It is possible that you may never find the original article that mentions a research article on endorphins.
However, I have found a popular article about natural ways to make endorphins reviewed by an M.D.
Here is the closest excerpt (from the middle of the article) I could find to the effect you mentioned in your example of why the Internet
is so addictive - it is probably why a good book (eg. the Harry Potter books is also addictive):

"Get moved
We're not talking about packing up and renting a U-Haul. Dr. Fuhrman says that viewing beautiful art, watching a touching dramatic scene or even listening to an inspiring piece of music can produce endorphins. "A person who gets pleasure in life, from whatever source, will keep endorphins at a healthy level," he says.
Endorphin factor: 2, unless you're overwhelmed with emotion (think swooning, tear-filled eyes and a quickened heartbeat); that counts for 3."
http://www.yourhealthportal.com/endorphins-101-your-guide-natural-euphoria.html?pageNum=2

I also went to www.pubmed.com which contains Medline - the research source of choice for medical doctors,
and selected some references that may have been related to that research mentioned in your lost article.

2: Prog Neurobiol. 2008 Sep;86(1):1-21. Epub 2008 Jun 18.

Beta-endorphin and drug-induced reward and reinforcement.

Roth-Deri I, Green-Sadan T, Yadid G.

Neuropharmacology Section, The Mina and Everard Goodman Faculty of Life Sciences
and The Leslie and Susan Gonda (Goldschmied) Multidisciplinary Brain Research
Center, Bar-Ilan University, Ramat-Gan, Israel.

Although drugs of abuse have different acute mechanisms of action, their brain
pathways of reward exhibit common functional effects upon both acute and chronic
administration. Long known for its analgesic effect, the opioid beta-endorphin is
now shown to induce euphoria, and to have rewarding and reinforcing properties.
In this review, we will summarize the present neurobiological and behavioral
evidences that support involvement of beta-endorphin in drug-induced reward and
reinforcement. Currently, evidence supports a prominent role for beta-endorphin
in the reward pathways of cocaine and alcohol. The existing information
indicating the importance of beta-endorphin neurotransmission in mediating the
reward pathways of nicotine and THC, is thus far circumstantial. The studies
described herein employed diverse techniques, such as biochemical measurements of
beta-endorphin in various brain sites and plasma, and behavioral measurements,
conducted following elimination (via administration of anti-beta-endorphin
antibodies or using mutant mice) or augmentation (by intracerebral
administration) of beta-endorphin. We suggest that the reward pathways for
different addictive drugs converge to a common pathway in which beta-endorphin is
a modulating element. Beta-endorphin is involved also with distress. However,
reviewing the data collected so far implies a discrete role, beyond that of a
stress response, for beta-endorphin in mediating the substance of abuse reward
pathway. This may occur via interacting with the mesolimbic dopaminergic system
and also by its interesting effects on learning and memory. The functional
meaning of beta-endorphin in the process of drug-seeking behavior is discussed.

Publication Types:
Review

PMID: 18602444 - indexed for MEDLINE

5: Pharmacol Rev. 2007 Mar;59(1):88-123.

The endomorphin system and its evolving neurophysiological role.

Fichna J, Janecka A, Costentin J, Do Rego JC.

Laboratory of Experimental Neuropsychopharmacology, CNRS FRE 2735, IFRMP 23,
Faculty of Medicine & Pharmacy, University of Rouen, 22, Boulevard Gambetta,
76183 Rouen cedex, France.

Endomorphin-1 (Tyr-Pro-Trp-Phe-NH2) and endomorphin-2 (Tyr-Pro-Phe-Phe-NH2) are
two endogenous opioid peptides with high affinity and remarkable selectivity for
the mu-opioid receptor. The neuroanatomical distribution of endomorphins reflects
their potential endogenous role in many major physiological processes, which
include perception of pain, responses related to stress, and complex functions
such as reward, arousal, and vigilance, as well as autonomic, cognitive,
neuroendocrine, and limbic homeostasis. In this review we discuss the biological
effects of endomorphin-1 and endomorphin-2 in relation to their distribution in
the central and peripheral nervous systems. We describe the relationship between
these two mu-opioid receptor-selective peptides and endogenous neurohormones and
neurotransmitters. We also evaluate the role of endomorphins from the
physiological point of view and report selectively on the most important findings
in their pharmacology.

