Re: For those with IBS, Crohn's, IBD, gastritis, etc.
- From: "TC" <tunderbar@xxxxxxxxxxx>
- Date: 5 May 2005 06:40:55 -0700
montygram wrote:
> One thing your doctor probably never told you was to avoid
unsaturated
> fatty acids, especially certain oils (corn, vegetable, soy, canola,
> sunflower, safflower, etc.), yet the evidence is overwhelming. You
can
> go to www.pubmed.com and do various searches, for example crohn
> oxidative will bring up all but the first, which came from
> www.sciencedaily.com:
>
>
> 5/2/2005
> Food Fried In Vegetable Oil May Contain Toxic Compound
>
> MINNEAPOLIS / ST. PAUL -- University of Minnesota researchers A.
Saari
> Csallany, a professor of food chemistry and nutritional biochemistry,
> and graduate student Christine Seppanen have shown that when highly
> unsaturated vegetable oils are heated at frying temperature (365 F)
for
> extended periods--or even for half an hour--a highly toxic compound,
> HNE (4-hydroxy-trans-2-nonenal) forms in the oil.
>
> Previously, vegetable oils such as soybean, sunflower and corn were
> regarded as heart-healthy because of their high levels of linoleic
> acid, a polyunsaturated fatty acid. HNE is incorporated into fried
food
> in the same concentration as it forms in the heated oil. Also,
Csallany
> and her colleagues have found three toxic HNE-related compounds
(known
> as HHE, HOE and HDE) in heated soybean oil. They will present their
> work at a poster session from 9 a.m. to 2 p.m. Wednesday, May 4, at
the
> 96th annual meeting of the American Oil Chemists Society in the Salt
> Lake City Convention Center.
>
> "HNE is a well known, highly toxic compound that is easily absorbed
> from the diet," said Csallany. "The toxicity arises because the
> compound is highly reactive with proteins, nucleic acids--DNA and
> RNA--and other biomolecules. HNE is formed from the oxidation of
> linoleic acid, and reports have related it to several diseases,
> including atherosclerosis, stroke, Parkinson's, Alzheimer's,
> Huntington's and liver diseases."
>
> Csallany's work underscores the risk of repeated heating, or reusing,
> highly unsaturated oils for frying because HNE accumulates with each
> heating cycle. In future studies, Csallany and her colleagues plan to
> determine how long polyunsaturated oil must be heated at lower
> temperatures in order to form HNE and its related compounds. The
study
> was funded by the University of Minnesota.
>
>
>
>
>
> Am J Physiol Gastrointest Liver Physiol. 2004 Apr;286(4):G528-37.
Epub
> 2003 Dec 4.
>
> Linoleic acid induces interleukin-8 production by Crohn's human
> intestinal smooth muscle cells via arachidonic acid metabolites.
>
> Alzoghaibi MA, Walsh SW, Willey A, Yager DR, Fowler AA 3rd, Graham
MF.
>
> Department of Physiology, Virginia Commonwealth University, Richmond,
> Virginia 23298-0034, USA. swwalsh@xxxxxxx
>
> Previously we reported that linoleic acid (LA), but not oleic acid,
> caused a marked increase in the secretion of IL-8 by Crohn's human
> intestinal smooth muscle (HISM) cells. Antioxidants inhibited this
> response, implicating a role for oxidative stress and NF-kappaB, a
> transcription factor for IL-8 that is activated by oxidative stress.
In
> this study, we examined two mechanisms whereby LA, the dietary
> precursor for arachidonic acid (AA), could increase the production of
> IL-8 via activation of AA pathways: 1) by generation of reactive
oxygen
> species by the AA-pathway enzymes to activate NF-kappaB or 2) by AA
> metabolites. Normal and Crohn's HISM cells were exposed to LA,
> oxidizing solution (Ox), or oxidizing solution enriched with LA
(OxLA).
> Exposure of cells to Ox or OxLA induced oxidative stress as
determined
> by thiobarbituric acid reactive substances. In normal cells, Ox but
not
> LA activated NF-kappaB as determined by transfection experiments and
> Western blot. In Crohn's cells, NF-kappaB was spontaneously activated
> and was not further activated by Ox or LA. In contrast, TNF-alpha
> markedly increased activation of NF-kappaB in both normal and Crohn's
> cells. These results indicated that LA did not increase IL-8 by
> activating NF-kappaB, so we evaluated the second mechanism of an
effect
> of AA metabolites. In normal cells, OxLA, but not LA, markedly
> stimulated IL-8, whereas in Crohn's cells, both OxLA and LA
stimulated
> IL-8. OxLA, also stimulated production of AA metabolites leukotriene
> B(4) (LTB(4)), PGE(2), and thromboxane B(2) (TXB(2)) by normal and
> Crohn's cells. To determine whether AA metabolites mediated the IL-8
> response, cells were treated with OxLA plus indomethacin (Indo), a
> cyclooxygenase inhibitor, and nordihydroguaiaretic acid (NDGA), a
> lipoxygenase inhibitor. Both Indo and NDGA blocked the IL-8 response
to
> OxLA. To determine more specifically a role for AA metabolites, AA
was
> used. Similar to OxLA, OxAA stimulated production of IL-8 and AA
> metabolites. Pinane thromboxane, a selective thromboxane synthase
> inhibitor and receptor blocker, inhibited OxAA stimulation of TXB(2)
> and IL-8 in a dose-response manner. MK886, a selective 5-lipoxygenase
> inhibitor, inhibited OxAA stimulation of LTB(4) and IL-8 also in a
> dose-response manner. Analysis of specific gene products by RT-PCR
> demonstrated that HISM cells expressed receptors for both thromboxane
> and LTB(4). We conclude that AA metabolites mediated the IL-8
response
> to LA in HISM cells. Both cyclooxygenase and lipoxygenase pathways
were
> involved. LA did not increase IL-8 by activating NF-kappaB, but
> NF-kappaB appeared to be involved, because LA increased IL-8 only in
> situations where NF-kappaB was activated, either spontaneously in
> Crohn's cells or by Ox in normal cells. We speculate that AA
> metabolites increased IL-8 production by enhancing
NF-kappaB-dependent
> transcription of IL-8.
