My dad’s story of cognitive steroid-responsiveness has perpetually intrigued doctors. Especially since much of our current knowledge of Alzheimer’s Disease asserts that steroids can cause delirium and agitation in patients with AD. But in Dad’s case, just the opposite is observed. The question therefore is why?
We searched the web to find our answers. And interestingly, a very probable solution can be found in how our body protects itself: It’s called The Immune System. This natural defense process is a very good thing when it’s in check. But sometimes and in some people, their Immune System turns onto itself. In these people – like Dr. Crandall – Instead of fighting off invaders like bacteria or viruses, their Immune System sees its own body as a foreign invader – and attacks it accordingly.
Whatever our Immune System attacks will experience inflammation. Which is fine when the thing being attacked needs to go. But when it’s your own body – say your joints, or your thyroid, or your pancreas, or your brain, this can’t be a good thing.
Did you ever wonder why people with Autoimmune diseases are up to 10 times more likely than people without auto-immune diseases to develop AD?
The answer, we believe, is in one of our genes that plays a role in auto-immunity. This gene is what allows some people to produce a newly identified Helper T cell that plays a role in both health and disease.
Our immune system is such a miraculous thing. Cells like TH1 and TH2 – which are good cells – take pride in fighting off infections within our bodies on a daily basis. But back in the early 2000’s, scientists discovered Helper T cell 17 and it’s lineage. This cell acts normally when produced in moderation, thereby providing a healthy benefit to the body. But when TH17 is produced in excess – which happens in auto-immune conditions – this cell begins to destroy the body. Inflammation ensues as the body’s good cell tissue is destroyed by the actions of the TH17 cells.
This is where Steroids come in. Steroids are able to shut down the cell causing the inflammation, in this case TH17. And once the TH17 is tamped down to moderate levels, it no longer causes inflammation. After awhile, the body returns to normal, which is when the auto-immune process is said to be in “Remission”.
There’s a lot of discussion about how it seems that auto-immune diseases are on the rise. Since the 1950s, rates of multiple sclerosis, Crohn’s disease, type 1 diabetes, and asthma have soared by 300% or more . And lots of literature discussing how having one auto-immune disease increases the likelihood of contracting another. Interested? This might be an interesting read:
Title: Multiple Autoimmune Syndrome on the Rise, Clinical Vigilance Needed
This is also an interesting recent study, Titled: US and UK stand out with higher disease prevalence of two autoimmune diseases which found that systemic lupus erythematosus (SLE) and Sjögren’s syndrome were more prevalent here in the US and in the UK than in any other country. What’s significant is that recent (2019) research is suggesting that Sjogren’s has a higher than average co-morbidity rate for AD than any other auto-immune disease, including Diabetes. Titled: Higher risk of dementia in primary Sjogren’s syndrome . Which corroborates an earlier (2017) study titled: Population-based study suggests an increased risk of Alzheimer’s disease in Sjögren’s syndrome.
In the meantime, take a look at this list of auto-immune diseases that statistically set those afflicted to being much more likely to develop Alzheimer’s Disease…
Diabetes
Lupus
Rheumatoid Arthritis
Periodontal Disease
Arteriosclerosis
Hoshimoto Thyroditis
PMR
Colitis
Some forms of COPD
Alzheimer’s Disease
[Okay, we put the last one in because it’s part of our working hypothesis…]
Because Dr. Crandall was a dentist, he looked first at autoimmune-related Periodontal Disease to better understand how TH17 attacks our own bone and tissue.
As a quick tutorial, Periodontal Disease is caused by the bacteria P. Gingivalis (TONS ON THAT LATER). We are not born with this bacteria in our mouths, but get it through contact with someone who has it. This bacteria is a very benign bacteria when the PH of the oral cavity is basic. Which it is for children…But as we age, the PH of our mouths change to acidic and when P. Gingivalis finds acid, it multiplies and begins to cause inflammation. Minor inflammation is called Gingivitis – a reversable condition that does not cause tooth or bone loss. But in some people, those who have the gene that allows their body to produce TH17, P. Gingivalis becomes destructive and leads to Periodontal Disease.
All right, on to the back up studies of relevance:
In the following 2018 paper that looked at TH17 and its role in the development of Periodontal disease, the primary author of the paper states “Our clinical observations point to the relevance of our animal studies to humans and provide further evidence that Th17 cells are drivers of periodontitis.” One study reviewed found that humans with generalized gum inflammation that are unable to produce TH17 did not develop Periodontal Disease despite have predisposed factors present.
Title: Researchers identify immune culprits linked to inflammation and bone loss in gum disease found at:
In the following 2008 paper, the authors discuss how TH17 was recently established as a unique T Helper cell lineage, and is thought to be a contributing factor to many inflammatory and autoimmune diseases:
Title: Th17 cells—a new T cell lineage
And in this 2012 study, which we believe is the most compelling data point of all three, the researchers were able to show that the auto-immune diseases PMR and GCA are both characterized by a significant change in the Th17 cell/Treg cell balance toward an increased Th17 cell response. The study also supports that steroids successfully decreased the frequency of Th17 lymphocytes without affecting the frequency and function of Treg cells.
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