Publication Types:
Research Support, Non-U.S. Gov't
Review

PMID: 17329549 - indexed for MEDLINE

6: Nicotine Tob Res. 2007 Jan;9(1):9-20.

Sensitization to nicotine: how the animal literature might inform future human
research.

DiFranza JR, Wellman RJ.

Department of Family Medicine and Community Health, University of Massachusetts
Medical School, Worcester, MA 01655. difranzj@ummhc.org

Despite a rich neuroscience literature on sensitization, this phenomenon has been
neglected in clinical nicotine research. This paper offers a primer on the
neuroscience of nicotine sensitization for behavioral scientists, identifying key
concepts, potential theoretical and clinical implications, and directions for
future research. Sensitization to a drug occurs when repeated exposures to the
same dose produce greater responses. In animals, sensitization to nicotine,
morphine, alcohol, cocaine, amphetamine, and methamphetamine manifests as
increased locomotor activity. In animals, sensitization to nicotine begins with
the first dose and is maximal within 5-7 days. It involves multiple
neurotransmitters, receptors, and brain structures and cannot be attributed to
any single alteration. The processes involved in its induction and expression are
not identical. The neurologic changes associated with sensitization are not
consistent across drugs, suggesting that sensitization is not an accident of
neurophysiology but perhaps an exaggerated adaptive response. Sensitization is
incorporated into two theories of addiction: incentive-sensitization and
sensitization-homeostasis. Whether sensitization occurs in humans and how it is
expressed is unclear, as is its role in human addiction.

Publication Types:
Research Support, N.I.H., Extramural
Review

PMID: 17365732 - indexed for MEDLINE

9: Eur Neuropsychopharmacol. 2006 Jan;16(1):25-32. Epub 2005 Jul 25.

A hypothalamic endorphinic lesion attenuates acquisition of cocaine
self-administration in the rat.

Roth-Deri I, Mayan R, Yadid G.

Neuropharmacology Section, Faculty of Life Sciences and The Leslie and Susan
Gonda (Goldschmied) Multidisciplinary Brain Research Center, Bar-Ilan University,
Ramat-Gan 52900, Israel.

The present study explores the role of beta-endorphin-producing neurons of the
arcuate nucleus in the behavioral effects of cocaine (i.e. acquisition of cocaine
self-administration). Eight-week-old female rats were treated with a single
estradiol valerate injection that causes a progressive lesion that is specific to
beta-endorphin-producing neurons throughout the arcuate nucleus. Cocaine
acquisition was suppressed following estradiol valerate pretreatment, while water
reinforced behavior was similar to controls. Since estradiol valerate treated
rats exhibit low estrogen plasma levels, estrogen replacement was performed but
cocaine self-administration acquisition remained suppressed. In addition,
analysis of beta-endorphin, dopamine, and DOPAC tissue levels confirmed the
specificity of the endorphinic lesion resulting from estradiol valerate
treatment. The suppression of cocaine self-administration acquisition following
estradiol valerate treatment provides evidence for a significant role for
beta-endorphin in cocaine reward.

Publication Types:
Comparative Study

PMID: 16043329 - indexed for MEDLINE

13: Peptides. 2005 Apr;26(4):701-5. Epub 2004 Dec 19.

Deficit in beta-endorphin peptide and tendency to alcohol abuse.

Zalewska-Kaszubska J, Czarnecka E.

