Dlaczego PALEO?

Masz dość wiecznych nieskutecznych diet? A może wciąż czujesz głód i nie potrafisz przestać myśleć o jedzeniu? Marzysz o tym aby jeść do syta i nie liczyć kalorii? Chcesz zrzucić tkankę tłuszczową, mieć więcej energii, lepsze samopoczucie? Cierpisz na otyłość, choroby autoimmunologiczne, cukrzycę, choroby serca, alergie, trądzik, depresję lub kiepski nastrój, problemy trawienne, PCO, zaburzenia hormonalne, brak energii? Jeżeli tak, jesteś w odpowiednim miejscu!

O paleo, medycynie naturalnej i odchudzaniu w oparciu o badania, fakty, doświadczenie. Analiza powszechnych przekonań dotyczących diety, odchudzania i zdrowia oraz holistyczne podejście do człowieka na podstawie konkretnych argumentów.

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24.09.2013

Jak ważne są zdrowe jelita - moja ostatnia praca naukowa (ang)

Parę osób było ciekawych jak wygląda przykładowa praca naukowa, które regularnie piszę. Niektórzy pytali bezpośrednio o ten temat. Poniżej można poczytać jak ważne są jelita dla naszego ogólnego zdrowia.
Niestety praca jest po angielsku, ale z powodu braku czasu nie jestem obecnie w stanie jej przetłumaczyć :(
Wszelkie prawa oczywiście zastrzeżone :)



The human bowel flora can be managed so as to produce a major positive impact on health”


