has been an abundance of research released over the past
18 months shedding new light on an old problem --the effects
of tobacco, alcohol and other drugs on the central nervous
system. Perhaps fueled by funds available through tobacco
settlement monies, we see a particular increase in the
amount of nicotine research published.
Three main themes arise. First, all drugs effect the brain
- some very substantially, particularly in adolescents. Second,
the plasticity of the brain and its amazing ability to compensate
for change, can lead to drug-crippled brains. Thirdly, certain
neurons appear to be more resilient than others to drug effects.
Most drugs (cocaine, alcohol, etc.) tend to work by increasing
dopamine levels in the amygdala and other pleasure regions
of the brain.
time a substance significantly changes a neurotransmitter
(nerve cell communication chemicals), it will cause damage
with chronic use. The reason for this is the brain's inherent
need and ability to repair its own systems.
what's going on. Think of a pleasant experience (a romantic
evening, sunbathing on the beach, a double decker hot fudge
sundae....). Feel the pleasure? What you are biologically
doing is secreting dopamine, a major brain chemical, into
the amygdala region of your brain. Receptor sites (dopamine
doorways) open up to receive the chemical and cause that pleasure
part of your brain to fire. It is nice, isn't it? That's what
most drugs do, only on a much more intense basis. They cause
huge amounts of dopamine to flood into the amygdala region.
problem comes with repeated use. The brain is efficient and
self-correcting. So once you start providing this intense
serge of dopamine on a regular basis, the brain tries to compensate
for the disturbance by either reducing production of dopamine
or locking and removing dopamine receptor sites. (The brain,
as living tissue, makes no value judgment on whether the feeling
was good or bad, it is just seeking to correct an imbalance
you have created). Now you have established tolerance. This
means a person will have to use more of the drug to get the
same effect because the brain has reduced its own production
and limited the dopamine doorways or receptor sites.
Imagine what happens after long-term chronic use. Natural
production of the neurotransmitter has all but been shut off
as the brain realizes it is being provided artificially, so
doesn't need to waste energy producing it on its own. Receptor
sites or avenues for the neurotransmitter to attach in the
brain have been limited and severely reduced in the brain's
attempt to reduce the overactive region. The brain has now
become crippled. It essentially has lost its natural ability
for pleasure. The drug addict who is attempting to withdraw,
is faced with a pleasure center that doesn't work. Not only
does the brain not produce dopamine in natural quantities,
it has removed many of the receptor sites or doorways in the
drug-free addict will feel no pleasure in imaging a candlelight
dinner, sunbathing on the beach, or even eating a double decker
hot fudge sundae. What has been created is a brain which can
feel no pleasure in anything unless done through artificial
means. It is easy to see how life would not feel worth living
and why the suicide rate during recovery is so high and successful
recovery rates are so low.
major effect of various drugs on the brain is the actual deterioration
of brain nerve cells. Alcohol, nicotine, cocaine and ecstasy
all are known to degenerate gray matter, and thereby reduce
the volume of some key brain regions. This loss can cause
processing problems in many of the decision-making areas of
the cortex as well as interfere with memory systems. Research
is now even showing that different aged brains are affected
in different ways. For example, it has been shown that alcohol
reduces the volume of the hippocampus in adolescent brains,
but apparently not in adult brains. The reduction is more
severe in teens that start alcohol use early and often. The
hippocampus is responsible for processing new information
Drugs do not affect all brain cells equally. There are two
main types of neurons in your brain. Fatty and plain. Some
nerve cells are covered in a fatty layer called a myelin sheath.
These cells are able to transmit electrical signals ten times
faster than than the uncoated neurons. The fatty covering
lends a somewhat whitish appearance to the cells, hence the
name white matter. Gray matter would be composed of unsheathed
or plain neurons. When nerve cells in the brain are damaged
from drugs, it tends to be the gray matter rather than the
white. This would indicate that the myelin sheath may offer
some protection against chemical substances.
there any "safe" drugs? Biologically speaking, it doesn't
appear so. It seems the brain's natural healing powers and
compensation skills can turn into our own worst enemy where
drugs are concerned. Obviously the brain's ability to move
into that compensation mode varies from person to person and
it seems that those with the systems quickest to adjust are
the brains most likely to become addicted.
there is any good news to this story it could come from the
pharmaceutical industry which is looking for some type of
recovery aid for addicted brains. There is hope that medicines
may become available to help persons through their recovery
by helping the brain heal faster, restore receptor sites sooner
or restore dopamine production. Until then, the only hope
for the addicted brain is time and continued research.
