Date:   4/21/2013 2:54:22 PM ( 11 y ago)
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OXYGEN AND ADRENAL DYSFUNCTION>>>>

The Cushinoid-Addisonian Epidemic

The core message of this brief essay on adrenal health and adrenal deficit is: All chronically dysoxic individuals suffer clinically significant adrenal dysfunction. Dysox is the state of disrupted oxygen signaling and oxygen-driven cellular energetics. This view of adrenal deficiency is significantly different from the prevailing thinking in endocrinology. Endocrinologists, with rare exception, continue to be preoccupied with named adrenal syndrome-Cushing's syndrome, Addison's disease, Conn's syndrome, and Sheehan's syndrome-as well as pituitary tumors and hypothalamic disorders. Such lesions account for an exceedingly small number of chronically ill individuals with objectively and quantifiably detected adrenal dysfunction. This, indeed, is one of the core messages of this column. My assertions in this column are based on extended clinical work with over 7,500 patients with chronic illness and on close analysis of over 900 profiles of the 24-hour urinary excretion of steroid compounds.

This column has nine other core points:

● First, the adrenal dysfunction of every individual requires individualized support for the gland.

● Second, the essential "adrenal question" is not what diagnostic label is chosen for someone with a dysfunctional gland-people everywhere are diminished by relentless habitat chemicalization and unrelenting frustration and anger-but how the adrenal function of that person can be assessed and restored.

● Third, the degrees of adrenal dysfunction are best assessed clinically, as well as with the measurement of 24-hour urinary excretion of adrenal and gonadal metabolites.

● Fourth, adrenal regeneration requires spiritual equilibrium and full restoration of oxygen homeostasis.

● Fifth, all disruptions of the bowel, blood, and liver ecosystems must be effectively addressed for adrenal homeostasis.

● Sixth, in my clinical experience, the direct short-term adrenal support is optimally provided with hydrocortisone, beginning with small doses of 2.5 mg twice daily to larger doses of ten to twenty mg daily.

● Seventh, the adrenal gland cannot be understood except through its inter-relationships with the hypothalamic-pituitary axis (HPA), gonadal output, insulin metabolism, energy economy of the body, the oxygen-driven bioenergetics, and chronic stress.

● Eighth, there is a "Cushinoid-Addisonian epidemic"-most people with adrenal dysfunction pass from an initial hyperadrenergic (Cushing's syndrome-like state) to a hypodrenergic (Addison's disease-like) state.

● Ninth, an increasing number of young people are "gender-skewed"-females are "male-like" and males are "female-like,"so to speak-and the adrenals play crucial roles in the phenomenon of gender devolution. For an in-depth discussion of these subjects, I refer the readers to Darwin and Dysox Trilogy, the tenth, eleventh, and twelfth volumes of The Principles and Practice of Integrative Medicine.1-3 Before discussing the above issues, below is an illuminating historical footnote.

The Adrenal Gland: Two Glands in One

The adrenal glands are a pair of structures capping the two kidneys. The word renal is an adjective for elements related to kidneys. The adrenal glands were so named centuries ago to refer to their relationship to the kidneys. Ad-renals for add-ons to the kidneys so to speak.. Adrenal cortex is the bright-yellow outer gland while adrenal m edulla accounts for the central 20 percent of the gland and is functionally related to the sympathetic system..The cortex includes zona glomerulosa, zona fasciclata, and zona reticularis, Over 50 steroids have been isolated from the adrenal cortex.. Two major types of hormones are called glucocorticoid. and mineralocorticoid and glucocorticoid. The primary glucocorticoid. is cortisol while the primary mineralocorticoid is called aldosterone.

The major clinical features of adrenal deficit include:

● Easily fatigued
● Persistent fatigue
● Undue cold sensitivity
● Low body temperature
● Orthostatic intolerance
● Skin discoloration, pigmentation
● Estrogen and testosterone deficit in older people as well as young people with chronic energy deficit states.

The major clinical features of adrenal overactivity include obesity, hypertension, and most of the above.

