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From the Townsend Letter
February / March 2018

Cortisol Deficiency: Frequent, Life-Impairing, and How to Give Patients Their Lives Back by Correcting It Part 2
by Thierry Hertoghe, MD
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Additional Use of DHEA and Other Anabolic Hormones
Adrenal glands simultaneously secrete cortisol and protective hormones, such as DHEA and aldosterone. In young adults, secretion of both cortisol and its protective hormone DHEA by the adrenal glands are similar – approximately 20 mg per day for women and 30 mg per day for men. Whenever increased amounts of cortisol are secreted, healthy adrenal glands also release proportionately more DHEA and other adrenal hormones.

In many medical offices, cortisol or one of its derivatives are generally prescribed alone without protective anabolic hormones. This imbalanced treatment produces a number of side effects – mostly tissue atrophy – as shown in Table 5. To avoid these undesirable catabolic effects, DHEA and other anabolic hormones such as testosterone, female hormones, and possibly even growth hormone should be systematically administered (if the patient is deficient in these hormones), whenever hydrocortisone or one of its derivatives is prescribed.

Intolerance to Cortisol
A minority of cortisol-deficient patients, usually those with the weakest adrenals, does not tolerate oral intake of cortisol. They may experience unbearable stomach acidity that can be overcome by enrobing the cortisol in a protective coat (a supplementary layer at the outside of the pill). Enteric coating protects the stomach against the pills' acidity by dissolving in the small intestine rather than in the stomach.

Patients may also feel weird, overwhelmed by a general malaise that spreads over the body with feelings of fainting and great weakness, when taking oral hydrocortisone or one of its synthetic derivatives. These patients find that cortisol therapy aggravates their cortisol deficiency symptoms. The usual cause is aldosterone deficiency induced or aggravated by glucocorticoid-induced reduction of pituitary secretion of ACTH, the hormone that stimulates secretion of all major hormones of the adrenal cortex. Aldosterone is another hormone secreted by the adrenal cortex. It keeps the blood pressure up. Treatment of aldosterone deficiency and its associated feeling of empty-headedness consists of adding fludrocortisone, the synthetic derivative of aldosterone.

A tiny minority of cortisol-deficient patients may still not tolerate or do well with cortisol, despite their desperate need for it. These cortisol-intolerant patients often experience all types of allergic or intolerance reactions to whatever medication they take. Their cortisol levels in blood and urine are usually dramatically low. Physicians may get headaches from trying to find strategies that could solve the problem.

Two alternate routes of administration may provide relief. Subcutaneous injections of cortisol at 30 to 50 mg a day may help, as may the application of 4–6 g/day of a liposomal gel with 5% cortisol applied to the buttocks, back, and belly in a very thin layer to avoid skin atrophy. A liposomal gel offers the best penetration of the body. If the applied layer is thin and if the patient rubs it ten times over a large surface, it should penetrate quickly, leaving the skin intact. I tried these two forms, and they provided the same efficacy as my daily 30 mg/day of hydrocortisone intake.

How to Make Cortisol Treatment Safe
First of all, avoid excess. Doses of 15–30 mg per day of hydrocortisone in women and 20–35 mg per day in men are usually physiologically safe28-31 but may need to be reduced for smaller individuals. High cortisol doses should only be administered for a limited time in exceptional crises – to rescue a patient or an organ, for example – but always with concomitant anabolic hormone treatment.

The best method is to inform patients of cortisol excess signs and recommend they reduce the dose by 25 to 50% if there are ever signs of cortisol excess, such as a swollen face, weight gain, high blood pressure, or excessive agitation.

Second, administer simultaneously protective anabolic hormones. DHEA is the number one anabolic hormone that neutralizes excessive catabolic effects of cortisol associated with cortisol treatment.35-39
Young adult adrenals secrete DHEA and other anabolic hormones concomitantly with cortisol. Because DHEA is anabolic and builds up tissue, its presence blocks the excessive catabolic effects of cortisol. Cortisol is predominantly catabolic because it hastens catabolism to eliminate excessive tissue and unblocks energy by breaking glycogen down into glucose.

Both catabolism and anabolism are essential for health, but they must be appropriately balanced. To do so, both cortisol and anabolic hormones, such as DHEA, should be given in equivalent doses. Physicians should therefore mimic nature and provide DHEA with cortisol to avoid tissue wasting.