1. Adolescent polydrug use and violence in the United States.
Dornbusch, Sanford M.; Lin, I- Chun; Munroe, Paul T.; Bianchi,
Alison J. International Journal of Adolescent Medicine &
Health. 1999 Jul-Dec Vol 11(3-4) 197-219
The association between cigarette smoking and drug abuse in
the United States. Lai, Shenghan; Lai, Hong; Page, J. Bryan;
McCoy, Clyde B. Journal of Addictive Diseases. 2000 Vol 19(4)
3. Anabolic androgenic steroids affects alcohol intake, defensive
behaviors and brain opioid peptides in the rat. Johansson,
Pia; Lindqvist, Ann-Sophie; Nyberg, Fred; Fahlke, Claudia.
Pharmacology, Biochemistry & Behavior. 2000 Oct Vol 67(2)
Age-related brain volume reductions in amphetamine and cocaine
addicts and normal controls: Implications for addiction research.
Bartzokis, George; Beckson, Mace; Lu, Po H.; Edwards, Nancy;
Rapoport, Ruth; Wiseman, Eve; Bridge, Peter. Psychiatry Research:
Neuroimaging. 2000 Apr Vol 98(2) 93-102.
Chronic cocaine treatment induces dysregulation in the circadian
pattern of rats' feeding behavior. Giorgetti, Marco; Zhdanova,
Irina V. Brain Research. 2000 Sep Vol 877(2) 170-175
Selective neurotoxic effects of nicotine on axons in fasciculus
retroflexus further support evidence that this a weak link
in brain across drugs of abuse. Carlson, Janice; Armstrong,
Brian; Switzer, Robert C., III; Ellison, Gaylord. Neuropharmacology.
2000 Oct Vol 39(13) 2792-2798
Running and cocaine both upregulate dynorphin mRNA in medial
caudate putamen. Werme, Martin; Thoren, Peter; Olson, Lars;
Brene, Stefan. European Journal of Neuroscience. 2000 Aug
Vol 12(8) 2967-2974.
Subacute onset of oculogyric crises and generalized dystonia
following intranasal administration of heroin. Schoser, Benedikt
G. T.; Groden, Christoph. Addiction. 1999 Mar Vol 94(3) 431-434
Self-administration behavior is maintained by the psychoactive
ingredient of marijuana in squirrel monkeys. Tanda, Gianluigi;
Munzar, Patrik; Goldberg, Steven R. Nature Neuroscience. 2000
Nov Vol 3(11) 1073-1074.
Memory disturbances in "Ecstacy" users are correlated with
an altered brain serotonin neurotransmission. Reneman, Liesbeth;
Booij, Jan; Schmand, Ben; van den Brink, Wim; Gunning, Boudewijn.
Psychopharmacology. 2000 Feb Vol 148(3) 322-324.
Brain atrophy and neuronal loss in alcoholism: A role for
DNA damage? Brooks, P. J. Neurochemistry International. 2000
Nov-Dec Vol 37(5-6) 403-412.
The influence of glycine on EEG parameters and sensorimotor
activity in normal and alcoholic subjects. Mashkova, V. M.
Human Physiology. 2000 Jul-Aug Vol 26(4) 388-392.
Alcohol enhances characteristic releases of dopamine and serotonin
in the central nucleus of the amygdala. Yoshimoto, K.; Ueda,
S.; Kato, B.; Takeuchi, Y.; Kawai, Y.; Noritake, K.; Yasuhara,
M. Neurochemistry International. 2000 Oct Vol 37(4) 369-376.
Hippocampal volume in adolescent-onset alcohol use disorders.
De Bellis, Michael D.; Clark, Duncan B.; Beers, Sue R.; Soloff,
Paul H.; Boring, Amy M.; Hall, Julie; Kersh, Adam; Keshavan,
Matcheri S. American Journal of Psychiatry. 2000 May Vol 157(5)
15. 1 /Impulsivity, suicide and violence risk in hospitalized
alcoholics: Sex differences. Moussas, G. I.; Dadoutis, G.;
Botsis, A.; Lykouras, L. Psychiatriki. 1999 Jul-Aug Vol 10(3)
228- 235 .
Suicidal ideation among college students in the United States.
Brener, Nancy D.; Hassan, Sohela Sabur; Barrios, Lisa Cohen.
Journal of Consulting & Clinical Psychology. 1999 Dec
Vol 67(6) 1004-1008.
Auditory and visual event-related potentials in alcoholics:
Abnormalities of components and brain electrical field. Olbrich,
H. M.; Maes, H.; Gann, H.; Hagenbuch, F.; Feige, B. European
Archives of Psychiatry & Clinical Neuroscience. 2000 Vol
"Loss of control" in alcoholism and drug addiction: A neuroscientific
interpretation. Lyvers, Michael. Experimental & Clinical
Psychopharmacology. 2000 May Vol 8(2) 225-245.
Marijuana, alcohol and actual driving performance. Ramaekers,
J. G.; Robbe, H. W. J.; O'Hanlon, J. F. Human Psychopharmacology
Clinical & Experimental. 2000 Oct Vol 15(7) 551- 558.