Diabetes and heart desease - article


#1

#2

It is great seeing this type of research. There also comes a time to act and take a progressive approach.

Based on the article we know the reason the heart gets messed up is because it can’t get energy from glucose because of lack of insulin. It would sure seem to me keeping non-diabetic time in range for the T2 would address this problem.

The problem is however Steps 1 through 3 and even Step 4 using of baslin insulin in the current ADA Standard of Care does not address non-diabetic time in range for T2s. In fact it is just the opposite. It promotes time out of range hoping to have the damaged pancreas work overtime and make up for the loss of insulin production and meal time release when it should be resting.

Just a few years ago the diabetes community could hide behind A1c but those days are over with CGMs. Knowing what the post meal sugars look like and knowing we can address them in real time with tools like afrezza should significantly reduce the burning of fat by the heart and as a result significantly reduce diabetic heart disease.

Like the researcher my father also died from a massive diabetic related heart attack.


#3

Either this article was poorly written, or this doctor is clueless.

Chances are the doctor did not write his interview, so most likely whoever did the interview and wrote the article did not quote the doctor properly.

This quote is wrong:

If insulin is working properly, then glucose [sugar] can get into the heart for energy. When insulin doesn’t work properly, the heart starts borrowing energy by burning fat.

Heart muscle functions almost exclusively aerobically. The heart has almost no glycogen reserve like skeletal muscle has. Fatty acids are the heart’s primary fuel source. Also ketone bodies and lactate can be used by the heart for fuel. Glucose is the heart’s last choice for fuel.

Certainly the doctor would not make such a mistake. It has to be whoever wrote it.


#4

Eddie - the heart needs a constant supply of glucose and oxygen so that its muscle cells can respire and continue to contract. Without proper insulin it relies more on the free fatty acids.

Here is a nice summary which I think is at the center of his research


#5

Of course it needs oxygen. I never said that it did not need oxygen. I said it functions aerobically.

The link you posted says the heart utilizes ketone bodies, which is also something I said in my post above.

But it does not need a constant supply of glucose. Don’t take my word for it, read Biochemistry. 5th edition. I have this book, and that is where I am getting my information.

Here is a link.
https://www.ncbi.nlm.nih.gov/books/NBK22436/

Unlike skeletal muscle, heart muscle functions almost exclusively aerobically, as evidenced by the density of mitochondria in heart muscle. Moreover, the heart has virtually no glycogen reserves. Fatty acids are the heart’s main source of fuel, although ketone bodies as well as lactate can serve as fuel for heart muscle. In fact, heart muscle consumes acetoacetate in preference to glucose.


#6

Eddie - what I can say for certain is we will not solve this here. What I think we can agree on is keeping near non-diabetic TIR can’t hurt and may have substantial benefit.

If you would like I would be more than happy to reach out to Dr. Thomas Pulinilkunnil directly and ask. If you would like to ask your questions directly his emails are tpulinil@dal.ca and tpulinil@unb.ca There is not much more info on their web site

Proteotoxic Basis for Metabolic Heart Disease

One of the major focus of the Pulinilkunnil laboratory is to assess how adaptive or causative changes in protein synthesis and degradation causes heart disease. To maintain cellular homeostasis, synthesized proteins are degraded and recycled inside cellular organelles called lysosomes by a process known as autophagy. Using a multispecies approach (rodents, yeast and zebrafish) Pulinilkunnil lab will specifically examine how different nutrients (glucose, fat and amino acids) influence lysosomal function to alter autophagy. Furthermore investigate whether aberrant lysosomal function impact mitochondrial metabolism and energetics thus governing cardiovascular outcomes in biology and disease.


#7

As did my father.


#8

@Eddie2
Thanks for the link. This is great information.

Granted a good deal is beyond my level of Biochemistry knowledge but it is worth the read and really provides a great deal of expert information. It is nice the publishers allowed a portion of their book to be made publicly accessible.