Reversing Diabetes Lesson Seven – Diabetes, Inflammations, and Infections

 

Majid Ali, M.D.

My Three Top Priorities for Patients With Inflammatory Disorders: 

First, Think of Coexisting Infections.

Second, Think of Cellular Energy and Insulin Status.

Third, Be Holistic and Integrative in the Science and Philosophy of Caring.


Two Core Messages

First, all forms of inflammations, with or without infections, increase the risk of diabetes, and diabetes increases the risk of all  types of inflammations and infections.

Second, for acute infections, microbes require first attention. For chronic infections, one’s own human cells require first attention.


Two Essentials

  1. All Inflammations and Infections begin with fermentation in the bowel and in the mind.

  2. Prevention and control of inflammation and infection must begin with control of fermentation in the gut and the mind.


A Treasured Lesson From My Patients:

Knowing Oxygen and Insulin for Health.

Knowing Inflammation For Healing.


Three Questions

Is inflammations always bad?

What weakens immunity to inflammations and infections in diabetes?

What causes insulin toxicity (hyperinsulinism)?


Think Seven

for Recurrent and Chronic Infections in Diabetes

  1. Think Prayer

  2. Think Oxygen

  3. Think Insulin

  4. Think Bowel

  5. Think Nutrients, Spices and Herbs

  6. Think Anti-inflammatory foods

  7. Think Specific Remedies 

Think Prayer

Pray, Just pray –  For whatever, whomever, wherever

Think Oxygen

Breathe slow, just breathe out slow – for however, however  long,  wherever

Think Insulin

Pray, Just pray –  For whatever, whomever, wherever

Think Bowel

Breathe slow, just breathe out slow – whereever, for however long.

Think Nutrient, Spices, Herbs

Begin low, build slow, be a scientist, try it, observe the effects, and move on.

Anti-Inflammatory Foods

Foods that cause sugar spikes which trigger insulin spikes are proinflammatory foods. Non- toxic foods that do not cause sugar spikes are anti-inflammatory foods.

Specific Remedies

Chromium, vanadyl, neem leaves, and others.



My First Encounter With the Diabetes-Infection Axis

One of my sharpest recollection of events in a medical clinic in 1961 is of how a professor diagnosed diabetes by looking at the neck of a new patient. The patients had a carbuncle of the neck which is considered diagnostic of diabetes because the disease does not allow to let this skin infection heal. That experience returns whenever I think of the diabetes-infection axis.


Four Historical Footnotes

1876 .          W. Epstein controls sugar leak in diabetes with aspirin.

                      Berliner Klinicsche 1876;3:337-340.

1901.           R. Williamson control sugar in urine in diabetes with aspirin. 

                      British Medical Journal. 1901;1:760-762.

1957.            Reid  J. Macdougall AL Stop insulin injections with aspirin.

                     British Medical Journal. 1957;8:418-428.   

1921.          Insulin discovered by the Canadian physician Frederick Banting

                    and Student Charles H. Best.


Types of Infections

  1. Acute .   Viral, Bacterial, yeast, parasitic

  2.  Subacute .  Viral, Bacterial, yeast, parasitic

  3.  Chronic .  Viral, Bacterial, yeast, parasitic

Two important microbial species causing infections in diabetes ate Staph aureus and Candida species.


The Gut-Diabetes Connections

 

  • Throat

  • Esophagus

  • Stomach

  • Small intestine

  • Large intestine


Molecular Mechanisms of the Diabetes-Infections Axis

1.  Less circulation, less oxygen

2. Reduced number and efficiency of hunter-immune cell function                              (decreased phagocytic function)