Rebecca Gerschman-An Unsung Hero
The unsung hero of the field of free radical pathobiology is Rebecca Gerschman, a physiologist at the University of Rochester. In the early 1950s, she investigated the relationships between oxygen toxicity and the adrenal gland, and proposed that oxygen toxicity was mediated by free radicals.4-7It is peculiar that Gerschman's seminal contributions escaped the notice of most researchers and writers interested in the energetic-molecular basis of health and disease. She observed that adrenalectomy protected rats from oxygen toxicity. She was aware of a 1934 report of Ozorio de Almeida,8 which documented the histological similarity between testicular tissue injury caused by ionizing radiation and oxygen toxicity. Gerschman also knew of the universal theory of Michaelis,9 which held that free radicals were intermediates in oxidation processes. Examining the effect of adrenalectomy on certain types of acutely injured tissues, she observed that the procedure exerted protective effects and deduced that adrenalectomy slowed the metabolic rate and consequently reduced the need for oxygen-driven reactions. Considering her findings in the larger context of the earlier work of de Almeida and Michaelis, she concluded that oxygen toxicity was mediated by free radicals.

The Cushingoid-Addisonian Transitions

I present the model of Cushnoid-Addisonian transitions to underscore an essential point: The adrenal glands regularly cope with environmental, nutritional, and anger-related stresses with an initial Cushinoid hyperactivity response, which is followed by Addinoid adrenal failure when decompnsation occurs. Both the initial Cushinoid and subsequent Addinoid responses are quantifiable. Endocrinology textbooks and journals rarely, if ever, address the crucial issue of the adverse effects of toxic environment, toxic foods, and toxic thoughts on the adrenal structure and function. Nor does the endocrinology literature recognize the Cushinouid-Addinoid sequence occurring in people without any of the above-mentioned syndromes. Not surprizingly, endocrinologists act as if their patients are immune to all environmental, dietary, and anger-related toxicities. They limit their work to textual models of the Cushing's syndrome, Addison's disease, Conn's syndrome, pituitary tumors, and hypothalamic disorders-entities which, as I show below, are exceedingly rare-and neglect adrenal dysfunctions that occurs in all chronically ill individuals.

The Cushing's syndrome-adrenal hyperactivity caused by adrenal neoplasms and hyperplasia-is a rare disorder, with an incidence of 1 per 100.000 per year, with a female-to-male ratio of 5 to 1.10 The clinical features of the syndrome include: fatigue, excess adipose tissue ("buffalo torso"), protein deficit, facial edema and fat build-up ("moon face"), acne, hirsutism, skin striae, hypokalemia and muscle weakness, adrenal diabetes, osteoporosis, and failure to fight common infections due to immunosuppression.

The Addisons's disease-adrenal failure putatively due to "primary atrophy," autoimmunity, tuberculosis, and adrenal destruction by neoplasms-is also a rare disorder. There are no accurate statistics concerning the incidence of Addison's disease in the United States. A British study reported the incidence of thirty nine cases per million. The clinical features of the syndrome include: low blood sodium and chloride levels, excess potassium, acidosis, hypotension, hypoglycemia, dehydration, fatigue, and immunosuppression. Among the striking signs of adrenal deficiency in some instances are cutaneous and mucosal pigmentation.

The Conn's syndrome (primary aldosteronism)-excess production of mineralocorticoid aldosterdue to hyperplasia or neoplasm of zona glomerulosa of the adrenal cortex-is also a rare disorder. Its clinical features include: retention of sodium and water, excessive loss of potassium, metabolic alkalosis, muscle cramps (due to neuronal hyperexcitability), muscle weakness (due to muscle cell hypoexcitability), headaches, and hypertension. In 1955, the prevalence of aldosteronism was estimated to be about one in 2,000 individuals with hypertension. Recently, substantially higher incidences of aldosteronism have been reported in hypertensive populations.12

I furnish the above synopsis is to make a point of crucial clinical significance: The Cushinoid-Addinoid transitions caused by toxicities of environment, diet, and anger produce all possible combinations of symptom-complexes seen in classical adrenal diseases. This is what endocrinologists refuse to accept. Their patients pay dearly for this ethical lapse.