Many doctors, from the ancients to the moderns, have noted the importance of the bowel in the body’s health. Ancient Hippocrates believed that “death begins in the colon.” Today we are aware of the importance and many functions of the bowel and bowel flora. There are two important and closely related variables that determine our gut health: the intestinal flora and the gut barrier.
It is said that a human has more bacteria in the body than human cells (1) or more than there is stars in the sky. Some source estimated that there are 100 trillion microorganisms in our bowel (2). Those bacteria is related to the health of the bowel and since many diseases start in the gut, it is crucial to focus on having a healthy gut flora
The gut flora has many functions like: nutrient uptake, protection against pathogens, viruses and opportunistic bacteria, nutrient creation (i.e.: Biotin, vitamin K2), regulation of metabolism or preventing systemic and gut inflammation. Deregulated gut flora has been linked to many different diseases, i.e.: autism, depression, autoimmune conditions, inflammatory bowel disease or type 1 diabetes and even cancer (3).
Moreover between 70-85% of our immunity resides in our gut. Beneficial bacteria provide antibiotic and antiviral substances for protection. Lactic acid bacteria enhance systemic immunity by increasing: B cells, phagocytic activity, IgA, IgG, IgM and secretory IgA which boast antibody activity (4). Furthermore it increases gamma interferon which supports white blood cells to fight infections and disease. Hence, when the essential gut flora becomes damaged and imbalanced, it causes disruptions in the function of the immune system.
Our immunity is partial determined early in a lifetime. Studies have shown that the gut flora has a profound influence on the development and maturation of the immune system after birth. It is believed that colonization of the gut begins when the unborn child swallows amniotic fluid containing microbes from the mother’s gut (5), (6).
The process of gut colonization with flora is influenced by method of delivery, with vaginal delivery resulting in significantly faster rates of colonization (7).
The intestinal barrier is the main interface between the immune system and the external environment and aim to prevent foreign substances from entering the body. If the intestinal lining gets damaged (causing leaky gut), some unwanted molecules get to pass through into the bloodstream and the body produce an immune response in order to attack them. It has been shown that the integrity of the intestinal barrier is a major factor in autoimmune disease (8) and leaky gut is a precondition to developing autoimmunity (9).
An immune response affects not only the gut itself, but also other organs and tissues. These include the skeletal system, the pancreas, the kidney, the liver and the brain (8).
Leaky gut can manifest as skin problems like eczema or psoriasis, heart failure, autoimmune conditions affecting the thyroid or joints (rheumatoid arthritis), mental illness, autism spectrum disorder, depression and many more.
Poor bowel health and poor mental health seems to be inextricably connected. Regarding to Michael Gershon 95% of the body’s serotonin resides in the gut. Moreover “serotonin plays a critical role in digestion and without it we would not have peristalsis (movement)”. Gut is often called the “second brain”, as it is the only organ with an independent nervous system, an intricate web of 100 million neurons embedded in the intestinal wall. Furthermore, human bowel bacteria produce hundreds of neurochemicals that the brain uses (10).
Some studies suggest that the bacteria that reside in the human gut influence children with autism spectrum disorder. There are new evidences that “autism is closely associated with a distinct gut microflora, that can be characterized by reduced richness and diversity as well as by altered composition and structure of microbial community”, and it is proven that children with autism had a lower diversity of gut microbiomes compared with healthy control individuals (11).
Moreover, researchers found evidence of abnormal energy metabolism in a group of autistic children, as a result compounds produced by gut bacteria frequently found in people with autism (12).
The human bowel flora is also important for skin heath. Almost 100 years ago study showed positive reactivity to stool-isolated bacteria compared to none of the control patients without active skin disease. Another study suggests that altered gut microbiota promotes, in both gut and the skin, the release of substance P., which plays major role in skin conditions (13).
Moreover the bowel microbiota has impact on lipids and tissue fatty acid profiles, and may influence sebum production as well as the fatty acid composition of the sebum (14).
It is hypothesized that bowel flora has an impact on weight gain. Although research into the many ways gut flora influence obesity is in early stages, there are some new studies suggest the important connection between bowel flora and the regulation of energy balance and weight (15), (16), (17). We can assume that intestinal flora have been implicated in many mechanisms that may contribute to weight gain, including enhanced lipopolysaccharide production leading to insulin resistance or suppression of fasting-induced adipose factor.
A healthy bowel flora is also crucial for thyroid health, because poor gut health can suppress thyroid function and trigger thyroid autoimmune diseases (When the intestinal barrier becomes permeable) (18).
Mo rover, human gut bacteria assist in converting inactive T4 into the active form of thyroid hormone, T3. About 20 percent of T4 is converted to T3 in the GI tract, in the forms of T3 sulfate (T3S) and triidothyroacetic acid (T3AC). The conversion of T3S and T3AC into active T3 requires an enzyme called intestinal sulfatase (19).
Furthermore, it seems that lipopolysaccharides reduce thyroid hormone levels; increase amounts of inactive T3; decrease TSH and promote autoimmune thyroid disease (20).
