Vasopressin, the Memory Hormone: Are Your Patients Thinking Straight

Vasopressin, the Memory Hormone: Are Your Patients Thinking Straight

Vasopressin is much more than a memory hormone. It is known to some as the learning hormone because people with vasopressin deficiency are forgetful.

Vasopressin is key to the architecture and function of the brain. Fourteen clinical studies attest to the fact that vasopressin supports long- and short-term memory, memory retrieval, and sound rapid-eye-movement (REM) quality of sleep. Vasopressin has even been successfully used to treat Alzheimer’s patients for mild improvement in memory (1-14).

However, vasopressin must be applied correctly to achieve these benefits. By correctly, I mean that it must be injected subcutaneously or sprayed intranasally for maximum effect. Most important, vasopressin must be used over a prolonged treatment period of at least three months before its benefits are realized. Such prolonged treatment is unlike that of melatonin, for example, where a single dose at bedtime improves sleep immediately that night.

Vasopressin is produced in the hypothalamus by the paraventricular and supraoptic cells that also produce the hormone oxytocin. Thus, vasopressin and oxytocin are structurally similar polypeptides with some overlapping functions, such as improving sleep quality. Subsequent to the production of these polypeptides, they are excreted into the bloodstream by ducts in the pituitary gland. In the past, this basic fact gave rise to the mistaken belief that vasopressin and oxytocin were produced in the pituitary. But that is not the case; they are hypothalamic hormones with many receptor sites in the hypothalamus and throughout the body (Figure 1).

Two-thirds of the body is composed of water. Vasopressin is the most potent hormone for keeping water in the body, particularly in the skin and blood vessels. It directly acts on the kidneys to retain water. On the other hand, the hormone aldosterone acts indirectly on water through sodium retention.

Both vasopressin and oxytocin have been well studied by prominent pharmaceutical companies since the 1940s. Interestingly, Parke Davis originally marketed and registered a glandular extract of these two key basic hormones in 1956. Their natural product was called Pituglandol®. In Parke-Davis’s double-blind clinical study of seventy-five patients, sixty-two with glaucoma showed significant improvement, namely a 20 percent average decrease in intraocular pressure (15).

Vasopressin alone suppresses aqueous humor flow by a resounding 60 percent, plus or minus 5 percent. Little wonder that such an amazing and completely natural hormone can dramatically impact memory.

However, as I mentioned at the beginning of this article, the correct dose must be used over a prolonged treatment period. Too high a dose causes a vasoconstrictive response of blood vessels in the brain, thus a physiologic dose of only 10 to 40 international units daily is preferred.  Indeed, endocrinologist Dr. Thierry Hertoghe, in both his lectures and in his Hormone Handbook, volumes one and two, always recommends that all hormone supplements be given at physiologic dose for best beneficial effects and to avoid side effects. Do not megadose your hormones.

Second, for best response from vasopressin, thyroid and hydrocortisone hormones should often be supplemented to correct deficiencies.

Vasopressin Studies with Memory

Vasopressin and memory research started with a lead article in the prestigious journal Lancet in 1979. Gold et al. published their unique finding that vasopressin functions by promoting processing of information. In a double-blind, placebo-controlled trial involving four patients, three of the four showed “highly significant and consistent improvements in tests designed to measure the formation, encoding, and organization of long-term trace events in memory” (1).

Subsequently, in 1982 and 1983 Laczi et al. found that diabetic patients injected or treated intranasally with vasopressin showed normalization of the deficits in short- and long-term memory. These effects were also noticed in normal, non-diabetic people (2,3).

Also in 1983 Laszlo showed that vasopressin promotes a “memory stimulation by influencing neural mechanisms” (4).

In 1984 Nebes et al. conducted a double-blind crossover study during two one-week periods in which subjects received 60 mg vasopressin daily. Vasopressin improved long-term retrieval time but did not benefit short-term memory in either young or old subjects. Also, it reduced memory comparison time and perceptual-motor time in short-term memory (5). Note that this 60 mg vasopressin overdosing likely caused the lack of any benefit in short-term memory.

In 1985 researchers Till and Beckwith concluded that a vasopressin analog “improved immediate memory more for low-verbal subjects and delayed memory more for high-verbal subjects” (6). Note that this limited response was probably due to analog and not pure bioidentical vasopressin.

In 1987 Hamburger-Bar et al. found that childhood learning disorders may benefit from repeated doses of vasopressin (7).

In 1987 Millar et al. found that, in healthy male volunteers, “vasopressin benefited initial processes of consolidation and learning” (8).

In 1997 Perras et al. used 40 IU vasopressin in twenty-six healthy elderly men for three months. They found that vasopressin improves sematic encoding after long-term administration (9).

In 1998 Van Londen et al. confirmed that the neuropeptide vasopressin, independently of other factors, “enhances memory, directly or indirectly, through increasing arousal and attention” (10).