3. Reduced number and functional deficits of immune white blood cells

4. Sluggish movements of immune cells

5. Increased apoptosis (planned cell suicide)

6.  Low levels of inflammatory cytokines

7. Compromised complement system defense molecules

8.  Low concentrations and efficiency of antibodies


Acute Infections and Chronic Infections

Preferred Natural Remedies

  1. Optimal hydration

  2. Dr. Ali’s Spicy Smoothie

  3. Probiotics (yogurt, Kiefer, Acidophillus)

  4. Turmeric and Vitamin C (1000 mg of each) four times a day

  5. Oregano oil

  6. Special Nutrients (Zinc lozenges, Magnesium, Potassium, Taurine)

  7. Antibiotics, If really needed

  8. Antifungal Spices, Herbs, and Medications. 

One of my sharpest recollection is of a patient that I saw as a student in 1961. He came to a medical clinic with a carbuncle (deep seated chronic skin infection) on the back of the neck. My professor took one look at the carbuncle and clinically diagnosed diabetes,  which proved right on blood tests. It would be 54 years before I learned the about the following three publications clearly establishing the insulin-inflammation connections.


Three Neglected Insulin Lessons From the Past.

1876 .          W. Epstein controls sugar leak in diabetes with aspirin.

                      Berliner Klinicsche 1876;3:337-340.

  1.           R. Williamson control sugar in urine in diabetes with aspirin. 

                      British Medical Journal. 1901;1:760-762.

  1.            Reid  J. Macdougall AL Stop insulin injections with aspirin.

                     British Medical Journal. 1957;8:418-428.   

 I anticipate three questions here: (1) the above three reports refer to Type 2 diabetes (T2D), why do is call them “three insulin lessons”? (2) what lights do the insulin-inflammation connections shed on neurodevelopmental biology? and (3) specifically, what clinical imperatives might be recognized to restore neuronal progenitor cell progression to mature “speech neurons, as well as other neurons involved involved with the autism spectrum, dysautonomia, and related neurodevelopemental disorders? Here are brief answers: (1) hyperinulinism predates T2D in all cases and maternal hyperinsulinism is a hazard for neuronal progenitor cell progression of the unborn child; (2) unrecognized hyperinsulinism in ASD and CID  during prenatal to threatens poses serious threats to developmental biology.


A Crucial Question

Why did I dig them out for investigations into the molecular basis of neurodevelopmental  studies discussing the results o I bring The answers: (1) unrecognized maternal hyperinsulinism is a hazard for neurobioilogy of the unborn baby; (2) unrecognized hyperinsulinism in early postnatal life is a hazard for progenitor cell progression; and (3)  for neurobioilogy of the unborn baby rain; T2D, is first and foremost, an insulin toxicity problem. Hyperinsulinism predates T2D. This relationship has been recognized for decades. The author has never seen T2D develop without hyperinsulinism preceding it. I have published many case studies toType 2 to illustrate these observayions. 

Proinflammatory Cytokines Induced Insulin Resistance

In 1993, 117 years after the first published report of antidiabetes effects of aspirin, the  effects of aspirin,  the proinflammatory cytokine NFK-a  was shown to induce insulin resistance.25,27 This seminal advance led to rapid recognition of similar anti-insulin, pro-diabetes effects of other inflammatory cytokines,  adipokines (leptin, adiponectin, and others produced by fat cells), resistin, visfatin, PAI-1, IL-6, angiotensinogen,  retinol-binding protein-4, serum amyloid A (SAA), and others.28-33  


Insulin Adjudicates Physiological and Pathological Inflammation


The Gut-Diabetes Connection

 

  • Throat

  • Esophagus

  • Stomach

  • Small intestine

  • Large intestine

Digestion starts within the mouth by the action of the enzymes in saliva. It then takes full effect within the stomach and some nutrients are also absorbed into the bloodstream here. Partially digested food known as chyme then undergoes further digestion mainly in the first part of the small intestine known as the duodenum. The small intestine, or small bowel, is the longest part of the gut and gradually the food is completely digested and almost all the nutrients are absorbed into the bloodstream.


