5-HTP for Age-Related Serotonin Decline
It's Time to Resign From:
The Sero-Less Gravity Club
Whose Members are Gravely Deficient in Serotonin

By Gail Valentine, D.O.

re you anxious about what the future might bring? Does worry keep you awake long after you should be sleeping? Do you get a sinking feeling in the pit of your stomach when someone confronts you? Are there days when you would rather stay home and not go out to face the world because you are depressed? Do you often find yourself inexplicably reaching for food when you're overwhelmed by your feelings?

Welcome to the "SERO-LESS" Gravity Club, whose member's brains are mildly to gravely deficient in serotonin. Serotonin is the molecule principally responsible for elevating mood. Being "sero-less" makes you heavier than you need to be, unable to escape the bonds of gravity. Serotonin can give you gravity freedom and make your worries weightless.

If you look around, you will notice that it's not the same Club it once was, comprised of people with formal medical diagnoses of major depression. The Club now includes a whole new class of additional members. Actually, these new members were eligible for membership before . . . but most of them just never knew it. We now know, as appalling as this is, that the new members of the "Sero-Less" Gravity Club potentially include everyone. And that means you. The reason for this is: it has now been established scientifically that the brain's serotonin system declines with age.1 In other words, the greater your age, the less serotonin you are likely to have.

The brain's serotonin system has now
been established to decline with age.

Serotonin is the primary brain molecule associated with mood and behavior. The reason for this widely-held recognition is due, in part, to the success of Prozac and other selective serotonin reuptake inhibitors (SSRIs). SSRIs work to increase the utility of serotonin in your brain. In so doing, SSRIs have achieved positive acclaim for those suffering from depression, anxiety, sleep disturbance, weight problems, migraine headaches, chronic pain and many other conditions.

However successful Prozac and other SSRIs have been at alleviating illness, there can be significant side effects associated with their use. Additionally, with items foreign to the brain and body (xenobiotics), there may be unknown effects on brain chemistry. Fortunately, however, drugs are not the only way to increase serotonergic activity or serotonin levels. There is now a safe and natural drug alternative for sero-less sufferers. The alternative is 5-HTP (5-hydroxytryptophan).

5-HTP is a natural plant extract from the plant griffonia simplicifolia. 5-HTP increases brain serotonin utility just like SSRIs do, but it does so in a different way. Prozac and other SSRIs work to prolong the use of serotonin in the brain by selectively and unnaturally blocking its uptake into the neuron, thus helping to maintain higher levels of serotonin in the synaptic spaces between neurons. This is why they are called selective serotonin reuptake inhibitors. Another way to explain this is that SSRIs prevent serotonin from being taken back up into the neuron, thereby leaving more serotonin available for "reuse." So SSRIs do not make more serotonin but keep reusing old serotonin. 5-HTP, which is the direct precursor for making serotonin in your brain, replenishes or creates more serotonin. Plus, unlike SSRIs, 5-HTP has no significant side effects.

There is now a safe and natural drug
alternative for sero-less sufferers.
The alternative is 5-HTP

Knowledge of serotonin did not start with SSRIs. There were a great many people taking the amino acid tryptophan during the pre-Prozac days of the 1980s - 15 million Americans according to the Center for Disease Control - and many, if not most, had at least a cursory knowledge of serotonin. So there was already a head of steam on the public's desire to think highly of serotonin. Tryptophan paved the way for general widespread acceptance of the benefits of serotonin for Prozac and other SSRIs and now for 5-HTP.

5-HTP is a metabolite of the amino acid tryptophan, both of which are precursors to serotonin. Tryptophan converts to 5-HTP, which converts to serotonin. The difference is that 5-HTP is the immediate precursor to serotonin and more easily restores adequate levels of serotonin. In fact, studies have shown it to work better than tryptophan in many cases, establishing benefits for 5-HTP that have never been clearly established for tryptophan. Moreover, unlike tryptophan, there is evidence that 5-HTP raises levels of the neurotransmitters noradrenaline and dopamine, providing an added tonic-like effect - a refreshing, restorative feeling. Thus, 5-HTP delivers a multiplicity of neurotransmitter bonuses, unlike SSRIs or even tryptophan,* and without the risks or side effects associated with drugs.

