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Larry, Re: Celiac disease and depression

Posted by McPac on June 30, 2003, at 2:23:54

In reply to Re: Celiac disease and depression » Deb R, posted by Larry Hoover on June 29, 2003, at 11:43:24

Lar, my question is at the END of this article.


How Modern Eating Habits May Contribute to Depression

By Ron Hoggan M.A. & James Braly M.D.

The causes of depression may vary as much as our individuality, yet we often fail to consider our eating habits as possible culprits. With each passing year's increased understanding of the biological complexities of the human animal, more data suggesting dietary factors are unveiled. The use of drugs such as SSRIs (selective serotonin re-uptake inhibitors) and herbal extracts such as St. John's Wort (1, 2, 3) and 5-hydroxytryptophan (4) to manipulate quantities of serotonin at the synapses within the brain has demonstrated that available serotonin beyond the blood brain barrier (BBB) is an important factor in alleviating depression for many people. The brand name of one such drug, Prozac, has become a household word in our North American culture. Protein, if consumed in excessive quantity, suppresses CNS serotonin levels. Carbohydrate intake, as well as alcohol and cocaine abuse increase levels initially, but if use is chronic, such use dramatically lowers CNS serotonin, resulting in depression, carbohydrate cravings, sleep disturbances, and proneness to argumentativeness, irritability. Violence can also be used to manipulate serotonin levels. Additionally, the morphine-like substances derived from the incomplete digests of dairy and cereal grain proteins are other dietary factors which may alter mood by depressing CNS serotonin, dopamine and norepinephrine levels (5). The reduced number of platelet receptors for serotonin found in patients with celiac disease, which is also caused, at least in part, by dietary factors, again points to food as a factor in some cases of depression. Such a propensity for depression, as is now seen in our modern world, seems to run counter to the process of natural selection. It is of more than passing interest that many of the foods which seem to be implicated in depression are also foods which Humanity has had only a relatively short time, on the evolutionary calendar, to adapt to (6). And we have been consuming more and more of these new foods during this century.

Regardless of the causes of the high frequency of depression in our contemporary world, we now have fairly effective drugs to treat this condition. One such group of drugs, SSRIs, act to reduce the rate of re-uptake of serotonin at the synapses, working to conserve serotonin and increase its synaptic concentration for longer periods of time. Serotonin is an important neurotransmitter which is needed for sleep onset, mood regulation, carbohydrate craving and consumption, and a host of other functions (7). But there are other means to manipulate its presence in the brain. If we have recently digested protein, resulting in an increased level of large neutral amino acids (LNAA) in the blood stream, and we subsequently eat enough carbohydrate to induce a significant rise of circulating insulin, most of these amino acids will be transported across cell walls, for storage or energy. Due to tryptophan's resistance to insulin, this will result in an increase of circulating tryptophan. Since LNAAs compete for transport across the BBB, and since its competitors have been reduced, the relative increase in tryptophan leads to increased quantities of tryptophan being moved into the brain. Since the BBB is the primary limiting factor in conversion of tryptophan to serotonin, this results in increased levels of serotonin within the brain (8).

Since such manipulations of serotonin are difficult to regulate, and unlikely to have long-lasting effects (although some of the mystery of obesity may be revealed in this dynamic) a much more important dietary factor in depression may be the morphine-like substances which derive from the incomplete digests of proteins in cereal grains and dairy products. These were first reported by Christine Zioudrou et al. who dubbed such peptides "exorphins"(9). Further elucidation of this issue has been provided through the extensive work of Fukudome and Yoshikawa, published over the last decade (10,11) who have identified and characterized five distinct exorphins in the pepsin digests of gluten. Eight distinct exorphins have also been identified in the pepsin digests of milk (12). This work has given us a clearer sense of the morphine-like psychoactive nature of the peptides which result from the incomplete digests of these dietary proteins, as well as offering a possible explanation for some of the reported psychiatric reactions to these proteins (13,14,15) including the sense of "brain fog" that often accompanies immune reactions to these foods.

