AGING, INFLAMMATION, THE MICROBIOME, AND FECAL MICROBIOTA TRANSPLANTS
Earlier this month, a dozen researchers from several universities in the Netherlands published a study in Frontiers in Immunology titled Aged Gut Microbiota Contributes to Systemical Inflammaging After Transfer to Germ-Free Mice. What’s especially interesting is that it deals with a subject I touched on in YESTERDAY’S POST on fascia and athletic injuries; “Inflammaging“. What is inflammaging and what relates it to fecal microbiota transplants?
It’s the combination of two words, ‘inflammation‘ and ‘aging‘. Although the word has been part of the scientific vernacular for nearly two decades, take a listen to what the experts are saying about inflammaging (BTW, there are over 300 studies with “inflammaging” in the title).
- In May of 2013 a group of researchers from the UK published Understanding How We Age: Insights Into Inflammaging in the journal, Longevity and Healthspan. The researchers concluded that “Inflammaging is characterized by the upregulation of the inflammatory response that occurs with advancing age and is believed to be a consequence of a remodelling of the innate and acquired immune system, resulting in chronic inflammatory cytokine production. Complex interrelated genetic, environmental and age-related factors determine an individual’s vulnerability or resilience to inflammaging. These factors include…… increased adiposity.” In other words, the chemicals we call “inflammation” are driven by many factors, including EPIGENETICS and OBESITY, and it’s all part of the inflammaging process.
- A year later, The Journals of Gerontology: Series A published Chronic Inflammation (Inflammaging) and Its Potential Contribution to Age-Associated Diseases that stated, “Human aging is characterized by a chronic, low-grade inflammation, and this phenomenon has been termed as “inflammaging.” Inflammaging is a highly significant risk factor for both morbidity and mortality in the elderly people, as most if not all age-related diseases share an inflammatory pathogenesis.” Aging is a natural part of living, and inflammation levels always increase as we age, and while you cannot stop either, you can slow both down by diminishing your inflammatory load. By the way, all DEGENERATIVE and AUTOIMMUNE diseases are based on inflammation.
- Then in 2016, a collaboration between teams from China and Australia published An Update on Inflamm-Aging: Mechanisms, Prevention, and Treatment in the Journal of Immunology Research. This study lists diseases I discuss in the previous two links (“Alzheimer’s disease, atherosclerosis, heart disease, type II diabetes, and cancer“), going on to say, “Inflamm-aging was first named in 2000, and it is a new addition to the types of aging studies. Inflamm-aging plays an increasingly important role in the rate of aging and age-related diseases. In the process of aging, some researchers pointed out that the phenomenon where adaptive immunity declines is called immunosenescence, while the phenomenon where innate immunity is activated, coupled with the rise of proinflammation, is called inflamm-aging. There is consensus that the primary feature of inflamm-aging is an increase in the body’s proinflammatory status with advancing age.” To better understand inflammaging’s foundational concepts, take a look at THIS POST or THIS POST.
- Here is what Life Extension Advocacy Foundation (Inflammaging and Age-related Disease) said about inflammaging (make sure to note DYSBIOSIS, THE LEAKIES, and OCCULT INFECTIONS are there for everyone to see). “The immune system relies on acute inflammation during the immune response to fight invading pathogens and to facilitate wound healing. This triggers cell turnover and tissue repair and is, in general, a desirable reason for inflammation. However, in direct contrast to this, inflammaging produces a chronic, low-grade, persistent background of inflammation that leads to poor tissue repair and degeneration. This chronic inflammation also contributes to the development of age-related diseases and is instrumental in driving the aging process in general. The oral and gut mucosa barriers that protect against bacterial invasion begin to both decline in effectiveness and break down as we age. Immunosenescence may also be accelerated and aggravated by persistent infections, such as CMV, HIV, and Epstein–Barr virus, linking it to microbial burden.” CMV & HBV are not only bad news for many people but are super common as well.
I already know what you’re thinking; what the heck does this have to do with FECAL MICROBIOTA TRANSPLANTS — one of the single hottest areas of research for the past five years? In previous studies, we saw where feces from obese mice was transplanted into thin mice, making them fat. The scientists turned right around and transplanted feces from thin mice back into the fat mice, making them thin. Back and forth, the outward expression of your health intimately related to the inward expression of your MICROBIOME.
This is why I have shown you time and time again that overall health is all about GUT HEALTH. Now, take a look at what this brand new study has to say concerning the relationship between aging and fecal microbiota transplants.
“Advanced age is associated with chronic low-grade inflammation, which is usually referred to as inflammaging. Elderly are also known to have an altered gut microbiota composition. However, whether inflammaging is a cause or consequence of an altered gut microbiota composition is not clear.
In this study, gut microbiota from young or old conventional mice was transferred to young germ-free (GF) mice. Four weeks after gut microbiota transfer immune cell populations were analyzed. Here, we show by transferring aged microbiota to young GF mice that certain bacterial species within the aged microbiota promote inflammaging. This effect was associated with lower levels of Akkermansia and higher levels of TM7 bacteria and Proteobacteria in the aged microbiota after transfer [dysbiosis].
The aged microbiota promoted inflammation in the small intestine in the GF mice and enhanced leakage of inflammatory bacterial components into the circulation was observed. Moreover, the aged microbiota promoted increased T cell activation in the systemic compartment. In conclusion, these data indicate that the gut microbiota from old mice contributes to inflammaging after transfer to young GF mice.”
Living the rest of your life with less inflammation is a noble goal, not so much because it will help you live longer (although it probably will), but because decreasing the amount of systemic inflammation coursing through your system will undoubtedly help you live better. And let’s be honest with ourselves for a moment; who really wants to live longer, if the quality of life is terrible? Unfortunately, this is the perfect scenario for generating obscene pharmaceutical profits, and exactly what’s going on in most Westernized countries, including America (HERE).
Think about it this way; How many people would purposefully choose to live the rest of their life with the aftermath of a stroke — or a nasty autoimmune disease — or cancer, if they could actually have avoided it / them in the first place? For those of you who believe that your specific disease is random or “GENETIC,” while certainly possible, is far less likely than you’ve been led to believe (go back and click on the “epigenetics” link above).
While I would never promote anything (particularly fecal microbiota transplants) as a ‘sure thing,’ I’ve created a starting point — a place to start gathering ideas for creating your own exit strategy (HERE) — a way to start slowing down the medical merry-go-round so that you can get off. If you find this sort of thing intriguing, be sure to spread the wealth by liking, sharing, or following on FACEBOOK.