>
>
>
> Cell Stress Chaperones. 2003 Winter;8(4):329-34.
>
> Expression of heat shock protein 32 (hemoxygenase-1) in the normal
and
> inflamed human stomach and colon: an immunohistochemical study.
>
> Barton SG, Rampton DS, Winrow VR, Domizio P, Feakins RM.
>
> Department of Adult and Paediatric Gastroenterology, Barts and the
> London, Queen Mary School of Medicine and Dentistry, London E1 2AD,
UK.
>
> Heat shock protein 32 (Hsp32, hemoxygenase-1) is induced by reactive
> oxygen metabolites (ROM) and degrades heme leading to the formation
of
> antioxidant bilirubin. Increased mucosal generation of ROM occurs in
> gastritis and inflammatory bowel disease. We aimed to assess mucosal
> expression of Hsp32 in normal stomach and colon and to test the
> hypothesis that disease-related differential expression occurs in
> inflamed tissue. Gastric body and antral mucosal biopsies were
obtained
> from 33 patients comprising Helicobacter pylori-negative normal
> controls (n = 8), H pylori-negative gastritis patients (n = 11), and
H
> pylori-positive gastritis patients (n = 14). Forty-seven archival
> colonic mucosal biopsies selected comprised normal histology (n =
10),
> active ulcerative colitis (UC) (n = 9), inactive UC (n = 8), active
> Crohn's disease (CD) (n = 8), inactive CD (n = 6), and other
colitides
> (n = 6). Hsp32 expression in formalin-fixed sections was assessed by
> avidin-biotin peroxidase immunohistochemistry using a polyclonal
rabbit
> anti-Hsp32 as the primary antibody. Immunohistochemical staining
> identified Hsp32 in all groups. Diffuse cytoplasmic staining was seen
> in gastric and colonic epithelial and lamina proprial inflammatory
> cells. Staining scores for Hsp32 were higher in antral H
> pylori-positive (P = 0.002) and H pylori-negative (P = 0.02)
gastritis
> than in controls and in body H pylori-positive gastritis than in the
> other 2 groups (P < 0.01). Expression of Hsp32 was increased in
active
> UC compared with inactive disease (P = 0.03) and normal controls (P =
> 0.02). In conclusion, Hsp32 is expressed constitutively in normal
> gastric and colonic mucosa, and differential expression occurs in
these
> tissues when they are inflamed. Upregulation of Hsp32 may be an
> adaptive response to protect mucosa from oxidative injury in patients
> with gastritis and inflammatory bowel disease.
>
>
>
> Dig Dis Sci. 2004 Sep;49(9):1433-7.
>
> Decreased total and corrected antioxidant capacity in patients with
> inflammatory bowel disease.
>
> Koutroubakis IE, Malliaraki N, Dimoulios PD, Karmiris K, Castanas E,
> Kouroumalis EA.
>
> Department of Gastroenterology, University Hospital Heraklion, P.O.
Box
> 1352, Heraklion 71110, Greece. ktjohn@xxxxxxxxxxxxxxx
>
> Oxidative stress and depletion of antioxidants may play a key role in
> the pathogenesis of inflammatory bowel disease (IBD)-related
intestinal
> damage. A new automated assay for the determination of blood total
> antioxidant capacity (TAC), based on the crocin bleaching method, has
> been used for the measurement of TAC and corrected TAC (cTAC) in
> patients with ulcerative colitis (UC) and Crohn's disease (CD) in
> comparison to healthy controls (HC). Ninety-four patients with UC, 97
> patients with CD, and 72 HC were included in this study. Serum TAC
was
> measured in all patients and controls on an Olympus AU-600 chemistry
> analyzer using a TAC kit. cTAC was calculated from TAC after
> subtraction of the interactions due to endogenous uric acid,
bilirubin
> and albumin. Mean serum TAC as well as cTAC levels were significantly
> lower in both UC and CD patients compared with HC (P < 0.0001).
