# Is refined starch the primary cause of IBS?



## tummyrumbles

It's possible that most forms of IBS are caused by bacterial overgrowth and constipation, and that these in turn are due to a highly refined diet of starches and sugars. IBS-C is generally regarded as being a completely separate disorder to IBS-D although IBS-D could be a natural progression from IBS-C. Inflammation is more pronounced in IBS-D however also occurs in IBS-C. While most forms of IBS might be caused by long-term effects of a westernised diet PI-IBS may be caused by a sudden and acute bacterial overgrowth, often from a gastrointestinal infection.

All forms of IBS involve a difficult or protracted bowel evacuation, one way or the other. All forms of IBS seem to involve bacterial dysbiosis.

A westernised diet doesn't explain why only a small percentage of people have IBS, however inflammation is often the precursor of disease, and diet the precursor of inflammation. This post could more accurately have asked - Is refined starch the primary cause of disease? Most high-carb eaters don't have IBS, although probably have digestive complaints of some type. A lifetime of poor diet could cause IBS - or heart disease, obesity or cancer. Genetics might play a role in which of these ailments any one individual succumbs to but the main point is that a diet high in dense carbohydrates is likely to be harmful in the long-term.

The following is a very good study which looks at the inflammatory effects of a refined starch diet. While the study is concerned with obesity, the main points are that a highly refined diet causes inflammation through bacterial lipopolysaccharide (LPS) and bacterial dysbiosis. There is also a strong correlation between inflammation and IBS.

The conclusion is that natural carbohydrates are healthy however this isn't an IBS study. Most of us find that fibre exacerbates IBS symptoms although this is because most of us already have bacterial dysbiosis and bacteria feeds on all carbohydrate, making symptoms worse. For anyone trying to heal an inflamed colon, a low-flatulogenic diet comprising of well-cooked low FODMAP vegetables and meat/fish might be the safest option. A very inflamed colon might benefit from longer cooking. Fibre should be very gradually introduced to enable healthy bacterial re-population.

Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402009/

The following are the main points taken directly from this study:

Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity

Due to being made up of cells, virtually all "ancestral foods"(e.g. Paleo) have markedly lower carbohydrate densities than flour and sugar containing foods.

Acellular flours, sugars, and processed foods (refined flours and starches) produce an inflammatory microbiota via the upper gastrointestinal tract.

A diet of grain-free whole foods with carbohydrate from cellular tubers, leaves, and fruits may produce a (different) gastrointestinal microbiota

The Paleo diet increases satiety

Refined starch (acellular carbohydrate), not dietary fat, is the main cause of obesity

The Western diet has a higher proportion of carbohydrate mass compared to the "locked-in" low carbohydrate density of cellular plant food

This heavy, carbohyrate density leads to over-eating

Bacterial homeostatis has maladapted to this food excess.

One study showed that Melanesian islanders consumed a diet high in fat (coconut), high in carbohydrates (root tubers and fruit) with a moderately high GI. Their leptin and glucose levels were still much lower than for a typical western diet.

Similar studies have shown that unless grains or refined starches have been introduced, other native people are equally free from western-type disease. Unprocessed meat also doesn't contribute to poor cardiovascular health.

Whole grains might not be all that healthy.

Removal of all grains and refined starches in the backbone of the Paleo diet.

Grain-free had a greater metabolic effect, and a higher satiety level.

Leptin and leptin resistance: a hormone produced by the body's fat stores that allows the hypothalamus of the brain to monitor the size of those stores, and regulate them by varying appetite and energy expenditure. In obesity, leptin often produces a smaller response at its receptors than it does in the lean, a phenomenon known as leptin resistance. This is believed to trigger hunger and reduced energy expenditure in an attempt to gain additional fat storage tissue, to increase leptin production levels, and overcome the leptin resistance. Thus, leptin resistance is analogous to a malfunctioning "fat thermostat."

Grains may increase leptin-resistance

Insulin receptor, epidermal growth factor receptor, or interleukin-2 receptor activities of cereal-grain lectins may be responsible for producing leptin resistance

Obesity is a disorder characterized by systemic low-level inflammation and higher bacterial lipopolysaccharide (LPS) concentrations

Bacterial endoxins are associated with chronic inflammation and intestinal permeability (leaky gut)

The source of the LPS is thought to be the GI tract, with ingestion of high-fat and high-carbohydrate Western-style meals found to produce postprandial "metabolic endotoxemia": an increase in circulating LPS levels and other inflammatory changes

LPS and other gastrointestinally derived pathogen-associated molecular patterns (PAMPs) have also been suggested to play a role in the etiology of many Western diseases

The small intestine has been implicated as a primary source for their systemic absorption

The far larger populations of Gram-negative bacteria in the large intestine are suggested to be less likely to act as a source for systemic PAMPs, due to the relatively small surface area of the bowel compared to the small intestine, the presumed evolutionary adaptations of the bowel to high concentrations of bacteria

The precise GI location of the alterations in microbiota underlying metabolic endotoxemia and inflammation in diet-induced obesity is not fully understood. The present hypothesis makes suggestions regarding the dietary triggers of these changes, wherever they are ultimately found to be located

The finding that glucose consumption elevates NFκB and inflammatory pathways57 without producing changes in LPS or TLR4 levels is important evidence that a glucose-induced non-LPS/TLR4 inflammatory pathway exists.

