Post by Billy BoyThanks Trig for your good sensible post.
All good info. I still sleep on the inclined bed and don't take GRJ now but keep some of
the roots always handy just in case.
I also take Melotonin for sleep. Never heard it was good for Gerd. Always learning new
stuff.
I'll bet Loretta doesn't accept any suggestions from you either. She is stuck in her
little box and wants a godlike doctor to write the magic prescription that will heal all.
Nothing against Loretta, by far most people are like this.
Sad.
I have relatives and close friends who are eaten up with Gerd and won't consider raising
the head of their bed because it won't look good. Can you imagaine that. It's true.
And, I have relatives and close friends who run to the bathroom with diarrhea after every
meal but won't consider doing an elimination diet to find out what foods cause the
diarrhea or won't consider 'probiotics' or will take one little pill of probiotics for a
few days and when they don't see any change stop the probiotics and say they don't work.
Again, they want the godlike doctor in the white coat to write the magic presecrption and
heal all.
Post by ***@gmail.com |Post by Loretta EisenbergSorry Bill, i dont know you and not being so trusting, it sounds like
snake oil to me
Billy Boy AKA Wild Bill has been posting here for years.
His bed tilting suggestion is a useful one. And you
will find my version of it back in the archive under
a different handle. The ginger doesn't hurt
and should be at least mildly helpful IMO though
I could never tell the difference back in the day
when I tried though perhaps I didn't try it enough.
You can buy fresh ginger at the supermarket
and there is evidence that the gingerols of ginger are
good for one in other ways as I recall.
For me the answer to my heartburn, reflux, and dyspepsia
came in steps. The PPI meds helped but in time they
caused nasty adverse effects. I had to quit them.
Even when using the meds I gradually started
sleeping on ever greater inclines. I went so
far as building a special adjustable that tilted
the whole surface of the bed in one plane quite
unlike a hospital bed. This helped but I still had
dyspepsia.
In time I went of alternative Doc (actually a longevity
clinic doc) he said that many with heartburn symptoms
actually have too little acid. At that point I was willing
to try anything. I started taking multiple capsules
of a digestive supplement containing betaine hydrochloride
with pepsin with meals (not after meal as one needs
this to be mixed in the food by stomach action) and
with it use my dyspepsia went away and that
had right away. I found I had to take it if I was
going to eat greasy starchy Chinese food and not
suffer. I slept on the inclined bed until perhaps
a ago or so. I was afraid to change what works.
I found I no longer needed the incline at night.
Also I am a melatonin taker, I take 6 milligrams
at bedtime and this also has been reported to
help with GERD symptoms. Do a Pubmed search
as see. I've also gone on a low carb diet to
improve blood glucose control and it with
a high dose alpha lipoic acid (1200 mgs per day in
divided doses) has me feeling pretty good.
Note alpha lipoic acid can be hard on the
stomach as high doses.
Note also there are some that are of the opinion
betaine base aka trimethylglycine is also helpful
for reflux/GERD.........google Larry Hoover postings
on the topic.
Anyway I've been good for 4 years or so now
after a nightmare decade from GERD plus
the adverse med effect. The PPI meds only
helped somewhat with GERD symptom.
!000 dollars for meds and I even had
the fundoplication which failed with time.
What worked for me worked for me but
if it will work for you I have no idea.
So I offered you my alternative view plus
a couple of others if you research the topic.
I gave you pretty everything here.............Trig
Thanks for the kind words. You got me to revisit the
ginger topic. Apparently it is a prokinetic that is
to say it helps the stomach to empty its contents
into the intestine which a really good way to help
prevent reflux plus it is an antiinflammatory.
I am including a selection of relatively recent absract
on the topic of melatonin for GERD and after them
a selection of abstracts on ginger for inflammation
and dyspepsia.
Anyway the evidence is such I going to restart using
fresh ginger root.
1: Altern Ther Health Med. 2008 Jul-Aug;14(4):54-8.
Melatonin for the treatment of gastroesophageal reflux disease.
Werbach MR.
The enterochromaffin cells of the gastrointestinal (GI) tract
secrete 400 times as much melatonin as the pineal gland;
therefore, it is not surprising that research is finding that this
indole plays an important role in GI functioning.