> Patients with active UC had no different TAC and cTAC compared to
those
> with inactive disease. Patients with active CD had significantly
lower
> mean TAC compared to those with inactive disease but cTAC was not
> different between the two phases of disease activity. Patients with
> proctitis had significantly higher TAC and cTAC compared to patients
> with left-sided colitis and total colitis. In CD patients no
> association between disease localization and these markers was found.
> TAC and cTAC are significantly reduced in IBD patients compared with
> controls irrespective of disease activity. The decreased antioxidant
> defenses may be a primary phenomenon severely compromising the mucosa
> and therefore increase susceptibility to oxidative tissue damage.
>
>
>
> World J Gastroenterol. 2005 Jan 21;11(3):403-6.
>
> Lipid peroxidation and antioxidant status in colorectal cancer.
>
> Skrzydlewska E, Sulkowski S, Koda M, Zalewski B, Kanczuga-Koda L,
> Sulkowska M.
>
> Department of Analytical Chemistry, Medical University of Bialystok,
> Mickiewicza 2, 15-230 Bialystok, Poland. skrzydle@xxxxxxxxxx
>
> AIM: Reactive oxygen species (ROS) can induce carcinogenesis via DNA
> injury. Both enzymatic and non-enzymatic parameters participate in
cell
> protection against harmful influence of oxidative stress. The aim of
> the present study was to assess the levels of final lipid
peroxidation
> products like malondialdehyde (MDA) and 4-hydroxy-2-nonenal (4-HNE)
in
> primary colorectal cancer. Moreover, we analysed the activity of main
> antioxidative enzymes, superoxide dismutase (Cu, Zn-SOD), catalase
> (CAT), glutathione peroxidase (GSH-Px) and glutathione reductase
> (GSSRG-R) and the level of non-enzymatic antioxidants (glutathione,
> vitamins C and E). METHODS: Investigations were conducted in 81
primary
> colorectal cancers. As a control, the same amount of sample was
> collected from macroscopically unchanged colon regions of the most
> distant location to the cancer. Homogenisation of specimens provided
> 10% homogenates for our evaluations. Activity of antioxidant enzymes
> and level of glutathione were determined by spectrophotometry. HPLC
> revealed levels of vitamins C and E and served as a method to detect
> terminal products of lipid peroxidation in colorectal cancer.
RESULTS:
> Our studies demonstrated a statistically significant increase in the
> level of lipid peroxidation products (MDA-Adc.muc.-2.65+/-0.48
nmol/g,
> Adc.G3-2.15+/-0.44 nmol/g, clinical IV stage 4.04+/-0.47 nmol/g,
> P<0.001 and 4-HNE-Adc.muc. -0.44+/-0.07 nmol/g, Adc.G3-0.44+/-0.10
> nmol/g, clinical IV stage 0.52+/-0.11 nmol/g, P<0.001) as well as
> increase of Cu,Zn-SOD (Adc.muc.-363+/-72 U/g, Adc.G3-318+/-48 U/g,
> clinical IV stage 421+/-58 U/g, P<0.001), GSH-Px (Adc.muc.
-2143+/-623
> U/g, Adc.G3-2005+/-591 U/g, clinical IV stage 2467+/-368 U/g,
P<0.001)
> and GSSG-R (Adc.muc.-880+/-194 U/g, Adc.G3-795+/-228 U/g, clinical IV
> stage 951+/-243 U/g, P<0.001) in primary tumour comparison with
normal
> colon (MDA-1.39+/-0.15 nmol/g, HNE-0.29+/-0.03 nmol/g, Cu,
> Zn-SOD-117+/-25 U/g, GSH-Px-1723+/-189 U/g, GSSG-R-625+/-112 U/g)
> especially in mucinous and G3-grade adenocarcinomas as well as
clinical
> IV stage of colorectal cancer. We also observed a decrease of CAT
> activity (Adc.muc. -40+/-14 U/g, clinical IV stage 33+/-18 U/g vs
> 84+/-17 U/g, P<0.001) as well as a decreased level of reduced
> glutathione (clinical IV stage 150+/-48 nmol/g vs 167+/-15 nmol/g,
> P<0.05) and vitamins C and E (vit. C-clinical IV stage 325+/-92
nmol/g
> vs 513+/-64 nmol/g, P<0.001; vit. E-clinical IV stage 13.3+/-10.3
> nmol/g vs 37.5+/-5.2 nmol/g). CONCLUSION: Colorectal carcinogenesis
is
> associated with serious oxidative stress and confirms that gradual
> advancement of oxidative-antioxidative disorders is followed by
> progression of colorectal cancer.
If you are interested in curing crohn's and/or colitis and/or ibd
and/or gastritis, read this book:
http://www.amazon.com/exec/obidos/ASIN/0969276818/qid=1115300284/sr=2-1/ref=pd_bbs_b_2_1/002-4089772-9359217
read the reviews
Those grains will get you every time.
TC
.
- References:
- For those with IBS, Crohn's, IBD, gastritis, etc.
- From: montygram
- For those with IBS, Crohn's, IBD, gastritis, etc.
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