Altered gut flora can result in constipation, hence elevations in estrogen levels might be observed due to impaired hormone clearance. High estrogen levels cause an increase in thyroid binding globulin, hence lower levels of unbound (free) thyroid hormone (21).
New research suggest that a microbial byproduct of intestinal bacteria contributes to heart disease and serves as an accurate screening tool for predicting future risks of heart attack, stroke and death in persons not otherwise identified by traditional risk factors and blood tests (22).
Moreover, there is a concern that bowel flora play an important role in cancer development. There are some suggestions that cancers mount an inflammatory response through microbial-dependent mechanisms that fuel their development and growth (23), (24).
Recently, researchers reported that specific bacteria found in the intestines might be major contributors to lymphoma. Furthermore, there are some studies suggest, that bacteria DNA gets transferred to human cells, in a process known as lateral gene transfer (LGT0), and that could have an important role in human diseases associated with mutation, hence may play a role in carcinogenesis (25).
Our modern lifestyle leads to a dysfunctional gut flora through various causes, although hereditary factor might be more important than it's believed. Gut flora is passed on from mother to child during birth, breastfeeding and other contact. The child also comes in contact with microorganisms through other family members.
Gut bacteria in infants born by c-section delivery may be disturbed for up to 6 months (26).
The research shows that antibiotic use in the immediate period after birth can severely alter the composition and population of gut microbiota in infants (27).
But they also suggest that breast milk can help re-establish a healthy balance of bacteria and antibodies even after use of antibiotics (28).
On the other hand, supplementing breast milk with even just a little bit of formula can affect the acidity of the gut environment, possibly promoting the presence of harmful bacteria and threatening the integrity of the gut lining (29), (30).
Antibiotic are in excessive use nowadays, although the consequences might be permanent. Studies have shown that antibiotic use causes a profound and rapid loss of diversity and a shift in the composition of the gut flora (31). The crucial point is that, this diversity is not recovered after antibiotic use without intervention. This damage to the gut flora promotes an overgrowth of opportunistic flora and especially yeasts like Candida (32), (33), (34). It is well proven, that unbalanced bowel flora is a contributing factor in autoimmunity (35) and in the formation of a proper immune response (36), (37).
Furthermore, other medicines have been connected with bowel flora damage. Non-steroidal anti-inflammatory drugs have been linked to increased gut permeability (38).
Steroid drugs, like Prednisolone, Hydrocortisone etc. also can damage gut flora (39) and corticosteroid therapy decreases the resistance of a host to C. Albicans (40).
Aspirin, ibuprofen, etc., that are often prescribed for long periods of time can stimulate the growth of pathogenic bacteria (39). Contraceptive pills cause damage to the gut flora (40) and has also been linked to impaired immunity to Candida Albicans (41).
Obviously the most important factor in person health is diet. Cereals seem to be very problematic, as they are contain antinutrients such as alkylresorcinols, alpha-amylase inhibitors, protease inhibitors and lectins. Gluten alters bowel barrier functions in patients with IBS-D and there are some evidences that non-celiac gluten intolerance is a real issue (42), (43), hence gluten might be problematic for everyone.
New research clearly shows gliadin, one of the proteins in gluten, increases intestinal permeability in both those with, and those without, celiac disease (44).
Gliadin causes zonulin levels to increase in people with the genetic pre-disposition to celiac disease (45). As zonulin levels go up, the tight junctions become lax, widening the space between the cells of the lining and increasing gut permeability (46), which allow large food particles out into the blood stream and interstitial fluids that shouldn't be there (vide leaky gut).
A lectin called wheat germ agglutinin, that is it found in higher concentrations in whole wheat, seems to be extremely problematic. WGA stimulates the synthesis of pro-inflammatory chemical messengers in intestinal and immune cells (47), and has been shown to play a causative role in chronic thin gut inflammation (48).
Diets that are high in animal products might be also harmful. Excess protein is available to gut bacteria for fermentation and that process produces a number of toxic byproducts.
Studies show that a typical diet high in sugar and grains promotes an unhealthy gut flora composition (49). Too many sugary foods and processed carbohydrates increase numbers of Candida species (351), Streptococci, Staphylococci, some Clostridia species, Bacteroids and some aerobic opportunistic bacteria (39).
Furthermore, some nightshades eaten in high amounts can be problematic to human bowel flora. The levels of glycoalkaloids in potatoes have been linked to increased intestinal permeability in animals and humans (51), (52), (53), (54).
Legumes also contain some toxins which suspend digestion and damage the gut. Phytohaemagglutinin, a kidney bean lectin, makes the gut leaky, blocks stomach acid production, promoting bacterial overgrowth of the small intestine, overpopulates the gut with immature cells that are easily colonized by E. coli and other pathogens and disturbs the mucus (55), (56), (57).
Alpha-amylase inhibitors in legumes (as well as in cereals) prevent starch digestion and leads to gut bloating and multiplication of pathogenic gut bacteria (58). Some antibodies to soy proteins have been identified in duodenitis, Crohn’s disease, ulcerative colitis, and coeliac disease (59).