Laboratory Evaluation of Cushnoid-to-Addinoid Transitions
The laboratory assessment of adrenal function presents four special problems: (1) The adrenal glands produce about 50 steroidal moieties by complex pathways and no single steroid can be relied upon for its functional assessment; (2) The adrenal steroidogenesis increases initially to cope with incremental demands followed by marked reductions, but not in any consistent pattern in the production of specific steroids or their metabolites; (3) Adrenal production of androgens, estrogens, and progesterone cannot be separated from gonadal production of these hormones; and (4) The laboratory range of some hormones is extremely widefor instance the value for the urinary excretion of DHEA used by the Mayo Clinic laboratory is 21 to 2170 mcg/24 hourmaking interpretation of the values of individual steroids difficult. Notwithstanding these problems, a suitable profile of steroidsthe composition of my choice is shown in Table 1is extremely valuable.

In cases of acute and severe demands on the adrenal glands, the glands mount a strong Cushnoid response with a marked increase in the urinary excretion of all hormones and their metabolites (Case 1, Table 1). The other end of the spectrum is the Addinoid depletion (complete adrenal failure) in which amazingly no steroids can be detected in the 24-hour urine samples (Case 6, Table 1). Between these two ends of the spectrum are seen examples of Cushinoid-to-Addinoid transitional stages representing varying patterns of overproduction of some and underproduction of other adrenal steroids.

The problem of extremely wide laboratory reference ranges for individual steroids, as mentioned earlier, is tedious. I find it useful to consider the mid-point of the laboratory range for individual hormones and metabolites rather than merely accept the "high" and "low" designations in the report. The data in Table 2 clarifies this point by displaying the 24-hour urinary steroid excretion values for 26 chronically ill adult individuals. Note than when related to the midpoints of the laboratory reference ranges, the aggregate data for these patients were "low" for five, "normal" for one, and "high" for two steroid compounds. Without such an approach, the laboratory values for most patients are designated in error as "normal," as was done by endocrinologists who reviewed the adrenal data of my patients.

Adrenal Therapies
I prescribe adrenal therapies for all patients with chronic illness. The crucial issues of spiritual equilibrium and the restoration of the bowel, blood, and liver ecosystems have been addressed in past columns. As for providing adrenal support until there is sufficient adrenal regeneration, there are two approaches: (1) direct support with hydrocortisone; and (2) indirect support with raw adrenal extract, phytofactors, and nutrients. Below, I relate how I concluded that direct adrenal support yields superior clinical results in most cases.

In the mid-1980s, I investigated the clinical benefits of bovine raw adrenal concentrate, as well as phytofactors and nutrients for adrenal support. Among the phytofactors, prescribed in combinations and rotations, were daily doses of roots of licorice (500 to 1,000 mg), rehmannia (500 to 750 mg), ashwargandha (100 to 200 mg), and Chinese yam (500 to 750 mg). Among the nutrients were daily doses of pantothenic acid (50 to 150 mg), pyridoxin (25 to 50 mg), riboflavin (10 to 20 mg), and ascorbic acid (1,000 to 2,000 mg). These adrenal factors were prescribed concurrently with antioxidants, minerals, and redox-restorative substances, such as glutathione, MSM, taurine, and others.

In the early 1990s, I compared the clinical benefits of the above factors with those of DHEA, pregnenolone, and androstenodione in daily doses of 25 to 50 mg each for men and for women half as much on alternate days. In the mid-1990s, I undertook a systematic study of hydrocortisone. Based on that experience, in my hands most patients with adrenal deficit respond best to direct adrenal support with hydrocortisone (daily doses of 5 to 20 mg). The short-term use of low-dose hydrocortisone is safe, effective, and without any adverse effects. It is widely misunderstood because it is confused with high-dose synthetic steroid therapy.

The subject of initial adrenal support with hydrocortisone creates unnecessary confusion in the minds of many people uninitiated in this therapy. They fail to see the difference between gentle adrenal support with low-dose hydrocortisone and massive synthetic steroid therapy in common use among the practitioners of pharmacologic medicine.

Adrenal Regeneration and Recovery

The essential points are:

(1) Clinical improvement in adrenal function is seen with optimal integrated and individualized plans within months in most cases;

(2) Clinical indications of improved adrenal status precede normalization of laboratory values;

(3) Some individuals with long-standing disabling illness and severe adrenal deficiency tolerate very low doses of hydrocortisone (1 to 3 mg daily) initially and take several months to accept larger doses (10 t 20 mg) until eventual adrenal recovery occurs in several months; and (

4) Individuals with major Depression and posttraumatic stress syndrome sometimes show poor clinical response despite robust efforts to support the gland.

 

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