With aging, the production of DHEA declines considerably more than that of cortisol, resulting in an imbalance that favors catabolism above anabolism, which explains the progressive acceleration of aging in individuals past the age of 45.

The third way to make cortisol treatment safe is to avoid consuming "bad" carbohydrates. In my experience, intake of sweet foods and cereals (that were not sprouted (such as traditional bread, pasta, muesli, porridge, etc.), tend to block the major beneficial effects of glucocorticoid treatment and to increase the occurrence and intensity of undesirable side effects, especially swelling and weight gain. Thus, patients should avoid bad carbs in their diet at least five days a week. A protein-rich diet (180 g/day or more of meat, fish, and poultry) is also protective against excess glucocorticoid catabolism.

Follow-Up
Follow-ups are mainly based on clinical assessments. More than for other hormone therapies, follow-ups of cortisol treatments should be done clinically for the most part, assessing for the presence of complaints and signs and avoiding any overdose signs.

Please note that saliva, serum, and 24-hour urine laboratory tests usually provide inconsistent results for follow-ups of bioidentical hydrocortisone and cortisone treatments. They are unstable and unreliable.
If hydrocortisone treatment is taken 30 minutes to three hours before blood and saliva tests, abnormally high free (and total) cortisol levels can be found in the serum due to peak levels of cortisol after absorption.

If hydrocortisone treatment at physiological doses is taken much later – seven to 24 hours after blood and saliva tests – cortisol levels usually drop back to their initial levels (from before treatment) or even to a supplementary 20-30% lower concentration (usually not more) because of transient and partial inhibition of the adrenal cortisol secretion.

In blood and saliva, cortisol levels are not stable during treatment. Not only is there a cortisol circadian rhythm, which makes cortisol levels fluctuate, with two to three times higher cortisol levels in the early morning than in late afternoon, but orally ingested cortisol does not bind strongly to cortisol-binding globulin (CBG), so the cortisol, which penetrates into the blood or saliva, quickly leaves for the target cells, decreasing cortisol levels.

The 24-hour urine test is not good for follow-ups either because it can show abnormally high levels of cortisol due to peak cortisol absorption with increased losses in urine, as well as unusually high excretion rates of cortisol metabolites (17-hydroxysteroids), even if cortisol treatment is adequate or insufficient. After intestinal absorption, the cortisol passes into the liver. Much of the cortisol is then broken down in the liver into inactive metabolites, which pass into the blood and then the urine, not reflecting real cortisol metabolic activity. The 24-hour urine is a must to control the reduction in adrenal androgens when dexamethasone is given to reduce body hair growth.

For non-bioidentical glucocorticoids, laboratory tests are even more inadequate for follow-up. None of the traditional laboratory tests can measure these synthetic glucocorticoids because of their different molecular structures. They might have some value to check the grade of adrenal suppression they may cause. Finding undetectable or nearly undetectable endogenous cortisol levels and very low metabolite levels in urine tests indicates that endogenous cortisol secretion by adrenal glands might be excessively suppressed by treatment, possibly by overdose.

Conclusion
Adrenal deficiency, particularly cortisol deficiency, is one of the most underestimated and misdiagnosed hormone deficiencies.

Untreated cortisol deficiency severely affects a patient's quality of life and brings a long road of unnecessary suffering. The hormone cortisol makes most stress bearable and considerably reduces suffering. Patients who remain in cortisol deficiency suffer excessively and continue to do so throughout their lives – the more severe the deficiency, the more suffering there is.

Many physicians and laypeople are reluctant to prescribe or take supplements of cortisol or one of its derivatives because of the unacceptable side effects of pharmacological doses of cortisol. These fears should not prevent physicians from treating cortisol-deficient patients with small, well-adjusted physiological doses of cortisol that are balanced with a protective DHEA supplement.

To correct a cortisol deficiency, the first things to do are to improve the environment, the lifestyle, and the diet. Let patients expose themselves to daylight and intense indoor light more. Recommend that they avoid pollutants – most pollutants are indoors. Regularly meditating or relaxing may also help increase cortisol levels when supplementary amounts are necessary. Avoiding unnecessary stress preserves cortisol stores from spillage. In addition, increasing the intake of protein- and fat-rich foods and avoiding sweets and cereals may also noticeably improve cortisol levels. In a minority of cases, these interventions may suffice.

In all other cases where cortisol treatment must be installed, these interventions optimize treatment results.

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References for Part 2 .pdf

References for Part 1 .pdf

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