In animal studies, it protects against GI ulcerations, and randomized
clinical trials suggest its efficacy in treating functional dyspepsia
and irritable bowel syndrome. Melatonin administration has been
shown to protect against esophageal lesions in animals. Moreover,
in a randomized, single-blind clinical trial of subjects with
gastroesophageal
reflux disease (GERD), the combination of melatonin with other
natural supplements was found to be superior to omeprazole,
a proton pump inhibitor (PPI). Its administration as a single
treatment
for GERD has not been previously reported. A 64-year-old Caucasian
female who required treatment with a PPI for symptoms of GERD
wished to substitute a naturaltreatment because of the risk of
worsening her osteoporosis. She experienced a
return of symptoms following each of three 20-day trials of a
proprietary
blend of D-limonene when attempts were made to discontinue the PPI.
She then underwent a trial of a natural formula consisting of
melatonin 6 mg, 5-hydroxytryptophan 100 mg, D,L-methionine 500 mg,
betaine 100 mg, L-taurine 50 mg, riboflavin 1.7 mg, vitamin B6 0.8
mg,
folic acid 400 microg, and calcium 50 mg. After 40 days, the PPI was
withdrawn without a return of symptoms. Subsequently, an attempt to
reduce melatonin to 3 mg resulted in symptoms, while all other
ingredients
were withdrawn with minimal symptoms during 10 months of follow-up.
PMID: 18616070
1: J Physiol Pharmacol. 2007 Jun;58(2):361-77.
Protective influence of melatonin against acute esophageal
lesions involves prostaglandins, nitric oxide and sensory nerves.
Konturek SJ, Zayachkivska O, Havryluk XO, Brzozowski T,
Sliwowski Z, Pawlik M, Konturek PC, Cześnikiewicz-Guzik M,
Gzhegotsky MR, Pawlik WW.
Department of Physiology, Jagiellonian University Medical College,
Cracow,
Poland. ***@cyf-kr.edu.pl
Melatonin (MT) is known to protect gastrointestinal mucosa against
various types of injury but its effects on esophageal damage have
not been studied. We examined the effects of MT on acute
esophageal injury and the mechanism involved in the
action of this indole. Acute esophageal lesions were induced
by perfusion with acid-pepsin solution using tube inserted through
the oral cavity into the mid of esophagus of anaesthetized rats with
or without inhibition of prostaglandin (PG)
generation by indomethacin (5 mg/kg/day), nitric oxide (NO) formation
by N(G)-nitro-L-arginine (L-NNA, 20 mg/kg/day) or sensory nerves
deactivation by capsaicin (125 mg/kg, sc). The esophageal injury
was assessed by macroscopic score and histologic activity index.
The esophageal mucosal blood flow (EBF) was determinated by H(2)-gas
clearance method. The plasma TNF-alpha and nitrate/nitrite (NOx)
levels and mucosal PGE(2) contents were assessed by immunoassays.
Esophageal acid-pepsin perfusion induced noticeable esophageal
mucosal injury as compared to perfusion with vehicle saline.
The pretreatment with MT prevented significantly esophageal injury,
raised EBF and mucosal content of PGE(2), while decreasing the levels
of TNF-alpha. Inhibition of COX/PG and NOS/NO systems by indomethacin
and L-NNA, respectively, or inactivation of sensory nerves by
capsaicin,
that manifested in further increase of esophageal injury, reduced the
levels of EBF, markedly raised the levels TNF-alpha and reduced
mucosal PGE(2), but the pretreatment with MT prevented significantly
esophageal injury, improved EBF and raised mucosal PGE(2) contents.
These studies suggest that MT can be considered as a
novel esophagoprotector, acting, at least
in part, through the COX/PG and NOS/NO systems and
activation of sensory nerves.
PMID: 17622703
1: J Physiol Pharmacol. 2006 Nov;57 Suppl 5:41-50.
Nocturnal secretion of melatonin in patients with upper digestive
tract
disorders.
Klupińska G, Wiśniewska-Jarosińska M, Harasiuk A, Chojnacki C, Stec-
Michalska K,
Błasiak J, Reiter RJ, Chojnacki J.
Department of Gastroenterology and Internal Diseases,
Medical University of Lodz,1 Haller's Square, 90-647 Lodz, Poland.
***@achilles.wam.lodz.pl
Recently, the results of many experimental investigations have shown
that melatonin possesses gastroprotective properties. On the other
hand
its role in pathogenesis of upper digestive tract diseases in man
still remains
unclear. The aim of the study was to investigate nocturnal secretion
of
melatonin in patients with functional and organic diseases of the
upper part of digestive tract. The investigations were carried out in
149 persons, aged 21-51 years, including healthy subjects (group I,
n=30),
and patients with non-erosive gastroduodenal
reflux (NERD, group II, n=24), with gastroesophageal reflux disease
(GERD,
group III, n=25), with functional dyspepsia (FD, according to the Rome
III Criteria,
group IV, n=36) and with recurrent duodenal ulcer (DUD, group V,
n=34).