There are some evidences that excessive omega-6 to omega-3 ratio can worsen inflammatory bowel disease. It is suggested that being in the upper quartile of intake of omega-6 fatty acids raised the risk of ulcerative colitis by 149% (60).
Fruits and vegetables are rightfully considered health foods, but in some situations even they can cause problems. FODMAP is an acronym for Fermentable Oligosaccharides, Disaccharides, Monosaccharides And Polyols. The biggest concern with FODMAP is fact, that they are poorly absorbed in the small intestine (61). As the bacteria ferment the nutrients, their waste products can increase intra-abdominal pressure causing both stomach pain and reflux problems (62). It is thought that some of their by-products activate a feedback loop that regulates gut motility, accelerating small bowel transit times (63). Furthermore, there is also an increase in osmotic load due to the size of some FODMAP molecules (64).
Even limited alcohol consumption can cause gastrointestinal problems too. “Just one drink per day for women - two for men - could lead to small intestinal bacterial overgrowth (SIBO) and subsequently cause gastrointestinal symptoms like bloating, gas, abdominal pain, constipation and diarrhea”, according to the results of a new study unveiled at the American College of Gastroenterology's (ACG) 76th Annual Scientific meeting in Washington (65).
Diet that lack vitamin in minerals can influence human bowel flora. Malnutrition contributes to bowel disease by impairing immunity and slowing intestinal healing, i.e. most inflammatory bowel disease patients are severely deficient in vitamin K2 (66).
Many other lifestyle factors, beyond diet and medicines, can have an impact on bowel health. Stress is one of them. There is some evidence suggest that gut microbiota may respond directly to stress-related host signals (67). It is proven that stress affect the physiological function of the gut and cause changes in gastric secretion, gut motility, mucosal permeability and barrier function, visceral sensitivity and mucosal blood flow (68).
Long term e
xposure to stress led to changes in composition, diversity and number of gut microorganisms, according to scientists from The Ohio State University (69).
Changes in the composition of the microbiota, can occur possibly due to the changes in neurotransmitter and inflammatory cytokine levels. Hence, chronic exposure to stress may lead to the development of a variety of gastrointestinal diseases such as gastroesophageal reflux disease (GERD), peptic ulcer disease, IBD, IBS, and even food allergies (68).
Psychological stress slows normal small intestinal transit time, encourages overgrowth of bacteria, and even compromises the intestinal barrier (70).
On the other hand, we can take some actions to better bowel health and hence better overall health. It is important to be aware, that we can and should try to restore our bowel health in many ways. Taking probiotic and prebiotic is one of them, Consuming probiotic foods and/or supplements might influence both mood and acne, by reducing systemic inflammatory cytokines and oxidative stress, increasing peripheral tryptophan levels, normalizing brain levels of stress hormones, modulating tissue lipid levels, and possibly even regulating glycemic control (71), (72), (73), (74).
Research suggests that certain probiotics may be useful in a number of ways, including modulating the immune system, reducing allergic response, shortening the length and severity of colds in children, relieving diarrhea, and inhibiting irritable bowel symptoms. Many beneficial bacteria can be obtained straight from the diet in the form of fermented or cultured foods, like sauerkraut, kimchi, kefir, beet kvass or yogurt (75).
Especially important are prebiotic foods or supplements, because fermentable fibers stimulate the growth and activity of bacteria.
Beyond restoring balance to the gut microflora and modulating the immune system, research has shown that administration of probiotics can have a direct effect on the tight junctions between enterocytes in the gut—resulting in decreased intestinal permeability (76 -85).
Furthermore, some studies have demonstrated significant improvements in depression, anger, anxiety, as well as lower levels of cortisol among otherwise healthy adults taking a daily probiotic supplement as compared to a placebo (86).
On the other hand, addressing the problem with pathogens and bacteria may be more complicated than taking a probiotic supplement. Most bacterial species will build biofilms - polysaccharide and protein meshworks built on bodily surfaces, like the gut lining, and protect bacteria from the immune system, antibiotics, and other bacterial species. Without dissolving pathogenic biofilms probiotics may not be successful therapy. Pathogenic species known to generate biofilms include Legionella pneumophila, S. aureus, Listeria monocytogenes, Campylobacter spp., E. coli O157:H7, Salmonella typhimurium, Vibrio cholerae, and Helicobacter pylori. (87).
Healthy bowel flora is crucial for our overall health, so one should be aware that taking a systematic approach that focuses on a gut flora is the most successful strategy in world full of innervations like Cesarean section, antibiotics, too much hygiene, lack of contact with animals and microbes or environmental toxins.
In practice that means eliminating problematic food like: gluten, sugar, refined flour and other highly processed and refined foods that inflame the gut; reducing use of certain medications; avoiding environmental toxins; managing stress or eating a natural diet rich in vegetables, fruits, meats, eggs, fermentable fibers and fermentable foods.
The 2005 Nobel prize in Physiology and Medicine awarded to Robin Warren and Barry Marshall is a reminder that the solution to some human diseases does not reside solely within the host but rather might be found at the interface with the microbial environment. Manipulation of the flora is becoming a realistic therapeutic and prophylactic strategy for many infectious, inflammatory and even neoplastic diseases within the gut” (88).

