Hi again Lisa,
I found the message that was sent to me awhile back. I just copied the
whole thing and pasted it here for you.
Maria
>this is the list of abstracts I found in Medline a year or so ago. there
>are a number of free entry points to search Medline; I think I used the
>Community of Scientists. the articles themselves can be located in a
>medical library at a medical school, or they can be purchased on line
>through CARL.
>
>I think the early ones predate the development of psychiatric
>medications, which are probably safer and more effective than things like
>megadoses of B6.
>
>the gist of it seems to be that there is a large mass of nerve tissue
>surrounding the gut that controls digestive function more or less
>independently of the central nervous system (e.g., brain). this tissue
>uses serotonin (5-HT) for its own communications and specifically to
>control smooth (involuntary) muscle such as that in the gut wall. the
>gut only releases what it doesn't need for its own purposes to rest of
>the body. in active celiac disease, the gut secretes so much serotonin
>that the central nervous system (e.g., brain) becomes deficient of both
>serotonin and the precursors (stuff it needs to make it).
>
>one of my early symptoms was an insomnia that would awaken me in the wee
>hours, my mind racing, and not let me fall asleep until just before I had
>to get up. my naive suspicion is that it was related to the excess of
>serotonin in the gut.
>
>when I succumbed to a major depressive episode (atypical) about a year
>after my thyroid quit (not Hashimoto's), they tried to give me (liquid, I
>don't tolerate corn either) Prozac, an SSRI (selective serotonin reuptake
>inhibitor). this prevented me from sleeping for a week or so before they
>decided to try something else. to me, it felt to me like the other
>insomnia, as if the SSRI further aggravated the excess of serotonin in my
>gut.
>
>the next thing they tried was (liquid, again) Sinequan, a tricyclic.
>this worked better for a while. but subsequent research suggests that
>people with driven, moody personalities and a history of hypothyroidism
>who are given a tricyclic have an increased risk of converting to Bipolar
>II (several days of hypomania (elevated mood and increased activity, not
>requiring hospitalization) separating weeks of marked depression).
>Bipolar II may be more closely related to atypical depression than to
>Bipolar I (manic depression). that is what happened to me.
>
>there is some evidence that a better prognosis might have been achieved
>with an MAOI (mono amine oxidase inhibitor), but they do not want to try
>switching me now because they are concerned with triggering full blown mania.
>
>the citation for that last paper, which is not celiac related but solely
>concerned with the conversion from unipolar depression to bipolar
>depression, has wandered off for now, but if you want it I'll run it down.
>
> Douglas in Pittsburgh to us will be years and long days
><[log in to unmask]> with false kings and withering fruit-crops
> - Merlin: Hoianau -
>-------------------------------
>
> Celiac Disease and Monoamine Metabolism
>
>78065469 DN Challacombe, Dawkins PD, Baker P,
> Increased tissue concentrations of
> 5-hydroxytryptamine in the duodenal mucosa of
> patients with coeliac disease,
> Gut 18: 11, 882-6, Nov 1977
>
> Tissue concentrations of 5-HT have been
> measured in the duodenal mucosa of adults
> and children with coeliac disease and were
> found to be significantly higher than
> those from a control group. This finding may
> be associated with hyperactivity or
> hyperplasia of enterochromaffin (EC) cells in
> the duodenum of patients with coeliac
> disease and could also be directly related to
> described abnormalities of 5-HT
> metabolism in this disease.
