Back to AVSJournals

Overview: the Pineal Gland Center of the Physical Brain

By Richard Bennett, Ph.D.

If anything could be called the center of the physical brain, it would have to be the Pineal Gland. This solid cone-shaped structure located at the roof of the posterior third ventricle is about the size of a grain of rice and weighs approximately 100 - 180 milligrams. It begins its composition at about the 36th day of gestation when two small cell masses-anlages-fuse together to form the gland. Almost undetectable at its beginning and still when it reaches differentiation at around birth, the gland is centered between the cerebellum and is attached to it. The gland is part of the circuitry involved in the translation of all visual messages received through the retina. Even though pineal glands have until recently been considered functionless phylogenetic relics, vestigiality has been imposed on the gland for no valid scientific reason as many advances in the past few decades have demonstrated its multi-faceted functions in humans and mammalians. The gland has also been referred to as the epiphysis, parietal eye, and in spiritual realms as the third eye. The pineal appears to be involved in synchronization of bodily functions(s) with the environment as a “regulator of regulators” and more recent research has demonstrated that the gland performs a pivotal, and perhaps critical role, in the identification of specific patterns of malignancies to include breast cancer and lymphomas. Strikingly, it has been changes in pineal activity that have been useful indicators in the identification of these other diseases and we see that changes in pineal activity and expression are indicators in compulsive behavior that leads to substance abuse and affective disorders.

As intriguing as the individuality of a fingerprint or the design of DNA, the gland varies so much that no two glands look alike. A lack of similarity in a normal functioning gland is of little or no importance, but when similar markers appear in specific forms of disease or in those who exhibit dramatic changes in behavior, it would seem imperative that the gland be examined in order to determine if its main function, that of synthesizing serotonin to melatonin, be impaired. An understanding of how the brain and body responds to a balanced - or imbalance - of melatonin presentation, and how disease or impairment of the gland could dramatically influence response, would be prognostic and therefore aid in treatment of disease or disease categories associated with a malfunctioning gland.

The synthesis of melatonin from serotonin takes place in the pineal gland. An N-acetylating enzyme converts serotonin to N-acetylserotonin; the latter is O-methylated through the action of hydroxyindole-O-methyltransferase (HIOMT). It is then metabolized to 5-hydroxyindoleacetaldehyde by the enzyme monoamine oxidase (MAO). The activity of MAO in the destruction of serotonin and that of hydroxyindole-O-methyltransferase in the O-methylation of N-acetylserotonin provide convenient vehicles for controlling the amount of melatonin, N-acetyl-5-methyoxytryptamine, present in an organism at anyone time. The presence of melatonin can now be quickly and accurately measured in bodily fluids and tissue, and though we have at hand the basic biochemistry and neuroanatomical connections of the gland so that we can see how normal and abnormal secretions occur, there is the unanswered question as to why. We do know that concretions of the gland can interfere with the synthesis of serotonin to melatonin and consequently the secretion of melatonin, but could these concretions of the gland be evidence of previous abnormalities that could be indicative of past, present, or impending physiological and/or psychological disease? Or could it be that healing has been achieved should there be a remission in such diseases as breast cancer or lymphoma? Or major change(s) in behavior? Considering all of this, serotonin and melatonin assay and Magnetic Resonance Imaging of the gland, applied together, could prove useful in the diagnosis, treatment, and monitoring of disease or impairment of the gland that cross-communicates to a specific disease category.

Pineal melatonin plays a major role in affective disorders such as Seasonal Affective Disorder and Binge Eating Disorder. These are just two disorders in which a single or a combination of maladies often couples with radical departures from normal behavior. Depression and self-imposed isolation are accompanied with little or no regulation of day/night cycles - a circadian rhythm - and are symptomatic of melatonin imbalance. These disorders are often resolved when circadian rhythm is restored. While circadian rhythm can be restored in a number of ways, Interactive Light Therapy that resets the biological clock is one way to induce a melatonin response as can the administration of endogenous melatonin. Sham or functional pinealectomy has also been an intervention that restores a circadian rhythm. Research has also demonstrated that the extent and action of pineal melatonin at certain melatonin receptors may account for its reputed oncostatic and immunological effects as experiments worldwide have cemented the relationship between neuroendocrine and immune systems. Other studies indicate that melatonin inhibits tumor growth when combined with Interluken-2, as it appears to restore a circadian rhythm in those with small cell cancers, thereby pointing to a somewhat direct relationship with the pineal gland. If this were so, it would be possible that a diseased gland that does not effectively control the synthesis of melatonin might do so if treated with IL-2.

Life could begin with a genetic mutation of the gland that could interfere with the normalcy and regularity of circadian rhythm(s). As example, rhythms could be other than circadian in that one could be genetically predisposed to either ultradian or infradian rhythms that could be markers of impending compulsive behavior that will -defiantly - lead to substance abuse. Here’s why. Ultradian cycles are those that occur more frequently than the normal 24-hour cycle and compares to the cycles of those who are dependent on opiates, barbiturates, alcohol, or any other depressant(s) where the wake/sleep cycle is manipulated by quantity and/or repetition. It is accepted universally that prolonged use of opiates or depressants create shorter duration of the effects and therefore requires more quantity or better quality to achieve the sought after satiation. Resultantly, the use of opiates or depressants may cause 3-4 or more wake/sleep cycles per 24 hour period, and therefore completely disrupt melatonin presentation that manage circadian rhythm. Infradian rhythms have similar responses but for very different reasons. As infradian rhythms are those that occur less frequently than 24-hour rhythms, they compare to the wake/sleep cycles of those who use psychoactive drugs such as cocaine and the amphetamines and where the single wake cycle often lasts for days at a time. Although conclusive evidence supporting the genetics of compulsive behavior that leads to substance abuse - whether infradian, ultradian, or circadian rhythms be a factor - is still in the research and mapping stage of the genome, we are finding that hormones and neurotransmitters as genetic components appear to be a result of genetic interaction on behavior. This argument for genetic influence seems to be winning out as we are learning that the switching on and off of genes can be influenced by many factors or actions that is now identified as complex behavior. It is also recognized that genes for behavior are no more unusual than genes for development and variations in both cases will be the substance for ongoing debate. Dysfunction or difference in gene characteristics can be responsible for all sorts of innate behavior simply because humans vary in the way they respond to most stimuli that is mediated through neurotransmitters or hormones. Yet once we identify the genetics that influence behavior, we can begin to design specific science-based interventions, effectively making the behavior as treatable as any other physiologically rooted disease or disorder whether the cause is a result of circadian, ultradian, or infradian rhythm that is a result of gene expression. As demonstrated over and over again, if the instruction is faulty from the very instant the cell begins to divide, the end result will be faulty. Not enough to cause cell death, but enough to build a protein that will build the being that will be predisposed to the behavior. With that thought, let us presume that altered synthesis of serotonin to melatonin as a result of a genetically altered pineal gland will certainly affect and alter circadian rhythms because of that gene expression. Should altered circadian rhythms parallel the schedule of one who is inclined to compulsive use of drugs, it would be a fair assumption that it would be easier for those with genetically induced non-circadian rhythms to slip into compulsive substance abuse or other forms of compulsive behavior that have a dysfunctional circadian component. That component - the relationship with day and night - ties to a common denominator: the Pineal Gland! Quite a role for something so small and once considered insignificant!

Back to AVSJournals