) containing refined carbohydrates while keeping fat almost constant.
It's worth watching the debate between Gary Taubes and Stephan Guyenet on JRE to see why there are so polarising views and which is more likely (does the brain drive hunger, and calorie consumption, and so excess energy storage as body fatness, or is it fat cells making body fatness) : https://www.youtube.com/watch?v=vA3QavPp1Ho
Interesting! Thanks for that link.