What Your Doctor Won't Tell You About Your Diabetes

What Your Doctor Won't Tell You About Your Diabetes

By Justin Nejbauer

There are certainly benefits when it comes to having a “for profit” healthcare system. One is that it drives innovation. It also allows capitalism to take effect, and (at least in theory) should result in lower costs of goods and services. One downside to a “for profit” healthcare system though is that there is unfortunately no money to be made from healthy patients. The monetary gain from preventative care is little to none. As a fitness professional, there is no disease where I see this to be more apparent than type 2 diabetes. Type 2 diabetes is essentially a loss of glycemic control due to severe reductions in sensitivity to the hormone insulin. If you are someone who has been diagnosed with type 2 diabetes, you have two options. One being to change the lifestyle factors that got you there in the first place. This often means reducing carbohydrate intake and increasing daily activity. The second option is to continue going on the way you have been, but to supplement with exogenous insulin. Both will technically improve glycemic control, and on paper look to have the same end result. This couldn’t be farther from the truth though. In fact, choosing between controlling blood sugar with changes in lifestyle vs. controlling blood sugar with exogenous insulin could literally be a life or death decision for you! I’m going to explain in detail, so be prepared to get into the science that will support this claim. Your doctor will not tell you this.

Natriuretic peptides (NP) are predominantly cardiac ventricular hormones that promote natriuresis and diuresis, inhibit the renin-angiotensin-aldosterone axis, and are vasodilators. (1) Insulin resistance is associated with lower NP levels, regardless if the individual is obese or not. (2) Low NP levels are also associated with increased visceral adiposity and hypertension (via fluid overload). 

It is interesting and notable that the standard treatment for diabetes mellitus type 2 (T2D) is to control blood sugar via the use of exogenous insulin, which can further increase insulin resistance (3), and subsequently exacerbates issues associated with low natriuretic peptide levels (including hypertension). Rather than reduce the amount of glucose being consumed (via a lower carbohydrate diet), the physician will prescribe supraphysiological amounts of insulin. Although both approaches do have an effect in improving glycemic control, one is done so at the expense of negative implications on natriuretic peptides, and would increase chances of having negative implications on cardiac functioning down the line. Furthermore, as insulin sensitivity inevitably declines over time due to receptor downregulation, more and more insulin is needed to continue to have a desired effect. 

It has been shown that negative implications on natriuretic peptides are due to the increase of circulating insulin associated with insulin resistance, rather than the downregulation of the insulin receptor itself. It has been demonstrated that acute doses of supraphysiological amounts of exogenous insulin result in modest reductions of NP (4), which supports this notion. In patients with T2D, glycemic control has been shown to make little difference in regards to negative cardiovascular events (5). This further supports the idea that it is the high levels of insulin that is the problem in regards to cardiovascular disease rather than the lack of glycemic control associated with T2D.

It is important to know that natriuretic peptides are released in response to the walls of the heart being put under stress. If fluid overload is great enough, the walls will be put under an especially large amount of stress, and will result in especially high NP output. If NP output is continuously elevated due to chronic fluid overload, NP receptor sensitivity is decreased (6), and eventually NPs can no longer take effect. This results in even more fluid overload, and can result in acute onset heart failure. Brain-natriuretic peptide levels will frequently be extremely elevated in heart failure patients in their body’s attempt to reduce fluid retention. The problem is not that NPs are lacking. The problem is that the NP receptor is burnt out, and the peptides cannot take effect. Just as chronically elevated insulin is associated with insulin resistance via receptor downregulation, chronically elevated natriuretic peptides are also associated with receptor downregulation and ultimately “natriuretic peptide resistance”. This results in a state where your body can not expel excess fluid.

Take away message here; if you are someone who is diagnosed with having diabetes mellitus type 2, and you have opted for glycemic control via exogenous insulin, it may be time to start taking your lifestyle more seriously. As has been shown, glycemic control is not the end all/be all in regards to your health when it comes to T2D. It is important to remember that there is no money to be made by pharmaceutical companies when it comes to reversing your disease with lifestyle factors alone. They make money when you purchase their insulin, and dare I say it, but they also make money when you are diagnosed with cardiovascular disease. The writing is on the wall. They have access to all the same studies I have referenced here. This is not secret information. As I have previously mentioned, this is just one of the unfortunate downsides of for profit healthcare. That being said, I highly suggest everyone do their own research, and be mindful of the sources they choose to listen to. At the end of the day, you can always rest assured that you have your own best interest at heart. 

Note: This is not intended to pose as medical advice. This article is for educational purposes only. Always consult your physician before adjusting your medication. 

(1)  https://pubmed.ncbi.nlm.nih.gov/12750764/

(2) https://academic.oup.com/jcem/article/96/10/3242/2834924

(3) https://www.ncbi.nlm.nih.gov/books/NBK507839/

(4) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5951576/

(5) https://pubmed.ncbi.nlm.nih.gov/23387439/

(6) https://pubmed.ncbi.nlm.nih.gov/23022110/