>
>82118189 K Sjolund, Alumets J, Berg NO, Hakanson R,
> Sundler F,
> Enteropathy of coeliac disease in adults:
> increased number of enterochromaffin
> cells in the duodenal mucosa,
> Gut 23: 1, 42-8, Jan 1982
>
> Twenty-nine adult patients with coeliac disease
> and 39 patients with a normal
> duodenal morphology were studied with respect
> to the 5-HT containing
> enterochromaffin cells. Their number in
> duodenal biopsies was assessed by
> flourescence histochemistry and they were
> examined by immunohistochemistry for
> peptides known or believed to occur in
> enterochromaffin cells. Antisera used were
> raised against substance P, motilin, and
> leu-enkephalin. In addition, the
> concentration of 5-HT was determined
> chemically. In adult coeliac disease there was
> a significant increase in the number of
> duodenal enterochromaffin cells compared
> with the control group. The concentration of
> 5-HT in the duodenal mucosa was also
> greatly increased. Substance P was found in a
> minority population of
> enterochromaffin cells. These cells were very
> few and did not increase in number in
> coeliac disease. Motilin cells were distinct
> from enterochromaffin cells. No
> enkephalin immunoreactive cells were found in
> the biopsies.
>
>83040896 C Hallert, Derefeldt T,
> Psychic disturbances in adult coeliac
> disease.
> I. Clinical observations,
> Scand J Gastroenterol 17: 1,
> 17-9, Jan 1982
>
> Adult coeliac patients living in a defined area
> of Sweden were examined for a
> history of major psychiatric illnesses
> occurring before the coeliac disease had been
> diagnosed. Eight of 42 patients without
> dermatitis herpetiformis (19%) and one
> medical control subject had attended a
> psychiatric clinic over a 10-year period for
> neurotic disorders (p less than 0.05), mostly
> depression. Our study shows that
> psychiatric illness may be severe in
> undiagnosed adult coeliac patients. It was
> found to be the commonest reason for granting
> disability pension in our series,
> having occurred in altogether six patients.
>
>83040897 C Hallert, Astrom J,
> Psychic disturbances in adult coeliac
> disease.
> II. Psychological findings,
> Scand J Gastroenterol 17: 1,
> 21-4, Jan 1982
>
> Psychiatric illness has been observed to be a
> main cause of disability in
> undiagnosed coeliac disease. A consecutive
> series of 16 patients with newly
> detected adult coeliac disease underwent
> assessment of personality by means of MMPI.
> The coeliacs scored high, 70.3 +/- 12.5, only
> on MMPI scale 2 ('depression'), which
> was the only significant difference from
> matched surgical controls. The score
> correlated 0.66 with daily fat excretion (p
> less than 0.05) but was unrelated to
> abdominal complaints. The general intellectual
> level, assessed by the SRB test, was
> similar in coeliacs and controls. Our results
> suggest that depressive
> psychopathology is a feature of adult coeliac
> disease and may be a consequence of
> malabsorption.
>
>
>
>83040898 C Hallert, Astrom J, Sedvall G,
> Psychic disturbances in adult coeliac
> disease.
> III. Reduced central monoamine metabolism and
> signs of depression,
> Scand J Gastroenterol 17: 1,
> 25-8, Jan 1982
>
> Untreated adult coeliac patients have
> previously been shown to have a high frequency
> of depressive symptoms as reported previously
> in a personality inventory (the MMPI).
> In the present study we determined the
> concentrations of three major monoamine
> metabolites in samples of lumbar cerebrospinal
> fluid of ten consecutive adults with
> newly detected coeliac disease. They showed
> significant reduction in levels of
> 5-HIAA (70.3 +/- 25.4 pmol/ml), HVA (128.2 +/-
> 58.3 pmol/ml), and MOPEG (27.7 +/-
> 7.4 pmol/ml), indicating reduced central
> metabolism in all three monoamine pathways.
> The concentrations, in particular that of
> MOPEG, were inversely correlated with
> depressive symptoms reported on the MMPI scale
> 2 ('depression'), which conforms with
> current concepts on the pathogenesis of
> depression.