Differing profiles of inflammation and PAMP translocation appear to be produced by different monosaccharides.

There is evidence that less Westernized diets can produce microbial communities with marked differences from those seen in industrialized countries. Children from rural Burkina Faso have a considerably different microbiota to those from Europe, a difference thought to be primarily dietarily mediated. With a lifestyle comparable to early Neolithic subsistence farmers, these children carry a large representation of Bacteroidetes, with an unusual prevalence of species suggested to bear genes for hydrolysis of dietary fiber

Dietary fat is an exacerbatory but not primary cause of human obesity

it is low-carbohydrate diets that are reported to produce the greatest weight loss in ad libitum diets, while ad libitum low-fat diets perform less well

To find the cause of the modern obesity epidemic, the properties of modern foods that perturb the homeostatic energy set point should be sought.

The universality of the negative effects of Western foods on indigenous populations indicates that these properties must be similarly widespread in modern foods.

A fundamental distinction between modern foods containing these and ancestral foods is carbohydrate density.

(Carbohydrate Density table)

Foods that would be permitted on a Paleolithic or "primal" diet - the "ancestral foods" - are those in the categories of root tubers, leafy vegetables, fruit, nuts, meats, eggs, and fish, and are shown in white. Tubers, fruits, or functional plant parts such as leaves and stems store their carbohydrates in organelles as part of fiber-walled living cells. These are thought to remain largely intact during cooking, which instead mostly breaks cell-to-cell adhesion.

This cellular storage appears to mandate a maximum density of around 23% non-fibrous carbohydrate by mass, the bulk of the cellular weight being made up of water. The acellular carbohydrates of flour,sugar and processed plant-starch products are considerably more dense. Grains themselves are also highly dense, dry stores of starch designed for rapid macroscopic enzymic mobilization during germination. Whereas foods with living cells will have their low carbohydrate density "locked in" until their cell walls are breached by digestive processes, the chyme produced after consumption of acellular flour and sugar-based foods is thus suggested to have a higher carbohydrate concentration than almost anything the microbiota of the upper GI tract from mouth to small bowel would have encountered during our co-evolution.

This may stimulate differing bacterial species to prosper or be outcompeted, or increase some microbial metabolic pathways and waste products in preference to others. It is proposed that the effects of these enhanced carbohydrate concentrations will include a more inflammatory GI microbiota, initially causing leptin resistance, hence the greatly elevated leptin levels seen in Western populations when compared to those eating a wholly cellular diet.

Once an inflammatory microbiota is in place, consumption of refined dietary fats and oils may effect a double hit by increasing the absorption of inflammatory PAMPs including LPS into the circulation or stabilizing and preserving the inflammatory microbiota itself. This would make a diet rich in both acellular carbohydrates and fat highly obesogenic, promoting a self-sustaining cycle of hyperphagia in an environment where such foods are abundant. Upon withdrawal of all acellular carbohydrates, the GI microbiota is proposed to return to a less inflammatory form consistent with our evolutionary experience, and one much more resistant to the exacerbatory effects of dietary fats

it increasingly appears that analogous microbial changes in the upper GI tract appear able to produce leptin resistance in vagal afferent endings, attenuating satiety signaling.The present hypothesis suggests that it is a diet of high-density carbohydrates that produces inflammatory microbiotal changes

If the high carbohydrate density of modern foods produces an inflammatory microbiota in both the mouth and small bowel, it may be this that is the root cause of both periodontal and atherosclerotic disease, as well as obesity and other metabolic syndrome-linked "diseases of affluence."

Hence a grain-free whole-food diet would be predicted to restore the GI microbiota to the less inflammatory state that humans coevolved with.

Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity

The proposed importance of the cellularity and low carbohydrate density of fruit and vegetables in maintaining an evolutionarily appropriate microbiota might explain the failure of supplementary fiber, vitamins, or antioxidants to replicate the health effects of a diet of fruit and vegetables when taken with a Western diet.

Glossary of terms (Wikipedia):

Lipopolysaccharide: Lipopolysaccharides (LPS), also known as lipoglycans and endotoxin, are large molecules consisting of a lipid and a polysaccharide composed of O-antigen, outer core and inner core joined by a covalent bond; they are found in the outer membrane of Gram-negative bacteria, and elicit strong immune responses in animals.

The term lipooligosaccharide ("LOS") is used to refer to a low molecular weight form of bacterial lipopolysaccharides.

Acellular: not consisting of, divided into, or containing cells.

Carbohydrate Density:

http://www.drweil.com/drw/u/ART03415/Using-The-Carbohydrate-Density-Index.html

HFHC: High-fat, high-carbohydrate

LEPTIN: Leptin the "satiety hormone", is a hormone made by fat cells which regulates the amount of fat stored in the body. It does this by adjusting both the sensation of hunger, and adjusting energy expenditures. Hunger is inhibited (satiety) when the amount of fat stored reaches a certain level. Leptin is then secreted and circulates through the body, eventually activating leptin receptors in the arcuate nucleus of the hypothalamus.