The field of serology has also provided us with some very clear evidence that such peptides, and the proteins from which they derive, can be absorbed through the intestinal mucosa, and into the circulation of a significant minority of apparently healthy members of the general population (16). Investigations of abnormal electrical activity in more than two thirds of untreated children with celiac disease has indicated that most of them normalize following dietary restriction (17, 18). These findings suggest that caseomorphin and gluten-derived exorphins are at the root of such abnormal electrical activity in the brain. Since such substances act as depressants, slowing neurotransmission, it should not be surprising if the intestinal permeability, and digestive enzyme deficiencies found in celiac disease were also found in many folks suffering depression. This is underscored by the reports that depression is a very common symptom of celiac disease (19, 20, 21, 22, 23, 24, 25, 26). More on this point can be found at: http://www.gluten-free.org/reichelt.html

Please don't misunderstand us. We do not mean to suggest that all, or even most people suffering from depression have celiac disease. Quite the contrary, we suspect that only a small minority will demonstrate celiac disease when tested (although screening this population for celiac disease makes good sense). It is my suspicion that many folks suffering from depression may have underlying intestinal permeability combined with digestive enzyme deficiencies. To have celiac disease, they would also need to have some degree of damage to, or lymphocyte infiltration of, their intestinal mucosa. So celiac disease would probably be found in a relatively small, but significant percentage, of those afflicted. The prior two conditions of enzyme deficiency and intestinal permeability are abundantly found when sought, and it is these features which, we suspect, dominate the segment of the population which is chronically depressed.

Humans have spent millions of years being naturally selected, in part, on the basis of a diet that included vegetables, seeds, fruit, insects, and subsequently, meat. Yet, at most, we have had only ~12,000 years to adapt to consumption of significant quantities of problematic cereal grains, with cultivation originating in southeastern Europe, and spreading to the northwest very slowly. The Romans spread it throughout their empire, reaching far flung parts of Europe, but places they never conquered, such as Ireland, Scotland, and Finland, have been consuming significant quantities of grains for less than 2,000 years. A Danish friend told me that prior to the end of World War II, many Danes considered wheaten bread to be a special treat, because wheat does not grow well in Denmark. North American natives have had a similarly limited exposure to gluten.

Humanity has also had a relatively short time to adapt to post-infancy consumption of significant quantities of milk from other species. This dietary practice probably arose out of animal husbandry. For a more extensive discussion of this topic, go to: http://www.PaleoDiet.com and http://www.gluten-free.org/hoggan/.

Our frequent difficulty with these recent foods seems congruent with the evolutionary data. Many of us simply have not had sufficient time to adapt to these recent additions to the human food supply. We would likely fare much better on foods to which our ancestors have adapted. The dramatic increase in our consumption of these recent foods during this century may have a very ominous element. Such dietary habits may well have been paving the way for Prozac.

The treatment for many cases of depression should begin with serological testing, and be followed by approximately the same treatment as that in celiac disease and milk protein intolerance. Dietary exclusion of the offending proteins will often mean exclusion of gluten-containing grains and/or dairy proteins. Such a diet would, in some cases, result in a few days of withdrawal symptoms, followed by a substantial improvement in mood. While we only know of anecdotal reports of such improvements, we find the above data, in combination with these anecdotal reports, to be quite compelling.

******Lar, re: the following statement from the article, what is the NAME of the specific enzyme that one could take to alleviate this enzyne deficiency? "The prior two conditions of enzyme deficiency and intestinal permeability are abundantly found when sought, and it is these features which, we suspect, dominate the segment of the population which is chronically depressed".