Department of Pharmacodynamics, Medical University of Lodz, Muszynskiego 1, PL
90-151 Lodz, Poland. jzalewska@pharm.am.lodz.pl

Human and animal studies suggest that there is a correlation between endogenous
opioid peptides, especially beta-endorphin, and alcohol abuse. It has been proven
that the consumption of alcohol activates the endogenous opioid system.
Consumption of alcohol results in an increase in beta-endorphin level in those
regions of the human brain, which are associated with a reward system. However,
it has also been observed that habitual alcohol consumption leads to a
beta-endorphin deficiency. It is a well-documented phenomenon that people with a
genetic deficit of beta-endorphin peptide are particularly susceptible to
alcoholism. The plasma level of beta-endorphin in subjects genetically at high
risk of excessive alcohol consumption shows lower basal activity of this peptide.
Its release increases significantly after alcohol consumption. Clinical and
laboratory studies confirm that certain genetically determined factors might
increase the individual's vulnerability to alcohol abuse.

Publication Types:
Review

PMID: 15752586 - indexed for MEDLINE

14: Neuropsychopharmacology. 2005 Feb;30(2):417-22.

Increased attributable risk related to a functional mu-opioid receptor gene
polymorphism in association with alcohol dependence in central Sweden.

Bart G, Kreek MJ, Ott J, LaForge KS, Proudnikov D, Pollak L, Heilig M.

The Laboratory of the Biology of Addictive Diseases, The Rockefeller University,
New York, NY 10021, USA. bartg@rockefeller.edu

The mu-opioid receptor (MOR), through its effects on reward and
stress-responsivity, modulates alcohol intake in both animal and human laboratory
studies. We have previously demonstrated that the frequently occurring A118G
single-nucleotide polymorphism (SNP) in exon 1 of the MORgene (OPRM1), which
encodes an amino-acid substitution, is functional and receptors encoded by the
variant 118G allele bind the endogenous opioid peptide beta-endorphin with
three-fold greater affinity than prototype receptors. Other groups subsequently
reported that this variant alters stress-responsivity in normal volunteers and
also increases the therapeutic response to naltrexone (a mu-preferring opioid
antagonist) in the treatment of alcohol dependence. We compared frequencies of
genotypes containing an 118G allele in 389 alcohol-dependent individuals and 170
population-based controls without drug or alcohol abuse or dependence. The A118G
SNP was present in the Hardy-Weinberg equilibrium with an overall frequency of
the 118G allele of 10.9%. There was a significant overall association between
genotypes with an 118G allele and alcohol dependence (p=0.0074). The attributable
risk for alcohol dependence in subjects with an 118G allele was 11.1%. There was
no difference in A118G genotype between type 1 and type 2 alcoholics. In central
Sweden, the functional variant 118G allele in exon 1 of OPRM1 is associated with
an increased attributable risk for alcohol dependence.

Publication Types:
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

PMID: 15525999 - indexed for MEDLINE

15: Psychoneuroendocrinology. 2004 Nov;29(10):1272-80.

Neuroendocrine response to casino gambling in problem gamblers.

Meyer G, Schwertfeger J, Exton MS, Janssen OE, Knapp W, Stadler MA, Schedlowski
M, Krüger TH.

Institute of Psychology and Cognition Research, University of Bremen, Grazer Str.
4, Postfach 33 04 40, 28359 Bremen, Federal Republic of Germany.

Problematic gambling is thought to be influenced by neurobiological mechanisms.
However, the neuroendocrine response to gambling is largely unknown. Therefore,
the effect of casino gambling on the sympathoadrenal system, the HPA-axis, and
pituitary hormones were analyzed. Fourteen male problem gamblers and 15
non-problem gamblers were examined in a balanced cross-over design. In the
experimental session, participants played blackjack in a casino wagering their
own money. During the control session, subjects played cards for accumulation of
points. Heart rate and endocrine measures were recorded at baseline, at 30, 60
and 90 min during gambling/card playing, and after the game. Heart rate and
norepinephrine levels increased with the onset of blackjack in both groups, with
problem gamblers showing significantly higher levels across the entire gambling
session. In addition, dopamine levels were significantly higher in problem
gamblers during casino gambling compared to non-problem gamblers. Cortisol levels
were transiently increased with the onset of blackjack in both groups. Casino
gambling as a "real life" situation induces activation of the HPA-axis and the
sympathoadrenergic system, with significantly more pronounced changes in problem
gamblers. These findings may contribute to a better understanding of
neuroendocrine disturbances in problem gambling.