>
>83040909 C Hallert, Martensson J, Allgen LG,
> Brain availability of monoamine precursors
> in adult coeliac disease,
> Scand J Gastroenterol 17: 1,
> 87-9, Jan 1982
>
> Adults with untreated coeliac disease show
> signs of reduced central monoamine
> metabolism. The reason is obscure, and in the
> present study we investigated the
> brain availability of the monoamine precursors
> tryptophan and tyrosine in 11
> untreated coeliac patients. The brain
> availability appeared to be unaffected in
> most of the patients, and the rise in serum
> tryptophan levels after oral casein
> administration was similar in coeliac and
> control subjects. Four of the 11 coeliac
> patients showed impaired brain availability
> with respect to tryptophan. Since they
> comprised all with a history of major
> psychiatric illness, this observation may have
> therapeutic implications for the management of
> depression in adult coeliac
> patients.
>
>83045491 C Hallert, Allenmark S, Larsson-Cohn U, Sedvall
> G,
> High level of pyridoxal 5'-phosphate in the
> cerebrospinal fluid of adult celiac
> patients,
> Am J Clin Nutr 36: 5, 851-4,
> Nov 1982
>
> Adults with intestinal malabsorption due to
> celiac disease show reduced central
> serotonin metabolism, probably induced by a
> lack of essential dietary factors.
> Investigating a role proposed for vitamin B6
> deficiency, a regular finding in
> untreated celiacs, the present study yields no
> support for the hypothesis that
> direct inhibition at the decarboxylation step
> by vitamin B6 deficiency accounts for
> low central serotonin turnover in adult
> celiacs: 11 untreated patients showing
> reduced 5-HIAA in the cerebrospinal fluid (71
> +/- 26.8 pmol/ml) had a significantly
> higher concentration of the metabolically
> active B6 vitamer pyridoxal 5'-phosphate
> in the lumbar cerebrospinal fluid (0.06 +/-
> 0.34 ng/ml) than controls (0.24 +/- 0.07
> ng/ml) (p less than 0.01). Cerebrospinal fluid
> tryptophan, precursor of serotonin,
> was normal (2035 +/- 649 pmol/ml). Raised
> pyridoxal 5'-phosphate in the
> cerebrospinal fluid in untreated celiac disease
> is an unexpected finding. Possibly
> it is secondary to the diminished central
> monoamine metabolism in these patients,
> but further studies are needed bearing in mind
> that mental depression is a major
> cause for disability in adult celiac
> disease.
>
>83186839 L Enerback, Hallert C, Norrby K,
> Raised 5-hydroxytryptamine concentrations in
> enterochromaffin cells in adult
> coeliac disease,
> J Clin Pathol 36: 5,
> 499-503, May 1983
>
> We measured cytofluorometrically the
> concentration of 5-hydroxytryptamine (5-HT,
> serotonin) of individual enterochromaffin (EC)
> cells in adult coeliac and
> non-coeliac small intestinal mucosa. The
> distributions of 5-HT concentration within
> populations of EC cells in control and coeliac
> mucosae were log normal and thus
> contained one single population of EC cells.
> The median 5-HT concentration per EC
> cell, and the number of EC cells both increased
> in coeliac disease, but showed signs
> of normalisation when gluten was withdrawn from
> the diet. The results indicate
> that, besides inducing EC cell hyperplasia,
> gluten is capable of producing
> reversible changes in functions of EC cells in
> adult coeliac disease.
>
>
>
>83274282 C Hallert, Sedvall G,
> Improvement in central monoamine metabolism
> in adult coeliac patients starting a
> gluten-free diet,
> Psychol Med 13: 2, 267-71,
> May 1983
>
> Adult coeliac patients taking a gluten-free
> diet for one year showed an increase of
> 33% in the concentrations in CSF of major
> monoamine metabolites (5-HIAA, HVA and
> MOPEG). Tryptophan in CSF rose 10%. There
> were concomitant morphological
> improvement in the jejunal mucosa, and the
> results would seem to indicate that the
> reduced central monoamine metabolism in
> untreated adult coeliacs is not primarily
> genetically determined but is probably related
> to the poor intestinal absorption.