Diagnoses were established on the basis of endoscopic imaging
and histological examination,24-hour pH-metry and laboratory tests.
Melatonin serum concentration was measured with ELISA method.
Blood samples were taken for examination in red-lighted room
at 10 p.m. and on the following day at 2 and 6 a.m.
The highest concentration of melatonin in all examined groups
was determined at 2 a.m. The average melatonin concentration in
healthy subjects was 34,7 +/- 4,8 pg/ml. In patients with GERD and
DUD melatonin concentration was lower than in healthy subjects - 27,2
+/- 8,5
pg/ml and 25,5 +/- 6,2 pg/ml respectively (p < 0,05; p < 0,01).
The highest concentration of melatonin was found in patients with
NERD and FD - 43,2 +/- 10,8 pg/ml and 42,4 +/- 10,1 pg/ml (p < 0,01; p
< 0,05).
The findings of this study support the notion that melatonin exerts
beneficial influences on the upper
digestive tract. It is likely that high or relatively correct
secretion of melatonin
is sufficient to prevent peptic changes in esophageal and duodenal
mucosa.
PMID: 17218759 [
1: J Pineal Res. 2006 Oct;41(3):195-200.
Regression of gastroesophageal reflux disease symptoms using dietary
supplementation with melatonin, vitamins and aminoacids: comparison
with omeprazole.
Pereira Rde S.
Depto. de Farmácia-Universidade Estadual da Paraíba, Av das Baraúnas,
351/Campus Universitário, Bodocongó/Campina Grande-PB-Brazil-CEP
58109-753, Brazil.
***@yahoo.com.br
The prevalence of gastroesophageal reflux disease (GERD) is
increasing.
GERD is a chronic disease and its treatment is problematic. It may
present
with various symptoms including heartburn, regurgitation, dysphagia,
coughing,
hoarseness or chest pain. The aim of this study was to investigate if
a dietary
supplementation containing: melatonin, l-tryptophan, vitamin B6, folic
acid,
vitamin B12, methionine and betaine would help patients with GERD, and
to
compare the preparation with 20 mg omeprazole. Melatonin has known
inhibitory activities on gastric acid secretion and nitric oxide
biosynthesis.
Nitric oxide has an important role in the transient lower esophageal
sphincter relaxation (TLESR), which is a major mechanism of reflux in
patients with GERD. Others biocompounds of the formula display
anti-inflammatory and analgesic effects. A single blind
randomized study was performed in which 176 patients underwent
treatment using the supplement cited above (group A) and 175
received treatment of 20 mg omeprazole (group B). Symptoms
were recorded in a diary and changes in severity of symptoms noted.
All patients of the group A (100%) reported a complete
regression of symptoms after 40 days of treatment.
On the other hand, 115 subjects (65.7%) of the omeprazole
reported regression of symptoms in the sameperiod.
There was statiscally significant difference between the groups (P
<0.05).
This formulation promotes regression of GERD symptoms with no
significant
side effects.
PMID: 16948779
=================================
Ginger and gingerol for fights inflammation,
is a prokinetic (gets the stomach to empty
as good thing), and cancer prevention.
Abstracts below.
1: Cancer Lett. 1998 Jul 17;129(2):139-44.
Erratum in:
Cancer Lett 1998 Sep 25;131(2):231.
Inhibitory effects of [6]-gingerol,
a major pungent principle of ginger,
on phorbol ester-induced inflammation,
epidermal ornithine decarboxylase activity and skin tumor promotion in
ICR mice.
Park KK, Chun KS, Lee JM, Lee SS, Surh YJ.
Yonsei University College of Dentistry, Seoul, South Korea.
A wide array of phytochemicals have been shown to possess potential
cancer chemopreventive properties. Ginger contains pungent phenolic
substances with pronounced antioxidative and antiinflammatory
activities.
In the present study, we have determined the antitumor promotional
activity of [6]-gingerol, a major pungent principle of ginger, using
a
two-stage mouse skin carcinogenesis model. Topical application of [6]-
gingerol
onto shaven backs of female ICR mice prior to each topical dose
of 12-O-tetradecanoylphorbol-13-acetate (TPA) significantly inhibited
7,12-dimethylbenz[a]anthracene-induced skin papillomagenesis.
The compound also suppressed TPA-induced epidermal ornithine
decarboxylase activity
and inflammation.
PMID: 9719454
1: Int Immunopharmacol. 2008 Dec 10;8(12):1626-32.
Epub 2008 Aug 8.
Ginger prevents Th2-mediated immune responses in
a mouse model of airway inflammation.
