Prevention and Treatment of Chronic Inflammatory Diseases: Sustained-Release Dihydroberberine Protocols for Diabetes, COVID-19, and Other Inflammatory Diseases

by Knox Van Dyke, PhD

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Sustained release dihydroberberine (DHB) is a dietary supplement that has therapeutic value for the prevention and treatment of a wide range of diseases associated with chronic inflammation, including pre-diabetes and diabetes, heart diseases, viral infections, chronic neuroinflammatory diseases, lung diseases, kidney diseases, liver diseases, and as adjunctive treatment in a variety of cancers. This article describes the rationale for such use, relevant research, add-on therapies, and suggested treatment protocols.


Prevalence of Diabetes

More than 46% of the US adult population–about 120 million people–have pre-diabetes or diabetes,1 making this category the proverbial mother of all diseases. Moreover, diabetes is often associated with hypertension, heart disease, cancer, vascular damage, and liver damage.2 Diabetic retinopathy is the leading cause of blindness.3 Moreover, diabetes increases the risk of developing neurodegenerative diseases such as Parkinson’s disease and Alzheimer’s disease, the latter of which is now referred to as “type 3 diabetes.”4


Diabetes and Inflammation

Chronic inflammation plays a key role in pre-diabetes and diabetes. The DNA of macrophages and other inflammatory cells is wrapped around spool-like histone proteins. When acute inflammation occurs, these proteins become acetylated by the enzyme histone acetyl transferase (HAT), which eliminates the positive charge of histones. This is the on-switch for acute inflammation. The negatively charged DNA then loosens from the histones, which allows for the transcription of inflammatory genes that produce inflammatory gene products and products of oxidative and nitrosative (O/N) stress.

Dihydroberberine crosses cell membranes more
readily than other berberine compounds.

Macrophages, in particular, become activated and generate peroxynitrite. This highly toxic peroxide can further react with carbon dioxide to produce an even more reactive product called peroxynitrite carbonate, which is a strong nitrating compound. As this inflammatory state continues for weeks to months to years, an increasing number of macrophages produce peroxynitrite in excess. This damages histone deacetylase 2 (HDAC2) — the “off switch” for acute inflammation — and allows peroxynitrite or its carbonate to continuously signal chronic inflammation. 


Type 1 Diabetes

Figure 1. Chemical Structure of Dihydroberberine
https://pubchem.ncbi.nlm.nih.gov/compound/Dihydroberberine

When acute inflammatory type 1 diabetes begins, T lymphocytes are stimulated and produce interleukins and chemokines that help trigger the chronic inflammatory state in macrophages described above. This state is toxic to pancreatic beta cells that produce and release insulin. The excessive peroxynitrite kills the beta cells, so insulin is not produced. Alpha cells replace the dead beta cells and begin to produce excessive glucagon that, when released, increases glucose in the blood. Without insulin’s ability to allow glucose to enter certain organs and tissues like muscle and fat, the high blood glucose becomes very toxic to tissues and blood vessels.

In type 1 diabetes, the proper amount and kinds of insulin must be given at the proper time of day. Insulin must be given to maintain healthy blood glucose levels and sustain life. Most often, treatment is a combination of short- and long-acting insulin to maintain normal blood glucose levels. But nothing is given to control the O/N stress that is toxic to mitochondria, the cellular organelle response for normal glucose and fat metabolism.


Type 2 Diabetes

Type 2 diabetes is the most common form of diabetes, accounting for about 90-95% of all diagnosed cases of diabetes. It is associated with insulin resistance, a condition where the insulin released is damaged and fails to be effective.

Dr. Theodore Banting, the co-discoverer of insulin, originally addressed the key question of what causes diabetes. In his 1920s Nobel address he said, “Insulin is not the cure for diabetes.” Since insulin helps control glucose and lipid levels in the blood and tissues, a logical inference from his idea is that glucose and fats are also not completely responsible for diabetes since they can be held in check by insulin. In addition, many children who eat considerable amounts of candy and sugary sweets do not develop diabetes. If sugars, which contain glucose, do not cause diabetes, how is it involved in the disease?

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