>
>84171964 C Hallert, Astrom J, Walan A,
> Reversal of psychopathology in adult coeliac
> disease with the aid of pyridoxine
> (vitamin B6),
> Scand J Gastroenterol 18: 2,
> 299-304, Mar 1983
>
> Signs of mental depression are typical in
> adults presenting with coeliac disease.
> The response to treatment was evaluated in 12
> consecutive patients by means of the
> Minnesota Multiphasic Personality Inventory
> (MMPI), with surgical patients serving
> as controls. The coeliacs reported no change
> in depressive symptoms after 1 year's
> gluten withdrawal despite evidence of
> improvement in the small intestine. When
> retested after 3 years, however, after 6 months
> of 80 mg/day of oral pyridoxine
> (vitamin B6) therapy, they showed a fall in
> score of scale 2 ('depression') from 70
> to 56 (p less than 0.01), which became
> normalized like other pretreatment
> abnormalities in the MMPI. Cholecystectomy in
> the control subjects produced no
> alterations in the MMPI profile. The results
> indicate a causal relationship between
> adult coeliac disease and concomitant
> depressive symptoms which seems to implicate
> metabolic effects from pyridoxine deficiency
> influencing central mechanisms
> regulating mood.
>
>84255784 EE Wheeler, Challacombe DN,
> Quantification of enterochromaffin cells
> with serotonin immunoreactivity in the
> duodenal mucosa in coeliac disease,
> Arch Dis Child 59: 6, 523-7,
> Jun 1984
>
> Enterochromaffin cells in the duodenal mucosa
> were stained by using a monoclonal
> antibody against serotonin immunoreactive sites
> and an indirect immunoperoxidase
> technique. A semi-automatic image analysing
> system showed increased numbers of
> these cells in patients with untreated coeliac
> disease compared with a control
> group. The number of serotonin positive
> granules in individual enterochromaffin
> cells also seemed to be increased in patients
> with coeliac disease, a factor which
> may be related to the pathogenesis of this
> disorder.
>
>85218445 K Sjolund, Nobin A,
> Increased levels of plasma
> 5-hydroxytryptamine in patients with coeliac
> disease,
> Scand J Gastroenterol 20: 3,
> 304-8, Apr 1985
>
> In 17 patients with coeliac disease the
> 5-hydroxytryptamine (5-HT) concentration was
> measured in platelet-poor plasma (PPP) and in
> whole blood and compared with that of
> a control group of 30 healthy persons. The
> 5-HT level was determined by
> high-pressure liquid chromatography and
> electrochemical detection. In patients with
> coeliac disease the concentration of 5-HT in
> whole blood was elevated compared with
> the control group (p less than 0.001). The
> 5-HT level in PPP was significantly
> increased in patients with coeliac disease in
> whom the disease was untreated or
> treated with gluten-free diet for less than a
> year (p less than 0.01) but also
> compared with the patients with coeliac disease
> treated with a gluten-free diet for
> more than a year (p less than 0.01). In some
> untreated patients with newly
> diagnosed disease the 5-HT levels in PPP were
> markedly elevated and exceeded the
> levels ordinarily found in patients with
> carcinoid tumors. In these patients with
> coeliac disease the 5-HT concentration in PPP
> was reduced when the enteropathy was
> healed. There was no significant correlation
> between the 5-HT concentration in PPP
> versus whole blood in the different groups.
>
>
>
>88175731 DN Challacombe, Wheeler EE,
> Are the changes of mood in children with
> coeliac disease due to abnormal
> serotonin metabolism?,
> Nutr Health 5: 3-4, 145-52,
> 1987
>
> Children with untreated coeliac disease are
> characteristically unhappy and after a
> few days of treatment with a gluten-free diet
> their mood improves. This improvement
> in mood can be rapidly reversed by introducing
> gluten into their diet again which
> suggests that a humoral agent could be involved
> in this process. As serotonin is a
> neurotransmitter in the brain and abnormalities
> of serotonin metabolism have been
> reported in coeliac disease, this biogenic
> amine could be the humoral agent that
> mediates the changes of mood in celiac disease.
