Joint pain from too much insulin


Majid Ali, M.D
jointpain

Nature created inflammation to gently remind people—animals and plants as well—to take a pulse of their lives. Inflammation is a response to injury. The inflammatory response is also essential part of healing. I do not know any form of healing that can take place without inflammation and I do not know any disease process in which inflammation does not begin tissue injury and, if unchecked, does not intensify it.

When the early signals of inflammation are ignored, Nature’s intelligent design is stressed and inflammation creates swelling and pain. If still ignored, the inflammatory response deepens, its message becomes angry, and it torments the whole body. If still unheeded, Nature plays its “inflammation card” and deeply sickens the individual. Finally, it gives up on the individual.

I reproduce some text from one of my other tutorials on inflammation to explain the above summary of what inflammation is and what it means. Life is an unending injury-healing-injury cycle. Injury is inevitable in an organism’s struggle for survival. Healing is the intrinsic capacity of the organism to repair damage inflicted by that injury. Inflammation is one aspect of the energetic-molecular mosaic of that intrinsic capacity. This view of inflammation extends far beyond the classical and wholly inadequate notion of it being a process characterized by edema, erythema, tenderness, pain, and infiltrate of inflammatory cells. Since oxygen is the organizing influence of human biology and governs the aging process in humans, it follows that inflammation, first and foremost, is one of the many face of oxygen homeostasis. In 1990, I devoted a large part of Oxygen and Aging to this subject.

Man-microbe conflicts are a legacy of microbe-microbe conflicts during the primordial period — long before humans appeared on the scene. Oxygen created and adjudicated microbe-microbe conflicts then, as it does the man-microbe conflicts now. I came to recognize that through my clinical work with persons who control microbial infections well — with or without antimicrobial drugs — as well as with those who cannot with anyantimicrobial. A large body of personal phase-contrast microscopic and biochemical findings in those patients led me to the conclusion that the fundamental molecular derangement in the latter is disruption of the oxygen homeostasis, including respiratory-to-fermentative shift in ATP production described previously.

Two Core Concepts of Crucial Clinical Significance

Below, I state two core concepts of crucial clinical significance that evolved from the view of inflammation given above:

1. Physiologic inflammation becomes pathologic inflammation when oxygen homeostasis is in jeopardy; and

2. The status of oxygen homeostasis determines the outcome in man-microbe conflicts. In this context, oxygen also resolves the long-standing Pasteur-BeChamp controversy about whether disease is caused by microbes invading from outside or by organisms multiplying from within.

Oxygen homeostasis has not been a consideration of immunologists and infectious disease specialists. It needs to be. Nor has oxygen been of interest to pediatricians, internists, and family practitioners who are the most frequent prescribers of antibiotics, since they take their cues from the specialists. I believe this to be the primary factors that leads to massive abuse of antibiotics. In a chapter entitled “Oxygen Settles the Great Pasteur-BeChamp Debate” in Oxygen and Aging (2000), I summarized my view of that matter with the following words:

When oxygen metabolism is optimal, Pasteur’s microbes from outside play more important roles in causing infectious disease. When oxygen metabolism is dysfunctional, BeChamp’s life forms multiplying from within the body become more important.

The Core Message

Physiologic inflammation is healing. Pathologic inflammation is disease-causing. It is crucial to learn how to keep inflammation in the healthful range and how not to allow it to slip into disease-causing mode.


The role of Insulin Toxicity

What is the most common blood lab testing error of doctors for which patients pay the highest price? The answer: Insulin profiling for detecting insulin toxicity. I recognize our age as the age of insulin toxicity. This should give the readers a real sense of the enormity of the problem created by doctors’ negligence of insulin toxicity.

The Age of Insulin Toxicity from Majid Ali on Vimeo.

In my writing, radio, and television work, I strive hard not to subordinate ethics to ideology. I define ethics as the study of the consequences of one’s action on others. Ethics is also the study of the consequences of one’s inaction on others when action is needed. If some doctors are offended by my opening statement, I hope they will read this article and at least two of my other articles on insulin toxicity and then decide if I have allowed ideology to subvert ethics.

Insulin Toxicity Majid Ali MD from Majid Ali on Vimeo.

Joint and Skin Inflammation Controlled by Correcting Hyperinsulinism

The incidence of inflammatory and autoimmune disorders of joints and skin is rising worldwide. When I see such patients, my first focus is on the possibility of insulin toxicity triggering and fanning such inflammations. When the insulin profiling establishes the presence of hyperinsulinism—an obsolete term which should be replaced by insulin toxicity—this becomes my top treatment strategy. This is where my best long-term clinical results are. Below I present a case study to illustrate my case.

Case Study

A 54-year-old woman weighing 120 lbs who presented with joint pain, areas of skin inflammation, mold allergy, tinnitus, and back pain. The table below presents her three insulin and glucose profiles, the first and the third were done following a standard 75 gram glucose load while the second was done after a healthy protein and healthy fat breakfast.

At the 5-month follow-up, she reported marked reduction of joint symptoms, skin inflammation, back pain, and allergy symptoms. At the one-year followup, she reported complete recovery from symptoms except some residual allergy symptoms. This clinical response was accompanied by marked reduction of fasting insulin from 25 mU/ ml to 8.7 mU/mL


Insulin and Glucose Profiles After 75 Grams Glucose Load of a 54-Year- Old Woman Weighing 120 Lbs Who Presented With Joint Pain, Areas of Skin Inflammation, Mold Allergy, Tinnitis, and Spine Discomfort. All Insulin Levels Expressed in mU/ml.

7/9/13

Fasting

½ HR

1 HR

2 HR

3 HR

Insulin

25.0

68.4

84.7

76.2

76.4

Glucose

85

187

178

141

112

7.19.2013, Post Protein/Breakfast

22.5

27.8

25.1

80

76

81

8.1.2014 Post Standard Glucose Load A1c 5.2

8.7

35.5

13.7

97

161

107

A1c Measurements

Blood A1c (glycated hemoglobin) values are widely used for screening for diabetes. Inn my experience, A1c is not unreliable for this purpose. It is, however, useful for monitoring the effectiveness of treatment plan. The A1c value in the case study presented above was 5.6% in the beginning of the program and was considered within normal limits even though she was insulin-toxic. The A1c values fell from to 5.4% and then to 4.2%.

A1c and Insulin Toxicity from Majid Ali on Vimeo.

Understanding Insulin Dysfunction Majid Ali MD from Majid Ali on Vimeo.

This case report is a part of my Insulin Case Studies Series

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Questions?

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