References:
1) Gill H.S., Guarner F., 2004, Probiotics and human health: a clinical perspective, http://pmj.bmj.com/content/80/947/516.abstract
2) Bäckhed F. et al., 2005, Host-Bacterial Mutualism in the Human Intestine, http://www.sciencemag.org/content/307/5717/1915.abstract
3) Holmes E, Li JV, Athanasiou T, Ashrafian H, Nicholson JK., 2011, Understanding the role of gut microbiome-host metabolic signal disruption in health and disease, Trends Microbiol.19(7), 349–359
4) Maldonado Galdeano, C., de Moreno de Leblanc, A., Dogi, C. and Perdigón, G., 2010, Lactic Acid Bacteria as Immunomodulators of the Gut-Associated Immune System, in Biotechnology of Lactic Acid Bacteria: Novel Applications, Wiley-Blackwell, Oxford, UK.
5) Bouskra D, Brézillon C, Bérard M, Werts C, Varona R, Boneca IG, Eberl G., 2008, Lymphoid tissue genesis induced by commensals through NOD1 regulates intestinal homeostasis, Institut Pasteur, Laboratory of Lymphoid Tissue Development, http://www.ncbi.nlm.nih.gov/pubmed/18987631
6). Kosiewicz M., Zirnheld A. L, Alard P., 2011, Gut Microbiota, Immunity, and Disease: A Complex Relationship, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3166766
7) Gronlund, M., Lehtonen O., Eerola E., & Kero, P., 1999. Fecal microflora in healthy infants born by different methods of delivery: permanent changes in intestinal flora after cesarean delivery, Journal of Pediatric Gastroenterology and Nutrition, 28, 19–25.
8) Fasano A., Shea-Donohue T., 2005, Mechanisms of Disease: the role of intestinal barrier function in the pathogenesis of gastrointestinal autoimmune diseases, http://www.direct-ms.org/pdf/LeakyGutMS/Fasano%20intestinal%20barrier%20autoimmunity.pdf
9) Visser J, Rozing J, Sapone A, Lammers K, Fasano A., 2009, Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms, University Medical Center Groningen, the Netherlands, http://www.ncbi.nlm.nih.gov/pubmed/19538307
10) Gershon M., 1999, The Second Brain: A Groundbreaking New Understanding of Nervous Disorders of the Stomach and Intestine, Harper Perennial, USA
11) Kang D-W, Park JG, Ilhan ZE, Wallstrom G, LaBaer J, et al. (2013) Reduced Incidence of Prevotella and Other Fermenters in Intestinal Microflora of Autistic Children, http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0068322
12) Frye R.E., Melnyk S., MacFabe D.F., 2013, Unique acyl-carnitine profiles are potential biomarkers for acquired mitochondrial disease in autism spectrum disorder, http://www.nature.com/tp/journal/v3/n1/abs/tp2012143a.html
13) Gueniche A, Benyacoub J, Philippe D, Bastien P, Kusy N, Breton L, Blum S, Castiel-Higounenc I., 2010, Lactobacillus paracasei CNCM I-2116 (ST11) inhibits substance P-induced skin inflammation and accelerates skin barrier function recovery in vitro, http://www.ncbi.nlm.nih.gov/pubmed/20965806
14) Bowe W.P., Logan A.C., 2011, Acne vulgaris, probiotics and the gut-brain-skin axis - back to the future?, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3038963/#__ffn_sectitle
15) Shen J, Obin MS, Zhao L., 2013, The gut microbiota, obesity and insulin resistance, http://www.ncbi.nlm.nih.gov/pubmed/23159341
16) DiBaise J.K et al., 2012, Impact of the Gut Microbiota on the Development of Obesity: Current Concepts, Division of Gastroenterology, Mayo Clinic, Scottsdale, Arizona, USA http://www.nature.com/ajgsup/journal/v1/n1/full/ajgsup20125a.html
17) Teixeira TF, Collado MC, Ferreira CL, Bressan J, Peluzio Mdo C., 2012, Potential mechanisms for the emerging link between obesity and increased intestinal permeability, Universidade Federal de Viçosa, Brazil, http://www.ncbi.nlm.nih.gov/pubmed/23084636
18) Arrieta M.C., Bistritz L., Meddings J.B., 2008, Alterations in intestinal permeability, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1856434/?tool=pubmed
19) Kharrazian D., Why Do I Still Have !yroid Symptoms? When My Lab Tests Are Normal, Morgan James Publishing, USA, 127
20) van der Poll T, Van Zee KJ, Endert E, Coyle SM, Stiles DM, Pribble JP, Catalano MA, Moldawer LL, Lowry SF, 1995, Interleukin-1 receptor blockade does not affect endotoxin-induced changes in plasma thyroid hormone and thyrotropin concentrations in man, http://www.ncbi.nlm.nih.gov/pubmed/7714108
21) Ben-Rafael Z, Struass JF 3rd, Arendash-Durand B, Mastroianni L Jr, Flickinger GL., 1987, Changes in thyroid function tests and sex hormone binding globulin associated with treatment by gonadotropin, http://www.ncbi.nlm.nih.gov/pubmed/3111894
23) Grivennikov SI, et al., 2012, Adenoma-linked barrier defects and microbial products drive IL-23/IL-17-mediated tumour growth, http://www.ncbi.nlm.nih.gov/pubmed/23034650
24) Rogers AB., 2011, Distance burning: how gut microbes promote extraintestinal cancers, http://www.ncbi.nlm.nih.gov/pubmed/21637019
25) Yamamoto M.L., 2013, Intestinal Bacteria Modify Lymphoma Incidence and Latency by Affecting Systemic Inflammatory State, Oxidative Stress, and Leukocyte Genotoxicity, http://cancerres.aacrjournals.org/content/73/14/4222.abstract
26) Grönlund MM, Lehtonen OP, Eerola E, Kero P., 1999, Fecal microflora in healthy infants born by different methods of delivery: permanent changes in intestinal flora after cesarean delivery, Turku University Central Hospital, Finland, http://www.ncbi.nlm.nih.gov/pubmed/9890463
27) Fallani, M., Young, D., Scott, J., Norin, E., Amarri, S., Adam, R., Aguilera, M., Khanna, S., Gil, A., Edwards, C. A., and Doré, J. ,2010, Intestinal microbiota of 6-week-old infants across Europe: geographic influence beyond delivery mode, breast-feeding, and antibiotics, http://www.ncbi.nlm.nih.gov/pubmed/20479681