Important Sites of Diabetes-Related Infections

  1.  Infections of the Urinary Tract

  2.  Vaginal Tract

  3. Skin

  4. Lungs and Pulmonary Tract


 Molecular Mechanisms of the Diabetes-Infections Axis

1.  Less circulation, less oxygen

2. Reduced number and efficiency of hunter-immune cell function                              (decreased phagocytic function)

3. Reduced number and functional deficits of immune white blood cells

4. Sluggish movements of immune cells

5. Increased apoptosis (planned cell suicide)

6.  Low levels of inflammatory cytokines

7. Compromised complement system defense molecules

8.  Low concentrations and efficiency of antibodies


Decreased mobilization of polymorphonuclear leukocytes, chemotaxis, and phagocytic activity may occur during hyperglycemia.[4,9,10] The hyperglycemic environment also blocks the antimicrobial function by inhibiting glucose-6-phosphate dehydrogenase (G6PD), increasing apoptosis of polymorphonuclear leukocytes, and reducing polymorphonuclear leukocyte transmigration through the endothelium.[4] In tWeak 

s

4.  Complement

Complement

The complement system is one of the main mechanisms responsible for the humoral immunity. It consists of serum and surface proteins whose main functions are to promote the opsonization and phagocytosis of microorganisms through macrophages and neutrophils and to induce the lysis of these microorganisms. Moreover, complement activation products provide the second signal for B-lymphocyte activation and antibody production.

Although some studies have detected a deficiency of the C4 component in DM,[5,6] this reduction of C4 is probably associated with polymorphonuclear dysfunction and reduced cytokine response.[2,5]

Inflammatory cytokines

Mononuclear cells and monocytes of persons with DM secrete less interleukin-1 (IL-1) and IL-6 in response to stimulation by lipopolysaccharides.[2,4] It appears that the low production of interleukins is a consequence of an intrinsic defect in the cells of individuals with DM.[2,7] However, other studies reported that the increased glycation could inhibit the production of IL-10 by myeloid cells, as well as that of interferon gamma (IFN-γ) and tumor necrosis factor (TNF)-α by T cells. Glycation would also reduce the expression of class I major histocompatibility complex (MHC) on the surface of myeloid cells, impairing cell immunity.[8]

Polymorphonuclear and mononuclear leukocytes

Decreased mobilization of polymorphonuclear leukocytes, chemotaxis, and phagocytic activity may occur during hyperglycemia.[4,9,10] The hyperglycemic environment also blocks the antimicrobial function by inhibiting glucose-6-phosphate dehydrogenase (G6PD), increasing apoptosis of polymorphonuclear leukocytes, and reducing polymorphonuclear leukocyte transmigration through the endothelium.[4] In tissues that do not need insulin for glucose transport, the hyperglycemic environment increases intracellular glucose levels, which are then metabolized, using NADPH as a cofactor. The decrease in the levels of NADPH prevents the regeneration of molecules that play a key role in antioxidant mechanisms of the cell, thereby increasing the susceptibility to oxidative stress.

Regarding the mononuclear lymphocytes, some studies had demonstrated that when the glycated hemoglobin (HbA1c) is <8.0%, the proliferative function of CD4 T lymphocytes and their response to antigens is not impaired.[4]

Antibodies

Glycation of immunoglobulin occurs in patients with diabetes in proportion with the increase in HbA1c, and this may harm the biological function of the antibodies.[4] However, the clinical relevance of these observations is not clear, since the response of antibodies after vaccination and to common infections is adequate in persons with DM.[4]


How Do You Reverse Diabetes Majid Ali MD on Vimeo


Reversing Diabetes – Lesson One

https://alidiabetes.org/?s=reversing+diabetes+-+lesson+-+one

Reversing Diabetes – Lesson Two

https://alidiabetes.org/?s=reversing+diabetes+-+lesson+-+two+

Reversing Diabetes – Lesson Three

https://alidiabetes.org/?s=reversing+diabetes+-+lesson+-+three


Reversing Diabetes – Lesson Four

https://alidiabetes.org/?s=reversing+diabetes+-+lesson+-+four

Reversing Diabetes – Lesson Five

https://alidiabetes.org/?s=reversing+diabetes+-+lesson+-+five

Reversing Diabetes – Lesson Six

https://alidiabetes.org/?s=reversing+diabetes+-+lesson+-+six


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