Wrzesień 24, 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 🙂

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).
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).
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).
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).
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).
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
bacteria in infants born by c-section delivery may be disturbed for
up to 6 months (26).
research shows that antibiotic use in the immediate period after
birth can severely alter the composition and population of gut
microbiota in infants (27).
they also suggest that breast milk can help re-establish a healthy
balance of bacteria and antibodies even after use of antibiotics
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).
drugs, like Prednisolone, Hydrocortisone etc. also can damage gut
flora (39) and corticosteroid therapy decreases the resistance of a
host to C. Albicans (40).
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.
research clearly shows gliadin, one of the proteins in gluten,
increases intestinal permeability in both those with, and those
without, celiac
disease (44).
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)
lectin called wheat germ agglutinin, that is it found in higher
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).
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).
term exposure to stress led to changes in
composition, diversity and number of gut microorganisms, according to
scientists from The Ohio State University (69).
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).
stress slows normal small intestinal transit time, encourages
overgrowth of bacteria, and even compromises the intestinal barrier
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).
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).
important are prebiotic foods or supplements, because fermentable
fibers stimulate the growth and activity of bacteria.
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).
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.
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.
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).
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,
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
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.
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,
Kosiewicz M., Zirnheld A. L, Alard P., 2011, Gut Microbiota,
Immunity, and Disease: A Complex Relationship,
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.
Fasano A., Shea-Donohue T., 2005, Mechanisms of Disease: the role of
intestinal barrier function in the pathogenesis of gastrointestinal
autoimmune diseases,
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
Gershon M., 1999, The Second Brain: A Groundbreaking New
Understanding of Nervous Disorders of the Stomach and Intestine,
Harper Perennial, USA
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,
Frye R.E., Melnyk S., MacFabe D.F., 2013, Unique acyl-carnitine
profiles are potential biomarkers for acquired mitochondrial disease
in autism spectrum disorder,
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,
Bowe W.P., Logan A.C., 2011, Acne vulgaris, probiotics and the
gut-brain-skin axis – back to the future?,
Shen J, Obin MS, Zhao L., 2013, The gut microbiota, obesity and
insulin resistance, http://www.ncbi.nlm.nih.gov/pubmed/23159341
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
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
Arrieta M.C., Bistritz L., Meddings J.B., 2008, Alterations in
intestinal permeability,
Kharrazian D., Why Do I Still Have !yroid Symptoms? When My Lab Tests
Are Normal, Morgan James Publishing, USA, 127
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,
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,
Grivennikov SI, et al., 2012, Adenoma-linked barrier defects and
microbial products drive IL-23/IL-17-mediated tumour growth,
Rogers AB., 2011, Distance burning: how gut microbes promote
extraintestinal cancers, http://www.ncbi.nlm.nih.gov/pubmed/21637019
Yamamoto M.L., 2013, Intestinal Bacteria Modify Lymphoma Incidence
and Latency by Affecting Systemic Inflammatory State, Oxidative
Stress, and Leukocyte Genotoxicity,
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
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
Zetterström R, Bennet R, Nord KE., 1994, Early infant feeding and
micro-ecology of the gut, http://www.ncbi.nlm.nih.gov/pubmed/7825464
Bullen CL, Tearle PV, Stewart MG., 1997, The effect of „humanised”
milks and supplemented breast feeding on the faecal flora of infants,
Mackie R.I., Sghir A., Gaskins H.R., 1999, Developmental microbial
ecology of the neonatal gastrointestinal tract,
Dethlefsen L., Relman D.A., 2010, Incomplete recovery and
individualized responses of the human distal gut microbiota to
repeated antibiotic perturbation,
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.,
65(2): 171–176
34) Seelig M.,1966,
The role of antibiotics in the pathogenesis of Candida infections.
Am. J.
Med. 40:887-917
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,
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
Hurley DL, Balow JE, Fauci AS., 1975, Experimental disseminated
candidiasis. II, Administration of glucocorticosteroids,
susceptibility to infection, and immunity,
Relloso M, Aragoneses-Fenoll L, Lasarte S, et al., 2011, Estradiol
impairs the Th17 immune response against Candida albicans,
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,
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
Drago S,et al., 2006, Gliadin, zonulin and gut permeability: Effects
on celiac and non-celiac intestinal mucosa and intestinal cell lines,
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
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
Dalla Pellegrina C., 2009, Effects of wheat germ agglutinin on human
gastrointestinal epithelium: insights from an experimental model of
immune/epithelial cell interaction,
Guzyeyeva G.V., 2008, Lectin glycosylation as a marker of thin gut
49) Maslowski K.,
Mackay C.R., 2011, Diet, gut microbiota and immune responses,
50) Knight L.,
Fletcher J., Growth of Candida albicans in Saliva: Stimulation by
Glucose Associated with Antibiotics, Corticosteroids, and Diabetes
51) Patel B.,
Schutte R., Sporns P., et al., 2002, Potato glycoalkaloids adversely
affect intestinal permeability and aggravate inflammatory bowel
52) Mensinga T.T.
Sips A.J., Rompelberg C.J., et al., 2004, Potato glycoalkaloids and
adverse effects in humans: an ascending dose study,
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,
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,
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,
57) Prykhod’ko O.,
et al., 2009, Precocious gut maturation and immune cell expansion by
single dose feeding the lectin phytohaemagglutinin to suckling rats,
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,
59) Haeney
M.R .,et al., 1982, Soya protein antibodies in man: their occurrence
and possible relevance in coeliac disease,
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
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.
Gibson PR, Shepherd SJ., 2012, Food choice as a key management
strategy for functional gastrointestinal symptoms,
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

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:

Kuwabara A., et al., 2009, High prevalence of vitamin K and D
deficiency and decreased BMD in inflammatory bowel disease,
67) Lyte M.,
Vulchanova L., Brown D.R., 2011, Stress at the intestinal surface:
catecholamines and mucosa-bacteria interactions,

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,
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,
73) Naruszewicz M.,
Johansson M.L., Zapolska-Downar D., Bukowska H., 2002, Effect of
Lactobacillus plantarum 299v on cardiovascular disease risk factors
in smokers,
74) Bowe W.P., Joshi
S.S., Shalita A.R., 2010, Diet and acne,
75) Parvez S., Malik
K.A., Ah Kang S., Kim H.Y. , 2006, Probiotics and their fermented
food products are beneficial for
76) Corridoni D, et
al.,2012, Probiotic bacteria regulate
intestinal epithelial permeability in experimental ileitis by a
TNF-dependent mechanism,
77) Barbara, G., et
al., 2012, Mucosal permeability and immune activation as potential
therapeutic targets of probiotics in irritable bowel syndrome,
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,
79) Chae, C.S., et
al., 2012, Prophylactic effect of probiotics on the development of
experimental autoimmune myasthenia gravis,
80) Fooks L.J.
,Gibson G.R., 2002, Probiotics as modulators of the gut flora,
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,
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,
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
87) Donlan R.M.,
2002, Biofilms: microbial life on surfaces,
88) O’Hara
A.M., Shanahan F., 2006, The gut flora as a forgotten organ,

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