Publication Types:
Clinical Trial
Comparative Study
Research Support, Non-U.S. Gov't

PMID: 15288706 - indexed for MEDLINE

17: Addict Biol. 2004 Sep-Dec;9(3-4):205-12.

Neuroendocrine pathways of addictive behaviour.

Kiefer F, Wiedemann K.

Department of Psychiatry and Psychotherapy, University Hospital of Hamburg,
Hamburg, Germany. kiefer@uke.uni-hamburg.de

Alcohol intake is known to modulate plasma concentrations of neuroendocrine
peptides. However, recent results suggest that the endocrine system may not only
respond passively to alcohol intake but that, vice versa, it also actively
modulates alcohol intake behaviour. The most coherent body of data concerns the
hypothalamo-pituitary-adrenocortical (HPA) axis, with low
corticotrophin-releasing hormone (CRH) being associated with more intense craving
and increased probability of relapse after acute detoxification. Leptin,
beta-endorphin and atrial natriuretic peptide (ANP), which indirectly regulate
the HPA system, also may modulate the intensity of craving or the intensity of
the alcohol withdrawal syndrome. Although most of the currently available data
demonstrate association rather than causality between neuroendocrine changes and
alcohol-related behaviours, they do provide testable hypotheses and open up
perspectives of treating alcohol dependence via manipulation of the
neuroendocrine axis.

Publication Types:
Review

PMID: 15511714 - indexed for MEDLINE

18: Neuro Endocrinol Lett. 2004 Aug;25(4):235-51.

The neurobiology of pleasure, reward processes, addiction and their health
implications.

Esch T, Stefano GB.

Charité - University Medicine Berlin, Institute for General Practice and Family
Medicine, Schumannstrasse 20/21, 10117 Berlin, Germany.

Modern science begins to understand pleasure as a potential component of
salutogenesis. Thereby, pleasure is described as a state or feeling of happiness
and satisfaction resulting from an experience that one enjoys. We examine the
neurobiological factors underlying reward processes and pleasure phenomena.
Further, health implications related to pleasurable activities are analyzed. With
regard to possible negative effects of pleasure, we focus on addiction and
motivational toxicity. Pleasure can serve cognition, productivity and health, but
simultaneously promotes addiction and other negative behaviors, i.e.,
motivational toxicity. It is a complex neurobiological phenomenon, relying on
reward circuitry or limbic activity. These processes involve dopaminergic
signaling. Moreover, endorphin and endogenous morphinergic mechanisms may play a
role. Natural rewarding activities are necessary for survival and appetitive
motivation, usually governing beneficial biological behaviors like eating, sex
and reproduction. Social contacts can further facilitate the positive effects
exerted by pleasurable experiences. However, artificial stimulants can be
detrimental, since flexibility and normal control of behavior are deteriorated.
Additionally, addictive drugs are capable of directly acting on reward pathways.
Thus, the concrete outcome of pleasant experiences may be a question of dose.
Moderate pleasurable experiences are able to enhance biological flexibility and
health. Hence, pleasure can be a resistance resource or may serve salutogenesis.
Natural rewards are mediated by sensory organ stimulation, thereby exhibiting a
potential association with complementary medical approaches. Trust and belief can
be part of a self-healing potential connected with rewarding stimuli. Further,
the placebo response physiologically resembles pleasure phenomena, since both
involve brain's reward circuitry stimulation and subjective feelings of
well-being. Pleasurable activities can stimulate personal growth and may help to
induce healthy behavioral changes, including stress management. However, more
research is needed to better understand the nature, neurobiology and maybe
dangerous aspects of pleasure. Also, a possible involvement of endogenous
morphinergic signaling has to be studied further.

Publication Types:
Research Support, U.S. Gov't, P.H.S.
Review

PMID: 15361811 - indexed for MEDLINE
Source(s):
http://www.pubmed.com
http://www.yourhealthportal.com/endorphins-101-your-guide-natural-euphoria....


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