Every November, we take time to explore and educate on an all-too-common chronic disease that affects 10% of Americans: diabetes mellitus. The relationship between diabetes and an imbalance of bacteria in your gut is incredibly complex and closely intertwined. For years, it has left most scientists wondering - which came first? Gut dysbiosis or diabetes?
This has been one of the most difficult challenges in diabetes research. Is gut dysbiosis a cause, or is it an effect of diabetes? Plenty of research has shown that the two are closely linked and continue to trend together, but most research stems from disease after it has already set in.
To determine which came first, studies must be conducted before a patient becomes sick. It’s easy to understand these cases are rare. And unfortunately, that’s a common theme in chronic disease research - we’re always one step behind the curve. Most clinical studies focus on illness after it has manifested rather than preventing it. We believe we should focus on the needs of the individual over the many to help promote a healthy and resilient body.
And as the science on diabetes has grown, scientists believe that the surprising answer may be found from learning the true impact of the gut on systemic inflammation.1
Understanding the Source of Diabetes
Diabetes is considered a ‘pro-inflammatory disease’, which is very common in autoimmune disorders. For example, type 1 diabetes (an autoimmune disease) occurs when a body’s own immune cells attack the pancreas and eliminate its ability to stabilize blood glucose (via insulin production). Although type 2 diabetes doesn’t necessarily face the same attack on the pancreas, an overactive immune system has been shown to heavily impact the development of the disease as well.
For researchers, it has become increasingly important to determine the source of inflammation influencing diabetes. Systemic inflammation has long been considered to be the underlying cause of diabetes’ impact on glycemic control. In both type 1 and type 2 diabetes, patients are unable to stabilize their blood sugar after meals. An imbalance in blood sugar can wreak havoc on a number of systems and have serious health consequences. Scientists have long speculated that inflammation may be what is perpetuating this cycle, but depending on which type of diabetes you’re talking about - very different things may be brewing beneath the surface.
Type 1 vs. Type 2
Although they share a name, the pathophysiology of type 1 and type 2 are quite different. They both lead to a disrupted ability to regulate glycemic control - or balance blood sugar (in the form of glucose). However - as we mentioned - type 1 diabetes occurs when our immune cells attack the pancreas and stop its production of insulin. Insulin is an essential hormone that communicates with our cells to bring circulating glucose from the blood into our tissues.
Only about 5% of diabetes cases are classified as type 1.2 It’s a rare, autoimmune disorder that is often genetically passed down (though recent studies have suggested that environmental assaults may also activate it).3 Those who develop type 1 diabetes require routine injections of insulin after feeding to help bring down their blood glucose levels. Without it, they risk significant consequences, including heart disease, stroke, coma, and death.
Type 2 diabetes is closely correlated with a high BMI and is considered a co-morbidity with obesity. Type 2 diabetes patients are still able to produce insulin from a functioning pancreas - but insulin loses its ability to properly communicate with other tissues. Rather than interacting with our cells, the cells become less sensitive to insulin’s presence.
Known as ‘insulin resistance,’ the cells fail to unlock the door for passing glucose to enter.
Studies have shown evidence that the all-too-often culprit of insulin resistance is actually systemic inflammation, which can harm or damage the glucose transporters on the outside of our cells. With the transporters damaged, insulin’s signaling falls on deaf ears, and the glucose remains circulating in the blood.
The Root Cause of Systemic Inflammation
Our digestive tract is closely associated with our immune system. The GALT - gut associated lymphoid tissue - is one of our body’s greatest immune hubs that stores nearly 70% of our immune cells.4 As science has shown - and we have seen - maintaining a healthy gut positively influences how well our immune system functions.
And if our gut health becomes compromised, our body becomes a breeding ground for an imbalanced gut ecosystem. Negative changes in our gut microbiome can develop into gut dysbiosis, resulting in a pro-inflammatory response. Maintaining a balanced microbiome decreases the chances of gut microbes secreting endotoxins that can degrade the lining of our digestive tract, therefore lessening the chance for stimulating inflammatory molecules and encouraging a healthy functioning gastrointestinal system.
When microbes are in harmony and in balance, they don’t penetrate other tissues to cause inflammatory reactions, which harms glucose transporters and contributes to insulin resistance.
Balanced Gut, Balanced Health
Diabetes specialists have shown significant evidence that gut dysbiosis is a common issue in diabetes cases.
Now, we’re even learning that some gut microbes also contribute to how we regulate blood sugar levels.5
Our gut microbiome interacts with so many aspects of our body. Whether it’s influencing our immune system or exchanging messages with our brain, there is so much more to learn.
But the easiest way to promote healthy interactions is by tapping into the true power of the food you eat. Understanding the dynamic between nutrition, the gut microbiome, and blood sugar management brings the world one step closer toward a healthier you.
And at Viome, we’re taking steps to learn just how. The research that comes out of our own laboratories is constantly giving us insight into the gut microbiome. And with every new study and every new test, we’re constantly evolving to bring you the most advanced and comprehensive technology in precision nutrition yet.
Originally published Nov. 20, 2020
Updated Oct. 25, 2023
References:
1 Grigorescu I, Dumitrascu DL. (2016). Acta Endocrinol (Buchar). 2016 Apr-Jun;12(2):206-214. doi: 10.4183/aeb.2016.206. PMID: 31149088; PMCID: PMC6535288.
2 Timmons, J. (updated Feb. 22, 2021). Online, infographic, healthline.com.
3 Simmons KM, Michels AW.(2015). World J Diabetes. 2015 Apr 15;6(3):380-90. doi: 10.4239/wjd.v6.i3.380. PMID: 25897349; PMCID: PMC4398895.
4 Vighi G, Marcucci F, Sensi L, Di Cara G, Frati F. (2008). Clin Exp Immunol. 2008 Sep;153 Suppl 1(Suppl 1):3-6. doi: 10.1111/j.1365-2249.2008.03713.x. PMID: 18721321; PMCID: PMC2515351.
5 Gérard C, Vidal H. (2019). Front Endocrinol (Lausanne). 2019 Jan 30;10:29. doi: 10.3389/fendo.2019.00029. PMID: 30761090; PMCID: PMC6363653.