Ahui ML, Champy P, Ramadan A, Pham Van L, Araujo L, Brou André K,
Diem S, Damotte D, Kati-Coulibaly S, Offoumou MA, Dy M, Thieblemont N,
Herbelin A.
CNRS UMR 8147,
Université Paris Descartes,
Faculté de Médecine, Hôpital Necker, 161 rue de Sèvres;
75783 Paris Cedex 15, France.
It is well documented that compounds from rhizomes of Zingiber
officinale,
commonly called ginger, have anti-inflammatory properties. Here, we
show that
ginger can exert such functions in vivo, namely in a mouse model of
Th2-mediated
pulmonary inflammation. The preparation of ginger aqueous extract
(Zo.Aq)
was characterized by mass spectrometry as an enriched fraction of n-
gingerols.
Intraperitoneal injections of this extract before airway challenge of
ovalbumin
(OVA)-sensitized mice resulted in a marked decrease in the recruitment
of
eosinophils to the lungs as attested by cell counts in bronchoalveolar
lavage
(BAL) fluids and histological examination. Resolution of airway
inflammation
induced by Zo.Aq was accompanied by a suppression of the Th2 cell-
driven
response to allergen in vivo. Thus, IL-4, IL-5 and eotaxin levels in
the lungs
as well as specific IgE titres in serum were clearly diminished in
ginger-treated
mice relative to their controls after allergen sensitization and
challenge. Finally,
we found that [6]-gingerol, a major constituent of ginger, was
sufficient to
suppress eosinophilia in our model of inflammation. This is the first
evidence
that ginger can suppress Th2-mediated immune responses and might thus
provide a possible therapeutic application in allergic asthma.
PMID: 18692598
1: J Surg Res. 2007 Apr;138(2):209-13. Epub 2007 Feb 8.
Effect of 6-gingerol on pro-inflammatory cytokine production and
costimulatory
molecule expression in murine peritoneal macrophages.
Tripathi S, Maier KG, Bruch D, Kittur DS.
Department of Surgery, SUNY Upstate Medical University,
Syracuse, New York 13210,USA.
BACKGROUND:
Pro-inflammatory cytokines produced primarily by macrophages
are key elements in many surgical conditions including sepsis,
ischemia-reperfusion injury, and transplant rejection.
Herbal products are being used as alternative
treatments in such inflammatory conditions. Ginger is known for its
ethno-botanical applications as an anti-inflammatory agent. 6-
gingerol
is one of the active ingredients of ginger that imparts ginger with
its
anti-inflammatory properties. We hypothesized that the
anti-inflammatory effect of 6-gingerol is because of inhibition of
macrophage activation, more specifically by an
inhibition of pro-inflammatory cytokines and antigen presentation by
lipopolysaccharide (LPS) activated macrophages.
METHODS:
To study the effect of 6-gingerol on pro-inflammatory cytokines,
we measured the liberation of TNF-alpha, IL-1beta, and IL-12 by
murine peritoneal macrophages exposed to several doses of 6-gingerol
in the presence of LPS stimulation. We also studied
the effect of 6-gingerol on the cell surface expression of
B7.1, B7.2, and MHC II. Finally, we examined the APC function
of the 6-gingerol treated macrophages by a primary mixed lymphocyte
reaction.
RESULTS:
6-gingerol inhibited the
production of pro-inflammatory cytokines from LPS stimulated
macrophages but had no effect on the LPS-induced expression of
B7.1, B7.2, and MHC II. The APC function of LPS stimulated
macrophages was also unaffected by 6-gingerol
treatment.
CONCLUSION:
Our data indicate that 6-gingerol selectively inhibits
production of pro-inflammatory cytokines from macrophages
but does not affect either the APC function or cell surface
expression of MHC II and costimulatory molecules.
We, thus, provide a mechanistic insight into the anti-inflammatory
properties of 6-gingerol that may be useful to treat inflammation
without interfering with the antigen presenting function of
macrophages.
PMID: 17291534
1: Eur J Gastroenterol Hepatol. 2008 May;20(5):436-40.
Effects of ginger on gastric emptying and motility in healthy humans.
Wu KL, Rayner CK, Chuah SK, Changchien CS, Lu SN, Chiu YC, Chiu KW,
Lee CM.
Division of Hepatogastroenterology, Department of Internal Medicine,
College of
Medicine, Chang Gung Memorial Hospital, Kaohsiung Medical Center,
Chang Gung
University, Kaohsiung, Taiwan. ***@yahoo.com.tw
OBJECTIVE:
Ginger has been reported to improve upper gastrointestinal symptoms.