> In this review the relationship
> between the mood changes in coeliac disease and
> serotonin metabolism will be further
> examined.
>
>92020818 TN Moyana, Shukoor S,
> Gastrointestinal endocrine cell hyperplasia
> in celiac disease: a selective
> proliferative process of serotonergic
> cells,
> Mod Pathol 4: 4, 419-23, Jul
> 1991
>
> Untreated celiac disease is characterized by
> gastrointestinal endocrine cell
> hyperplasia (ECH). This study investigated the
> constitutive nature of the ECH. Ten
> duodenal biopsies showing villous atrophy from
> adult celiacs were evaluated against
> ten sex- and age-matched controls. The mean
> number of endocrine cells per unit
> length of mucosa in the celiacs was compared
> with the control group using the
> Student t test. These values, respectively,
> were as follows: Churukian-Schenk
> method, 52.4 versus 29.6 (P = 0.001);
> Fontana-Masson, 32.5 versus 18.4 (P = 0.016);
> chromogranin, 33.4 versus 23.6 (P = 0.017);
> serotonin, 44.7 versus 26.7 (P = 0.006);
> somatostatin, 5.0 versus 5.4 (P = 0.631); and
> gastrin, 0.37 versus 0.37 (P = 1.000).
> There was thus ECH as shown by the first four
> stains with, in some areas, the
> endocrine cells continuously abutting against
> each other to form linear profiles.
> With respect to specific hormonal products,
> only serotonin showed ECH. These
> results suggest that the ECH in celiac disease
> is not a haphazard process but,
> instead, a selective proliferation of certain
> endocrine cell types.
>
>92128770 A Hernanz, Polanco I,
> Plasma precursor amino acids of central
> nervous system monoamines in children
> with coeliac disease,
> Gut 32: 12, 1478-81, Dec
> 1991
>
> Some children with coeliac disease show
> behavioural disorders such as depression and
> other signs which have been correlated with
> reduced central monoamine metabolism.
> We have therefore investigated the brain
> availablity of the monoamine precursors
> tryptophan and tyrosine in 15 untreated
> children with coeliac disease and 12 treated
> children with coeliac disease as well as 12
> control children. Significantly
> decreased plasma concentrations of tryptophan
> were found in untreated children (mean
> (SD) 13 (4) mumols/l, p less than 0.001)
> compared with treated children (31 (13)
> mumols/l), and in both groups of coeliac
> children when compared with control
> children (81 (22) mumols/l). A significantly
> lower ratio of plasma tryptophan to
> large neutral amino acids (tyrosine, valine,
> isoleucine, leucine, and phenylalanine)
> was also observed, which could indicate
> impaired brain availability of tryptophan in
> coeliac children and was more pronounced in
> untreated children. The impaired
> availability of tryptophan could produce
> decreased central serotonin synthesis and
> in turn behavior disorders in children with
> coeliac disease.
>
>92342686 ZE Kozlowska,
> [Evaluation of mental status of children
> with malabsorption syndrome after
> long-term treatment with gluten-free diet
> (preliminary report)], (Ocena stanu
> psychicznego dzieci z zespolem zlego
> wchlaniania po wieloletnim stosowaniu diety
> bezglutenowej (doniesienie wstepne).),
> Psychiatr Pol 25: 2, 130-4,
> Mar-Apr 1991
>
> The author examined 41 children, suffering from
> celiac disease with psychiatric
> methods and EEG. The children, aged 7-17 y.,
> were many years on gluten-free diets.
> Various psychiatric symptoms were found in
> 48.8%, and EEG abnormalities in 70.7%.
> Only 9 children (21.9%) were free from any
> psychiatric disorders and EEG
> abnormalities.
>
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