28) Zetterström R, Bennet R, Nord KE., 1994, Early infant feeding and micro-ecology of the gut, http://www.ncbi.nlm.nih.gov/pubmed/7825464
29) Bullen CL, Tearle PV, Stewart MG., 1997, The effect of "humanised" milks and supplemented breast feeding on the faecal flora of infants, http://www.ncbi.nlm.nih.gov/pubmed/21296
30) Mackie R.I., Sghir A., Gaskins H.R., 1999, Developmental microbial ecology of the neonatal gastrointestinal tract, http://ajcn.nutrition.org/content/69/5/1035s.full#fn-group-1
31) Dethlefsen L., Relman D.A., 2010, Incomplete recovery and individualized responses of the human distal gut microbiota to repeated antibiotic perturbation, http://www.pnas.org/content/early/2010/09/14/1000087107
32) Seelig M., Mechanisms by which antibiotics increase the incidence and severity of candidiasis and alter the immunological defenses, Bacteriol Rev. 1966 June; 30(2): 442–459
33) Huppert M., MacPherson D.A., Cazin J., PATHOGENESIS OF CANDIDA ALBICANS INFECTION FOLLOWING ANTIBIOTIC THERAPY, J Bacteriol. 1953 February; 65(2): 171–176
34) Seelig M.,1966, The role of antibiotics in the pathogenesis of Candida infections. Am. J.
Med. 40:887-917
35) Tlaskalová-Hogenová H., 2004, Commensal bacteria (normal microflora), mucosal immunity and chronic inflammatory and autoimmune diseases, http://www.ncbi.nlm.nih.gov/pubmed/15158604
37) Rook G.A.W, Brunet L.R., 2005, Microbes, immunoregulation, and the gut, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1774411/
38) Sigthorssona G., et al., 1998, Intestinal permeability and inflammation in patients on NSAIDs, http://gut.bmj.com/content/43/4/506
39) D Campbell-McBride N., Gut and Pysychology Syndrome, Revised and Expanded edition.
United Kingdom. Medinform Publishing, 2010
40) Hurley DL, Balow JE, Fauci AS., 1975, Experimental disseminated candidiasis. II, Administration of glucocorticosteroids, susceptibility to infection, and immunity, http://www.ncbi.nlm.nih.gov/pubmed/1185009
41) Relloso M, Aragoneses-Fenoll L, Lasarte S, et al., 2011, Estradiol impairs the Th17 immune response against Candida albicans, http://www.ncbi.nlm.nih.gov/pubmed/21965175
42) Vazquez-Roque MI et al., 2013, A controlled trial of gluten-free diet in patients with irritable bowel syndrome-diarrhea: effects on bowel frequency and intestinal function, http://www.ncbi.nlm.nih.gov/pubmed/23357715
43) Biesiekierski J.R., 2011, Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial, http://www.ncbi.nlm.nih.gov/pubmed/21224837
44) Drago S,et al., 2006, Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines, http://www.ncbi.nlm.nih.gov/pubmed/16635908
45) Thomas KE, Sapone A, Fasano A, Vogel SN., 2006, Gliadin stimulation of murine macrophage inflammatory gene expression and intestinal permeability are MyD88-dependent: role of the innate immune response in Celiac disease, http://www.ncbi.nlm.nih.gov/pubmed/16456012
46) Lammers K.M., et al., 2006, Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3, http://www.ncbi.nlm.nih.gov/pubmed/18485912
47) Dalla Pellegrina C., 2009, Effects of wheat germ agglutinin on human gastrointestinal epithelium: insights from an experimental model of immune/epithelial cell interaction, http://www.ncbi.nlm.nih.gov/pubmed/19332085
48) Guzyeyeva G.V., 2008, Lectin glycosylation as a marker of thin gut inflammation, http://www.fasebj.org/cgi/content/meeting_abstract/22/1_MeetingAbstracts/898.3
49) Maslowski K., Mackay C.R., 2011, Diet, gut microbiota and immune responses, http://www.nature.com/ni/journal/v12/n1/full/ni0111-5.html
50) Knight L., Fletcher J., Growth of Candida albicans in Saliva: Stimulation by Glucose Associated with Antibiotics, Corticosteroids, and Diabetes Mellitus,
http://jid.oxfordjournals.org/content/123/4/371.extract
51) Patel B., Schutte R., Sporns P., et al., 2002, Potato glycoalkaloids adversely affect intestinal permeability and aggravate inflammatory bowel disease,
52) Mensinga T.T. Sips A.J., Rompelberg C.J., et al., 2004, Potato glycoalkaloids and adverse effects in humans: an ascending dose study, http://www.ncbi.nlm.nih.gov/pubmed/15649828
53) Keukens E.A., de Vrije T., van den Boom C., de Waard P., Plasman H.H., Thiel F., Chupin V., Jongen W.M., de Kruijff B., 1995, Molecular basis of glycoalkaloid induced membrane disruption, http://www.ncbi.nlm.nih.gov/pubmed/8541293
54) Smith D.B., Roddick J.G., Jones J.L., Potato glycoalkaloids: some unanswered questions, Trends in Food Sci Technol 1996;7:126-131
55) Kordás K., et al., 2011, Phytohaemagglutinin inhibits gastric acid but not pepsin secretion in conscious rats, http://www.ncbi.nlm.nih.gov/pubmed/11595455
56) Pusztai A., et al., 1993, Kidney bean lectin-induced Escherichia coli overgrowth in the small intestine is blocked by GNA, a mannose-specific lectin, http://www.ncbi.nlm.nih.gov/pubmed/8226393
57) Prykhod’ko O., et al., 2009, Precocious gut maturation and immune cell expansion by single dose feeding the lectin phytohaemagglutinin to suckling rats, http://www.ncbi.nlm.nih.gov/pubmed/18644165
58) Pusztai A., et al., 1995, Inhibition of starch digestion by alpha-amylase inhibitor reduces the efficiency of utilization of dietary proteins and lipids and retards the growth of rats, http://www.ncbi.nlm.nih.gov/pubmed/7782910
59) Haeney M.R .,et al., 1982, Soya protein antibodies in man: their occurrence and possible relevance in coeliac disease, http://www.ncbi.nlm.nih.gov/pubmed/7040491