Little information about the effects of ginger on gastric motor
function,
exists, however. Our aim was to investigate the effects of ginger on
gastric emptying,
antral motility, proximal gastric dimensions, and postprandial
symptoms.
METHODS:
Twenty-four healthy volunteers were studied twice in a randomized
double-blind manner.
After an 8 h fast, the volunteers ingested three ginger capsules
(total 1200 mg)
or placebo, followed after 1 h by 500 ml low-nutrient soup. Antral
area,
fundus area and diameter, and the frequency of antral contractions
were measured using ultrasound at frequent intervals over 90 min, and
the gastric half-emptying time was calculated from the change in
antral area. Gastrointestinal sensations and appetite were scored
using visual analog questionnaires. Data are expressed in terms of
mean+/-standard error.
RESULTS:
Antral area decreased more rapidly (P<0.001) and the gastric
half-emptying time was less after ginger than placebo
ingestion (13.1+/-1.1 vs. 26.7+/-3.1 min, P<0.01), whereas the
frequency of antral contractions was greater (P<0.005).
Fundus dimensions did not differ, and there was no significant
difference in any gastrointestinal symptoms.
CONCLUSION:
Ginger accelerates gastric emptying and stimulates antral
contractions in healthy volunteers. These effects could potentially
be beneficial in symptomatic patient
groups.
PMID: 18403946
1: Curr Gastroenterol Rep. 2007 Dec;9(6):447-55.
Dyspepsia in childhood and adolescence: insights and treatment
considerations.
Perez ME, Youssef NN.
Center for Pediatric Irritable Bowel and Motility Disorders, Goryeb
Children's
Hospital at Atlantic Health, 100 Madison Avenue, Internal Box 82,
Morristown, NJ
07962, USA.
Functional dyspepsia (FD) is common in children, with as many as 80%
of those being evaluated for chronic abdominal pain reporting
symptoms
of epigastric discomfort, nausea, or fullness. It is known that
patients with
persistent complaints have increased comorbidities such as depression
and anxiety. The interaction with psychopathologic variables has been
found to mediate the association between upper abdominal pain and
gastric hypersensitivity. These observations suggest that abnormal
central nervous system processing of gastric stimuli may be a
relevant
pathophysiologic mechanism in FD. Despite increased
understanding, no specific therapy has emerged; however, recent
nonpharmacological-based options such as hypnosis may be effective.
Novel approaches, including dietary manipulation and use of
nutraceuticals such as ginger and Iberogast
(Medical Futures Inc., Ontario, Canada), may also be
considered.
PMID: 18377794
1: Pak J Pharm Sci. 2007 Jul;20(3):231-5.
Ginger facilitates cholinergic activity possibly due to blockade of
muscarinic autoreceptors in rat stomach fundus.
Ghayur MN, Khan AH, Gilani AH.
Department of Biological and Biomedical Sciences, Aga Khan University
Medical
College, Karachi-74800, Sind, Pakistan.
Ginger (Zingiber officinale) is a universally known food plant reputed
for its
medicinal use in gastrointestinal disorders as a prokinetic and
laxative.
We recently showed that 70% aqueous-methanolic extract of ginger
(Zo.Cr) exhibits
prokinetic activity in rats via activation of post-synaptic muscarinic
M3
receptor in rat stomach fundus. In view of the physiological
significance of
pre-synaptic muscarinic M1 and M2 autoreceptors, this study was
undertaken
to further look into the possible mode of action of the prokinetic
effect of
ginger through inhibition of pre-synaptic muscarinic receptors.
Isolated tissue bath experiments were performed with Sprague-Dawley
rat
stomach fundus strip preparations immersed in Kreb's solution at 37
degrees C.
Carbachol (CCh) maximum responses (1 microM) were obtained in rat
stomach fundus. Zo.Cr, given in multiple increasing bolus
concentrations
(0.01-0.1 mg/ml) 10 min prior to administration of CCh, potentiated
the CCh peak responses showing that it is possibly inhibiting the
pre-synaptic muscarinic receptors. Like wise, increasing bolus
concentrations of pirenzepine (0.03-0.3 microM) and himbacine
(0.01-0.03
microM), standard muscarinic M1 and M2 antagonists respectively,
also potentiated the CCh responses. These results show that ginger,
in addition to having a direct cholinergic agonistic effect on the
post-synaptic M3 receptors, also has a possible inhibitory effect on
pre-synaptic muscarinic autoreceptors, similar to standard
muscarinic antagonists, thus reiterating the gastric stimulant effect
of
this age-old plant.
PMID: 17545109