In 1999 Perras et al. stated that sleep in the elderly is characterized by disturbed sleep architecture. This means that the elderly experience reduced time spent in slow wave sleep and REM sleep. The researchers did a pilot study whereby twenty-six healthy elderly subjects were given intranasally 20 IU vasopressin at bedtime for three months. Vasopressin increased total sleep time by an average of forty-five minutes, slow wave sleep time by twenty-one minutes, and REM sleep time by ten minutes. However, subjective sleep quality did not change. The researchers concluded: “Vasopressin promotes sleep time and improves sleep architecture after prolonged intranasal administration in elderly subjects” (11).

In 2002 Neveus et al. found that ten children responded positively to desmopressin (synthetic vasopressin), and they had more REM during sleep (12).

In 2003 Perras et al. found in twenty-six elderly men that arginine (bio-identical) vasopressin promoted only improved slow wave sleep and a general improvement in the neuroendocrine pattern of sleep (13).

Also in 2003 Lose et al. found in 144 female patients that desmopressin is an effective and well-tolerated treatment for nocturia (14).

Signs and Symptoms of Vasopressin Deficiency

Generally speaking, lack of vasopressin means ubiquitous dehydration of our bodies, especially our faces, causing fine wrinkles. In addition, I have found other clear signs of deficiency including low blood pressure (systolic less than 110 mm Hg and diastolic less than 60 mm Hg), crow’s feet, deeply sunken eyes backed into darkened eye sockets, double upper-eyelid fold (figure 2), soft eyeballs, dizziness when standing up after lying down, frequent bathroom trips—especially during daytime (polyuria)—and a blank stare due to constant low blood pressure.

For example, I recognize vasopressin-deficient patients by their blatant, definitive blank stares combined with deeply sunken eyes and adjacent crow’s feet. These signs stand out to even an unobservant medical practitioner.

These blank stares combined with dizziness symptoms indicate to me that both humans and lab animals have problems with memory when vasopressin is deficient.

Actor Sean Penn, age 47, appearing in the film, Milk; notice the crow’s feet, sunken eyes, blank stare, and double eyelid fold at an early age of only 47 years.

Dr. Hertoghe Explains the Advantages of Vasopressin

Dr. Thierry Hertoghe recently spoke in London, England, about the advantages of supplemental vasopressin. He said that vasopressin improves kidney health. He stated emphatically that signs and symptoms of a vasopressin deficiency are deep and sunken eyes, sharp wrinkles, soft eyeballs, poor memory, and dehydration folds on the upper eyelids. In his practice in Belgium he recommends bioidentical vasopressin to improve sleep by approximately forty-five minutes per night. He stated that vasopressin spray combined with oxytocin spray is often his effective treatment for schizophrenia. In reference to aging, Dr. Hertoghe said that vasopressin increases one’s chance of survival by a factor of four. He also advised that a lack of vasopressin might be a cause of short-term memory loss and low electrolytes, such as sodium.

Conclusions

Older Being Wiser

Vasopressin is key to the architecture and function of the brain. It is the learning hormone, and without it we become forgetful. Vasopressin significantly helps with improving processing speed and memory that decline from their peaks in the late teens. However, an older brain moving more slowly than its younger self is often just as accurate in other areas and may be more adept at reading others’ moods in addition to being more knowledgeable.

Thus, older can really mean being wiser when one supplements with vasopressin. And by being wiser I mean one becomes more diplomatic and more easily heads off interpersonal misjudgments and better navigates tricky social situations.

It behooves everyone to add an additional forty-five minutes of sound and needed sleep, especially during one’s senior years. That extra forty-five minutes allows the microglial cells in the brain to do their jobs and clean the brain (phagocytosis) of unwanted and dangerous amyloid toxins that accumulate during aging and that eventually result in plaques, tangles, and even Alzheimer’s disease.

References

  1. Gold PW et al, Nov. 1979, Lancet, 10;2(8150), pp. 992-994.
  2. Laczi F et al, 1982, Psychoneuroendocrinology, 7(2-3), pp. 185- 193.
  3. Laczi F, et al, Feb. 1983, Acta Endocrinol, 102(2), pp. 205-212.
  4. Laszio FA, Aug 1983, Z Gesamte, 1;38(15), pp. 413-415.
  5. Nebes RD et al, Jan 1984, Z Research, 11(1), pp.49-59.
  6. Till RE and Beckwith BE, May-June 1985, Peptides, 6(3), pp. 397-402.
  7. Hamburger-Bar R et al, Jan-Feb 1987, J Med Science, 23(1-2), pp.12-18.
  8. Millar K et al, May 1987, Psychol Med, 17(2), pp. 335-341.
  9. Perras B et al, Aug 1997, Psychoneuroendocrinology, 22(6), pp.387-396.
  10. Van Londen et al, Mar 1998, Psychol Med, 28(2), pp. 275-284.
  11. Perras et al, Feb 1999, Clinical Psychopharmacol, 19(1), pp. 28-36.
  12. Neveus et al, 2002, Acta Paediatr, 91(10), pp. 1121-1125.
  13. Perras et al, Feb 2003, J Clinical Psychopharmacol, 23(1), pp. 35-44.
  14. Lose G et al, Oct 2003, AM J Obstet Gynecol, 189(4), pp. 1106-1113.
  15. Becker, B. and R. E. Christensen. 1956, AMA Arch Opthalmol 56, pp. 1-9.