60) IBD in EPIC Study Investigators, 2009, Linoleic acid, a dietary n-6 polyunsaturated fatty acid, and the aetiology of ulcerative colitis: a nested case-control study within a European prospective cohort study, http://www.ncbi.nlm.nih.gov/pubmed/19628674
61) Gibson, P. R. and Shepherd, S. J., 2010, Evidence-based dietary management of functional gastrointestinal symptoms: The FODMAP approach. Journal of Gastroenterology and Hepatology, 25: 252–258. doi: 10.1111/j.1440-1746.2009.06149.x
http://onlinelibrary.wiley.com/doi/10.1111/j.1440-1746.2009.06149.x/full
62) Gibson PR, Shepherd SJ., 2012, Food choice as a key management strategy for functional gastrointestinal symptoms, http://www.ncbi.nlm.nih.gov/pubmed/22488077
63) GIBSON, P. R., NEWNHAM, E., BARRETT, J. S., SHEPHERD, S. J. and MUIR, J. G. ,2007, Review article: fructose malabsorption and the bigger picture. Alimentary Pharmacology & Therapeutics, 25: 349–363. doi: 10.1111/j.1365-2036.2006.03186.x
http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2036.2006.03186.x/full
64) BARRETT, J. S., GEARRY, R. B., MUIR, J. G., IRVING, P. M., ROSE, R., ROSELLA, O., HAINES, M. L., SHEPHERD, S. J. and GIBSON, P. R. ,2010, Dietary poorly absorbed, short-chain carbohydrates increase delivery of water and fermentable substrates to the proximal colon. Alimentary Pharmacology & Therapeutics, 31: 874–882. doi: 10.1111/j.1365-2036.2010.04237.x
http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2036.2010.04237.x/full
66) Kuwabara A., et al., 2009, High prevalence of vitamin K and D deficiency and decreased BMD in inflammatory bowel disease, http://www.ncbi.nlm.nih.gov/pubmed/18825300
67) Lyte M., Vulchanova L., Brown D.R., 2011, Stress at the intestinal surface: catecholamines and mucosa-bacteria interactions, http://www.ncbi.nlm.nih.gov/pubmed/20941511
68) KONTUREK P., et al., 2011, STRESS AND THE GUT: PATHOPHYSIOLOGY, CLINICAL CONSEQUENCES, DIAGNOSTIC APPROACH AND TREATMENT OPTIONS
http://www.jpp.krakow.pl/journal/archive/12_11/pdf/591_12_11_article.pdf
69).http://www.sciencedirect.com/science/article/pii/S0889159110005295
70) Bowe W.P., , Logan A.C., 2011,Acne vulgaris, probiotics and the gut-brain-skin axis - back to the future?, http://www.gutpathogens.com/content/3/1/1
71) Li W., Dowd S.E., Scurlock B., Acosta-Martinez V., Lyte M., 2009, Memory and learning behavior in mice is temporally associated with diet-induced alterations in gut bacteria, http://www.ncbi.nlm.nih.gov/pubmed/19135464
72) Desbonnet L. Garrett L., Clarke G., Bienenstock J., Dinan T.G. , 2008, The probiotic Bifidobacteria infantis: An assessment of potential antidepressant properties in the rat, www.ncbi.nlm.nih.gov/pubmed/18456279
73) Naruszewicz M., Johansson M.L., Zapolska-Downar D., Bukowska H., 2002, Effect of Lactobacillus plantarum 299v on cardiovascular disease risk factors in smokers,
http://www.ncbi.nlm.nih.gov/pubmed/12450890
74) Bowe W.P., Joshi S.S., Shalita A.R., 2010, Diet and acne, http://www.ncbi.nlm.nih.gov/pubmed/20338665
75) Parvez S., Malik K.A., Ah Kang S., Kim H.Y. , 2006, Probiotics and their fermented food products are beneficial for health,
http://www.ncbi.nlm.nih.gov/pubmed/16696665
76) Corridoni D, et al.,2012, Probiotic bacteria regulate intestinal epithelial permeability in experimental ileitis by a TNF-dependent mechanism, http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042067
77) Barbara, G., et al., 2012, Mucosal permeability and immune activation as potential therapeutic targets of probiotics in irritable bowel syndrome, http://www.ncbi.nlm.nih.gov/pubmed/22955358
78) Bittner, A.C., et al., 2007, Prescript-assist probiotic-prebiotic treatment for irritable bowel syndrome: an open-label, partially controlled, 1-year extension of a previously published controlled clinical trial, http://www.ncbi.nlm.nih.gov/pubmed/17692729
79) Chae, C.S., et al., 2012, Prophylactic effect of probiotics on the development of experimental autoimmune myasthenia gravis, http://www.ncbi.nlm.nih.gov/pubmed/23284891
80) Fooks L.J. ,Gibson G.R., 2002, Probiotics as modulators of the gut flora, http://www.ncbi.nlm.nih.gov/pubmed/12215180
81) Kiseleva, E.P., et al., 2011, The role of components of Bifidobacterium and Lactobacillus in pathogenesis and serologic diagnosis of autoimmune thyroid disease, http://www.ncbi.nlm.nih.gov/pubmed/21831795
82) Ng S.C., et al., Mechanisms of action of probiotics: recent advances, http://www.ncbi.nlm.nih.gov/pubmed/18626975
83) Ruemmele F.M., et al., Clinical evidence for immunomodulatory effects of probiotic bacteria, http://www.ncbi.nlm.nih.gov/pubmed/19179874
84) Shida K., et al., Flexible cytokine production by macrophages and T cells in response to probiotic bacteria: a possible mechanism by which probiotics exert multifunctional immune regulatory activities, http://www.ncbi.nlm.nih.gov/pubmed/21637028
85) Schiffer, C., et al., A strain of Lactobacillus casei inhibits the effector phase of immune inflammation, http://www.ncbi.nlm.nih.gov/pubmed/21810608
86) Messaoudi M, et al.,2011, Assessment of psychotropic-like properties of a probiotic formulation (Lactobacillus helveticus R0052 and Bifidobacterium longum R0175) in rats and human subjects,
http://www.ncbi.nlm.nih.gov/pubmed/20974015
87) Donlan R.M., 2002, Biofilms: microbial life on surfaces, http://www.ncbi.nlm.nih.gov/pubmed/12194761
88) O'Hara A.M., Shanahan F., 2006, The gut flora as a forgotten organ, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1500832/