*Use of tryptophan is rather moot because the FDA ban, following the Showa Denko batch contamination of 1989, is still in effect.

Serotonin also operates in another way. It plays a principal role in appetite satisfaction through its effect on the release of a hormone produced in the gut, cholecystokinin (CCK). When released, CCK travels up the vagus nerve to the brain's hypothalamus where it interacts with serotonin to lessen appetite or modulate feeding and satiety systems.2,3 There are different types of serotonin receptors (the sensors through which serotonin exerts its influence) in the brain which have been found to have a variety of different applications. The now infamous anorectic drug dexfenfluramine (Redux) produced its anorectic effect (reduced desire to eat) by selectively enhancing serotonin's impact on specific receptors and by presumably enhancing release of dopamine.4 However, Redux was a drug (it has now been recalled) with clearly unacceptable risks.

Another mechanism for weight control is the process of thermogenesis whereby the supervisory mitochondria of adipose (brown) fats cells are induced to working overtime by burning more fat for energy than the body might normally require. Certain serotonergic drugs such as the discredited dexfenfluramine are thought to possibly operate through thermogenesis. Although this has never been established. There is a probe component of the serotonergic system that is thought to play a possible role in thermoregulatory activity. It does this by activating a mode of metabolic thermogenesis governed by a mechanism that operates while we sleep.5 What we do know, however, is that 5-HTP has been found to increase thermogenesis as it increases serotonin. 5-HTP increases thermogenesis, independently too, even when it doesn't increase serotonin.6,7

There are other functions associated with serotonin that enhance spatial memory, reduce anxiety, lessen headaches, and provide relief from fibromyalgia, PMS, panic attacks, and obsessive-compulsive behavior. Inadequate levels of serotonin have been found to accompany aggressive or violent outbursts and to impede recovery from alcoholism. It is hardly necessary to go further. Serotonin is one of the most important molecules in the body and maintaining adequate levels may be one of the most important goals of your life.

5-HTP, which is the direct precursor for
making serotonin in your brain, replenishes
or creates more serotonin. Plus, unlike
SSRIs, 5-HTP has no significant side effects.

A breakthrough study has now established that serotonin production and utility falls off with age. Conducted by Carolyn Meltzer, M.D., and her colleagues at Pittsburgh Medical Center this study represents the first solid evidence of age-related serotonin decline (first announced last fall at the annual meeting of the Society for Neuroscience).7 Given the impact of her findings, it is odd that her presentation was not picked up by the press. This is even more noteworthy an omission when you realize that serotonin is probably the molecule of the entire 1990s, about which far more has been written than any other molecule in the human brain.

What Dr. Meltzer did was to give a radioactive form of the drug altanserin (a radiotracer that adheres to specific serotonergic receptors) to a range of younger and older healthy people (ages ranging from 18 to 76). Then she scanned and took pictures of the areas of their brains where a specific binding site (a receptor) for serotonin is known to be distributed, where these specific receptors for serotonin are most dense. When compared to detailed pictures of the participant's brain anatomy taken with magnetic resonance imaging (MRI) equipment, prior to the binding-site brain scans, the researchers found a clear correlation of age to serotonin: the older the participants, the less serotonin and serotonin activity. Although prior postmortem studies have suggested that the serotonergic system winds down with age, this is the first study to demonstrate that this is indeed the case.