For more information on changing diet see:
The Gluten-Free Page: http://www.gluten-free.org/hoggan/
The No Milk Page: http://www.NoMilk.com/
The Paleolithic Diet Page: http://www.PaleoDiet.com/
PaleoFood Recipe Collection: http://www.PaleoFood.com/

References

Ernst E. St. John's Wort, an antidepressant? A systematic, criteria-based review. Phytomed; volume 2: pages 67-71, 1995.
Linde K, et al. St. John's Wort for depression: an overview and meta-analysis of randomized clinical trials. British Journal of Medicine; volume 313: pages 253-258, 1996.
Perovic S and Muller WEG. Pharmacological profile of hypericum extract [St. John's Wort]. Effect of serotonin uptake by post-synaptic receptors. Arzneim Forsch; volume 45: pages 1145-1148, 1995.
Fibromyalgia and the serotonin pathway. Juhl JH Altern Med Rev, 1998 Oct, 3:5, pages 367-375.
Hallert C et al. Psychic disturbances in adult coeliac disease III. Reduced central monoamine metabolism and signs of depression. Scand J Gastroenterol, 1982; volume 17: pages 25-28.
Lutz W, The Colonization of Europe and Our Western Diseases. Medical Hypotheses 1995; 45: 115-120
Tortora & Grabowski _Principles of Anatomy & Physiology_ Harper Collins, N.Y. 1996; p. 417
Young S, The Effect on Aggression and Mood of Altering Tryptophan Levels. _Nutrition Reviews_ 1986; May Supplement: 112-122
Zioudrou C, Streaty RA, Klee WA, Opioid peptides derived from food proteins. The exorphins. J Biol Chem. 1979 Apr 10;254(7): 2446-9.
Fukudome S, Shimatsu A, Suganuma H, Yoshikawa M Effect of gluten exorphins A5 and B5 on the postprandial plasma insulin level in conscious rats. Life Sci. 1995;57(7):729-34.
Fukudome S, Yoshikawa M Opioid peptides derived from wheat gluten: their isolation and characterization. FEBS Lett. 1992 Jan 13;296(1):107-11.
Mycroft FJ, et al. MIF-like sequences in milk and wheat proteins. N Engl. J Med. 1982 Sep 30;307(14):895.
Dohan FC. Genetic hypothesis of idiopathic schizophrenia: its exorphin connection. Schizophr Bull. 1988;14(4):489-94.
Saelid G, Haug JO, Heiberg T, Reichelt KL Peptide-containing fractions in depression. Biol. Psychiatry. 1985 Mar;20(3):245-56.
Hoggan, R. Absolutism's Hidden Message for Medical Scientism. Interchange. 1997; 28(2/3): 183-189.
Husby S, Jensenius JC, Svehag SE Passage of undegraded dietary antigen into the blood of healthy adults. Quantification, estimation of size distribution, and relation of uptake to levels of specific antibodies. Scand J Immunol. 1985 Jul;22(1):83-92.
Kozlowska ZE. [Evaluation of mental status of children with malabsorption syndrome after long-term treatment with gluten-free diet]. Psychiatr Pol. 1991 Mar-Apr;25(2):130-4.
Paul K, Todt J, Eysold R, [EEG Research Findings in Children with Celiac Disease According to Dietary Variations] _Zeitschrift der Klinische Medizin_ 1985;40: 707-709
Corvaglia L, et al. Depression in adult untreated celiac subjects: diagnosis by the pediatrician. Am J Gastroenterol. 1999 Mar;94(3):839-43.
Ciacci C, et al. Depressive symptoms in adult coeliac disease. Scand J Gastroenterol. 1998 Mar;33(3):247-50.
Addolorato G, et al. Anxiety and depression in adult untreated celiac subjects and in patients affected by inflammatory bowel disease: a personality "trait" or a reactive illness? Hepatogastroenterology. 1996 Nov-Dec;43(12):1513-7.
Pellegrino M, et al. Untreated coeliac disease and attempted suicide. Lancet. 1995 Sep 30;346(8979):915.
Cheliout W. [A misleading depression]. Encephale. 1994 Sep-Oct;20(5):531-4. French.
Hernanz A, et al. Plasma precursor amino acids of central nervous system monoamines in children with coeliac disease. Gut. 1991 Dec;32(12):1478-81.
van Praag HM. Affective disorders and aggression disorders: evidence for a common biological mechanism.
Suicide Life Threat Behav. 1986 Summer;16(2):103-32. Review.
Hallert C, et al. Psychic disturbances in adult coeliac disease. I. Clinical observations. Scand J Gastroenterol. 1982 Jan;17(1):17-9.


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poster:McPac thread:237849
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