18 komentarzy:

  1. świetna robota! : ) nie mam teraz czasu, żeby przeczytać całe, ale na pewno przeczytam : )

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  2. A po polsku to przepraszam gdzie?

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  3. Brzmi to raczej jak dobrze udokumentowany i dobrze napisany artykuł niż praca naukowa (jak na pracę naukową tekst jest zbyt powierzchowny). Ale i tak bardzo ciekawy.

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    Odpowiedzi
    1. Zdecydowanie się zgadzam, jest to raczej wyliczanka konkretnych wniosków z przywołanych prac, niż gruntowna analiza. Zresztą domyślam się, że osoba oceniająca powyższe zwróci Ci uwagę na konstrukcję pracy, choćby wnioski zupełnie oderwane od reszty materiału.
      Ale gratuluję napisania, praktyka czyni mistrza.

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    2. No niestety żaden z Was nie trafił z przewidywaniem...
      Osoba oceniająca miała inne zastrzeżenia i zdecydowanie dostałam minus za zbyt dużo szczegółów. Tym się właśnie różni naturopatyczne podejście od konwencjonalnego. Myślę, że jestem po środku...

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    3. Również zgadzam się z tym, że jak na pracę naukową jest to powierzchowna praca. Szczegółów to nie było dużo. Za to było sporo przykładów.
      Nie mniej jednak bardzo fajnie się czytało.
      Wyłapałem błąd w bodajże piątym akapicie:
      partial -> partially

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  4. Witam. Ja odnosnie jelit i zoladka. Wykryto u mnie Helicobacter i w dodatku mam zapalenie blony sluzowej zoladka i dwunastnicy. W dodatku na tle zapalnym z gastroskopii wyszlo ze mam czesciowy zanik kosmkow jelitowych, Mysle ze tu pewnie sama dieta nie starczy by jednak pozbyc sie Helicobacter oraz stanu zapalnego. Jak mam sobie pomoc bo dostalem az 3 antybiotyki, IPP, probiotyki i sytuacja mnie po prostu przeraza. Jak moge sobie pomoc naturalnie? Czytalem na tym blogu wiele ciekawych informacji odnosnie kwasu solnego, no ale jak mam zapalenie w zoladku i dwunastnicy to chyba tego kwasu mam az za duzo i sie rozlewa ? Co ma mrobic jakies rady poza byciem na diecie Paleo co jestem juz 2 miesiace niestety problem dalej wystepuje :///

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    Odpowiedzi
    1. Przede wszystkim musisz zdecydować w jaki sposób chcesz się leczyć, albo konwencjonalnie albo naturalnie. Łączenie tego daje bardzo kiepskie rezultaty. Antybiotyki i IPP to leki hamujące objawy, mocno naruszające równowagę organizmu. Plus mające destrukcyjny wpływ na wątrobę. O ile toksyny możemy usunąć to szkody jakie wywołają zostają dłużej.
      Jest wiele naturalnych sposobów na HP i problemy jelitowe, jednak trzeba przeprowadzić diagnozę, zobaczyć jakie inne nierównowagi są w organizmie, jakie organy są dysfunkcyjne itd. Podałam kilka sposobów na samodzielne leczenie jelit nie tak dawno w osobnym poście :)

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    2. dziekuje bardzo :) poczytam jeszcze, przeraza mnie fakt brania antybiotykow :( zaryzykuje ten raz jak po miesiacu ich brania dalej nie bedzie poprawy czy cos to chyba dam sobie spokoj :)

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    3. MS, zapraszam do skomentowania.
      O nieszczelności naukowo przez naszego znajomego napisane:
      http://www.bioslone.pl/forum/index.php?topic=28138.msg195377#msg195377

      http://www.bioslone.pl/forum/index.php?topic=28348.0;topicseen

      W Polsce też o tym myślimy. Twój blog jest bardzo zbliżony. Podobnie myślimy. Czytałaś już trochę o Biosłone? Pewien doktor wykonał badania. Może więcej ludzi zrozumie jak ważne są jelita. Ja tego kiedyś nie rozumiałam albo nie doceniałam ich roli.

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    4. Bartek zdecyduj się czy jesteś kobietą czy mężczyzną.
      Jak dla mnie biosłone trochę zalatuje sektą...

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    5. Anonimowy, Bartek to zalogowany na googlu mój syn. Korzystam czasem z jego loginu. Niektórym nie podoba się styl Biosłone, bo nie pozwalają krytykować i podważać tam zawartej wiedzy, która ma te same podwaliny i brzmienie jak tutejszy blok MS. Dlatego tak bardzo jestem ciekawa jej opinii.
      Mama Bartka, Magda

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    6. Przepraszam za błąd, blog.:)

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    7. Sektą może i tak :) Ale nie powiedziałabym, że to celowe...czytałam, widziałam, nawet radia słuchałam...to wszystko wygląda hermetycznie, na zasadzie jest prawda i tylko jedna prawda. Nie jest to zarzuty, bo pod wieloma rzeczami mogę się podpisać rękami i nogami, ale myślę że wielu ludzi odstrasza takie podejście. Podoba mi się podejście do szczepień i tak radykalny głos w tej sprawie. W ogóle mam wrażenie, że bioslone wywodzi sie z dosc radykalnej naturoterapii, myle się? :)

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  5. Czy mieta może nasilac zgage?

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    Odpowiedzi
    1. Tak. Mięta rozluźnia zwieracz przełyku, co może powodować przepuszczanie treści żołądkowej.

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