Prior research with rats has shown that aging affects the ability of the brain to process neurological information, according to findings published in the January issue of the Journal of Neuroscience Research.8 In this research report, the authors conclude that serotonin neuron loss and reduced serotonin production are occurrences of normal aging. By extrapolating from animals to humans, they conclude that late-life diseases characterizable as neuropsychiatric may contribute to behavioral changes commonly observed in the elderly population. This may seem like a "no brainer" because ample research shows that depression is causally related to deficits in serotonergic neurotransmission. Yet it is another nail in the coffin of the belief in "normal" aging, which suggests that depression is a consequence of aging and something that we can do nothing about. Age-related changes in serotonin neurons may predispose the elderly to develop depression, but serotonin can be replaced and the associated problems lessened or eliminated.

What we do know, however, is that 5-HTP
has been found to increase thermogenesis
as it increases serotonin. 5-HTP increases
thermogenesis, independently too, even
when it doesn't increase serotonin.

A body of evidence seems to indicate that the cognitive impairment of Alzheimer's disease may be accelerated by disturbances of cholinergic and serotonergic function, with more emphasis on serotonergic dysfunction. There is increasing support that serotonergic dysfunction is responsible for a significant portion of the behavioral aspects of Alzheimer's disease.

Up until the Meltzer study, the connection between aging - and age-related cognitive and mood disorders - and serotonin decline has depended largely on post mortem studies. These post mortem studies are limited in their ability to predict the influence of less serotonin on human biochemistry in terms of mood or behavior.

Groucho Marx once said that he would resign if anyone ever made him a member of their club, because he would not want his reputation tarnished by any organization with standards so low that it would accept him as member. The joke very well applies to the Sero-Less Gravity Club. Only it is not a joke, because the consequences are too severe. Being caught anywhere without adequate levels of serotonin is not funny. Accepting the idea of serotonin decline as inevitable, as just part of "natural" aging, is as silly as acquiescing to the notion that it is unnatural to supplement with hormones such as natural estrogen or natural progesterone. Fortunately, the advent of 5-HTP enables us to overturn the hourglass and resign in advance from the Sero-Less Gravity Club.


  1. Meltzer CC, Smith G, DeKosky ST, Pollock BG, Mathis CA, Moore RY, Kupfer DJ, Reynolds CF 3rd. Serotonin in aging, late-life depression, and Alzheimer's disease: the emerging role of functional imaging. Neuropsychopharmacology 1998;18:407-430.
  2. Balleine B, Davies A, Dickinson A. Cholecystokinin attenuates incentive learning in rats. Behav Neurosci 1995 Apr;109(2):312-319.
  3. Hoebel BG. Brain neurotransmitters in food and drug reward. Am J Clin Nutr. 1985 Nov;42(5 Suppl):1133-1150.
  4. Balcioglu A, Wurtman RJ. Dexfenfluramine enhances striatal dopamine release in conscious rats via a serotoninergic mechanism. J Pharmacol Exp Ther. 1998 Mar;284(3):991-997.
  5. Schwartz PJ, Wehr TA, Rosenthal NE, Bartko JJ, Oren DA, Luetke C, Murphy DL. Serotonin and thermoregulation. Physiologic and pharmacologic aspects of control revealed by intravenous m-CPP in normal human subjects. Neuropsychopharmacology 1995 Oct;13(2):105-115.
  6. Serra F, LeFeuvre RA, Slater D, Palou A, Rothwell NJ. Thermogenic actions of tryptophan in the rat are mediated independently of 5-HT. Brain Res. 1992 Apr 24;578(1-2):327-334.
  7. Lin MT, Tsay HJ, Su WH, Chueh FY. Changes in extracellular serotonin in rat hypothalamus affect thermoregulatory function. Am J Physiol 1998 May;274(5 Pt 2):R1260-R1267.
  8. Dugar A, Lakoski JM. Serotonergic function of aging hippocampal CA3 pyramidal neurons: electrophysiological assessment following administration of 5,7-dihydroxytryptamine in the fimbria-fornix and cingulum bundle. J Neurosci Res 1997;47:58-67.

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