by Will Block

DHEA and Depression

f all the studies conducted since the 1950s indicating a wide variety of successful usages of DHEA, one finding stands out: people feel better on DHEA. According to University of California researcher Dr. Owen Wolkowitz, the most consistent finding is that DHEA seems to increase a person's sense of well-being.1

It comes as no surprise, therefore, that DHEA has now been found to alleviate depression. In a recent study involving six middle-aged and elderly subjects suffering from major depression, all were found to have low basal levels of DHEA.2 After administration of 30-90 mg/day of oral DHEA over a period of four weeks, circulating levels of DHEA were restored to levels characteristic of younger individuals.

It comes as no surprise, therefore, that DHEA
has now been found to alleviate depression.

Memory performance, by certain measures, improved significantly. Depression ratings were also significantly reduced, demonstrating that DHEA can have powerful neuropsychiatric effects. The researchers increased the treatment span of one resistant patient for 6 added months and her depression ratings improved dramatically (48-72%) and her word identification memory also lunged forward (63%).

When treatment stopped, all measures of improvement returned to what they had been before supplementation, suggesting a deficiency syndrome. The scientists also noticed that the increased benefits were directly tied to serum increases of DHEA and to increases in the plasma DHEA/cortisol ratios. The more pronounced suggestion to come from the study, however, is that DHEA may have antidepressant and promemory effects.

Wolkowitz also conveyed that studies of brain cells suggest that DHEA may help preserve dendrites - outgrowths that branch from one brain cell to another - which serve as the circuitry for signaling between cells. Additionally, he says, there is evidence that DHEA acts by affecting the activity of signaling chemicals called neurotransmitters in the brain.

  1. Healthbeat. KRON-TV (Ch 4). Nov. 6, 1996.
  2. Wolkowitz OM, Reus VI, Roberts E, Manfredi F, Chan T, Raum WJ, Ormiston S, Johnson R, Canick J, Brizendine L, Weingartner H. Dehydroepiandrosterone (DHEA) treatment of depression. Biol Psych. 1997;41:311-318.
  3. Norris J. UCSF begins clinical trial of DHEA to treat Alzheimer's. UCSF Newswire. 12/13/1995.

DHEA Levels Decline in the Brain with Age

The graphs of age-related declines in DHEA have all referenced the amounts found in serum in the bloodstream. Now we have a study showing that the amounts in the cerebrospinal fluid (CSF) also decline with age. Given what we know about DHEA and its neurosteroidal properties, including its correspondence to intelligence and memory, this is an important finding. Because the CSF bathes the brain and spinal cord, this information is but another reason to start supplementing with DHEA as levels decline. These findings emphasize that our DHEA levels come down by approximately 2% per year from about the end of our twenties. At age 70, our levels may be only 10% of what they were as a young adult, in our brains as well our blood.

Scientists measured DHEA and cortisol in 62 subjects aged 3-85 years old, 36 of whom were males and 36 females. Also noteworthy, the researchers from the University of Cambridge in England also determined that the ratio of cortisol to DHEA increased with age in the brain. Due to the decrease in DHEA, the result was relative hyper-cortisolemia. Because cortisol tends to exacerbate stress, and DHEA to lessen it (DHEA has antiglucocorticoidal activity), relative hyper-cortisolemia is an ominous sign of the inevitable ravages of the aging process that may be ameliorated with DHEA supplementation.

  • Guazzo EP, Kirkpatrick PJ, Goodyer IM, Shiers HM, Herbert J. Cortisol, DHEA, and DHEAS in the CSF fluid of man: Relation to blood levels and the effects of age. J Clin Endo Met 1996;81:3951-3960.

Creatine Uploading May Be Unnecessary

Information on the best protocol for creatine use has been scant, but an important new study indicates that the same muscle mass increase may be obtainable without the need to preload with higher amounts. Until now, most studies have indicated that optimal results are obtained when the loading dose is up to 20 g of creatine for 5-6 days, followed by a dose of 2-3 g for four weeks.

However, a recent article published in the British Journal of Sports Medicine reports that 3 g/day for one month works as well. Conducted by Dr. Paul Greenhaff, who has established himself as one of the world's most knowledgeable creatine researchers, this is good news for several reasons. First, it is easier to comply with a schedule that doesn't require calculation, and, more important, the benefits of a creatine regimen are now available to those users who have proven sensitive to the larger uploading levels. It also cuts on costs.

Several other important conclusions are found in the study, including the idea that when creatine is taken with simple carbohydrates such as fruit or vegetable juice, creatine concentration can be increased 60%. The study also found that when caffeine is taken with creatine, the results of creatine are counteracted.

  • Greenhaff P. Creatine supplementation: recent developments. Br J Sports Med. 1996;30: 276-281.

ALC May Enhance Brain Structure

When acetyl-L-carnitine (ALC) was given to 6-, 12- and 22-month-old rats, measurable changes in brain structure were found to occur in the hippocampus region. In control rats, certain characteristics of the synapse, the space between the junction of the neurons in a neural pathways, were found to decline with age. While the surface area of the neuronal endings did not change with age, the density changed.

In ALC-treated rats, the density was found to increase. Also, the number of synapses with very small distances between neurons increased. Collectively, these changes represent positive modulation of the synaptic structural dynamics in ALC-treated animals. ALC increased energy economy and provision at the nerve terminals. This may account for ALC's ability to enhance certain aspects of memory.

  • Bertoni-Freddari C, Fattoretti P, Caselli U, Paoloni R. Acetylcarnitine modulation of the morphology of rat hippocampal synapses. Anal Quant Cytol Histol. 1996;18:275-278.

High Levels of Vitamin E Slow Alzheimer's Disease

Many life extenders take the drug selegiline (deprenyl) to protect their brains from oxidative damage, increase the levels of brain catecholamine activity, reduce neuronal damage, and possibly slow the progression of Alzheimer's disease (which may be a disease we all will suffer from if we live long enough). A recent study has shown for the first time that the benefits of deprenyl may also be available for those taking high levels (2000 IU) of vitamin E daily.

Vitamin E slowed the progression of
Alzheimer's disease slightly more
than the treatment of choice, deprenyl

When a total of 341 patients with Alzheimer's disease received 10 mg of deprenyl (a MAO-B inhibitor) or 2000 IU of vitamin E (alpha tocopherol) or a placebo every day for two years, the time of onset for what the scientists termed a primary outcome was measured. (Primary outcomes included death, institutionalization, loss of the ability to perform basic activities of daily living, or severe dementia.)

Those taking deprenyl outlasted placebo by an additional 215 days (49% longer) before encountering a primary outcome (655 days for deprenyl vs 440 days for placebo) and those taking the 2000 IU of vitamin E/day outlasted placebo by 230 days (52% longer) before they encountered any negative event from the same set of primary outcomes (670 days for vitamin E vs 440 days for placebo). These were significant delays. Vitamin E slowed the progression of Alzheimer's disease slightly more than the treatment of choice, deprenyl, for patients with moderately severe impairment.

  • Sano M, Ernesto C, Thomas RG, Klauber MR, Schafer K, Grundman M, Woodbury P, Growdon J, Cotman CW, Pfeiffer E, Schneider LS, Thal LJ. A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer's disease. N Engl J Med. 1997;336:1216-1222.

Dietary and Production Sources of Melatonin

To obtain the equivalent of 3 mg of oral supplementary melatonin from your diet you would have to consume 120 bananas or 30 large bowls of rice at one time, according to MIT brain and cognitive science professor Richard J. Wurtman, MD.1 Dr. Wurtman has warned the public that taking melatonin can cause people to crash into telephone poles. He believes melatonin should be available by prescription only.

Curiously, Dr. Wurtman also has a "use patent" on melatonin. The arrival in the drug "pipeline" of his prescription melatonin, Melzone, is anticipated any day now.

Speaking of rats, melatonin levels were determined in serum and gastrointestinal tract tissue of rats that had had their pineal glands removed.2 This surgical procedure resulted in substantially lower levels of melatonin in serum but did not alter levels of melatonin in the gastrointestinal tract. This finding supports the hypothesis that melatonin concentrations in the tissues of the GI tract are independent of pineal production. In another animal experiment, when melatonin levels were bolstered in the GI tract, the formation of gastric lesions was significantly reduced. Further, there was also a reduction of free radicals in the bloodstream at the same time that gastric blood flow slowed.3 Melatonin may be able to protect mucosa from the damage caused by ischemia-reperfusion (blood restriction and reflow), an action thought to be mediated, in part, by antioxidant activity.

  1. Lamberg L. Medical News & Perspectives. JAMA. October 2, 1996.
  2. Bubenik GA, Brown GM. Pinealectomy reduces melatonin levels in the serum but not in the gastrointestinal tract of rats. Biolog Sig. 1997;6:40-44.
  3. Konturek PC, Konturek SJ, Majka J, Zembala M, Hahn EG. Melatonin affords protection against gastric lesions induced by ischemia-reperfusion possibly due to its antioxidant and mucosal microcirculatory effects. Eur J Pharm. 1997;322:73-77.

Melatonin Works

After largely ignoring melatonin - several years after the Harvard Health Newsletter gave it thumbs up - The New England Journal of Medicine has finally come around and conceded that melatonin works! It should come as no surprise, however, that NEJM still cautions that the time has not yet arrived to advocate the use of melatonin - not until the long-term big studies are done, i.e., not until well into the 21st century when many of us who might have profited from it will be dead. More than 5400 scientific articles appear in the electronic literature, as well as hundreds of articles in the popular press. Moreover, there have been more than 20 million Americans who have tried melatonin, which has been available since the mid-1980s, yet NEJM, widely held as the most "prestigious" medical journal in this country, still cautions that we should wait. Here are the highlights of the study:

  • Melatonin possesses significant antioxidant abilities, and it may be possible to achieve these advantages at physiologic doses rather than pharmacologic amounts.
  • Strong animal study evidence exists showing that melatonin can significantly strengthen the immune system.
  • Melatonin has the ability to inhibit certain tumors.
  • Melatonin has a sleep-inducing effect in humans.
  1. Brzezinski A. Melatonin in humans. N Engl J Med. 1997;336:186-195.

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