What is Leptin?

http://www.wellnessresources.com/weight/articles/what_is_leptin/

Reactive oxygen species: (ROS) are chemically reactive molecules containing oxygen. Examples include oxygen ions and peroxides. ROS are formed as a natural byproduct of the normal metabolism of oxygen and have important roles in cell signaling and homeostasis.

PAMPS: Pathogen-associated molecular patterns, or PAMPs, are molecules associated with groups of pathogens, that are recognized by cells of the innate immune system. These molecules can be referred to as small molecular motifs conserved within a class of microbes. They are recognized by Toll-like receptors (TLRs) and other pattern recognition receptors(PRRs) in both plants and animals.

They activate innate immune responses, protecting the host from infection, by identifying some conserved non-self molecules. Bacterial lipopolysaccharide (LPS), an endotoxin found on the bacterial cell membrane of a bacterium, is considered to be the prototypical PAMP. LPS is specifically recognised by TLR 4, a recognition receptor of the innate immune system. PAMPS are molecules that are commonly part of or shed by microbes, and are used by the innate immune system to recognize and mount a response to bacteria.

Pathogen: is anything that can produce disease. Typically the term is used to mean an infectious agent (colloquially known as agerm) - a microorganism, in the widest sense such as a virus, bacterium, prion, fungus or protozoan, that causes disease in its host.

SOCS3: Suppressor of cytokine signaling 3 (SOCS3 or SOCS-3) is aprotein that in humans is encoded by the SOCS3 gene. This gene encodes a member of the STAT-induced STAT inhibitor (SSI), also known as suppressor of cytokine signaling (SOCS), family. SSI family members are cytokine-inducible negative regulators of cytokine signaling.

NF-κB: (nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex that controls transcription of DNA. NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, oxidized LDL, and bacterial or viralantigens. NF-κB plays a key role in regulating the immune response to infection (κ light chains are critical components of immunoglobulins). Incorrect regulation of NF-κB has been linked to cancer, inflammatory, andautoimmune diseases, septic shock, viral infection, and improper immune development. NF-κB has also been implicated in processes ofsynaptic plasticity and memory. In brief, NF-κB can be understood to be a protein responsible for cytokine production and cell survival.

Vagal afferents: The fibers of the vagus nerve that carry information from the internal organs to the brain. From the upper gut, these fibers convey information about when food has been eaten, physical stretching of the gut by food, and the chemical nature of that food as it is digested. They are thought to play an important role in the signaling of satiety.

Obesogenic: causing obesity


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## tummyrumbles

Starch can be toxic. We weren't meant to eat highly dense carbohydrates like breads, pizza bases etc. These types of starches, referred to as acellular flours in the previous post, are considered to be the major cause of bowel diseases such as inflammatory bowel disease and Crohn's Disease.

This study shows the link between a particular bacteria, Klebsiella, starch consumption and Ankylosing Spondylitis (AK) and Crohn's Disease.

http://www.hindawi.com/journals/jir/2013/872632/

This study doesn't differentiate between harmful and less harmful starches, as did the study in the previous post.

Man-made starches made from wheat and non-gluten grains have a lot more concentrated "locked-in" starch than natural plants such as potato, sweet potato, corn etc. Natural vegetable carbohydrates, or cellular carbohydrates, have a much lower density of starch and the bulk of their cellular weight is water.

This study proves the link between high starch intake, the presence of Klebsiella bacteria, AK, IgA antibodies and bowel inflammation. Most of these patients had reduced symptoms after following a nine month low starch diet.

Many IBS-D people believe that white breads, pizza etc settles their colon. Rice, white bread and other refined starches are known to be anti-diarrheals. The problem is that these refined starches might be causing their IBS. They continue to eat these harmful foods in the belief that they cure the diarrhea. Instead these foods probably cause diarrhea through their constipating effects and through worsening inflammation caused by bacterial dysbiosis and bacterial endotoxins such as lipopolysaccharides.

IBS should be thought of as a progressive disease. It might begin with vague feelings of gassiness or incomplete evacuation. The longer a harmful diet is maintained, the more that inflammation in increased. The only real difference between IBS and inflammatory bowel disease is the number of inflammatory markers. IBS-C has less inflammation than IBS-D, generally. IBS as a "functional" disorder has less inflammatory markers than bowel diseases such as Crohn's and Inflammatory Bowel Disease. IBS, as a low-level disease, can increase in severity.

A low starch diet will heal the colon, but it shouldn't be necessary to exclude all starch. Well mashed potatoes won't have the high starch levels of bread or other flours. Grains may also cause leptin-resistance, where our appetite signaling is disrupted, which means we keep craving these foods.

FODMAPs may exacerbate IBS symptoms because of existing bacterial dysbiosis. This doesn't mean that all FODMAPs are bad food, it's simply that bacteria feed on carbohydrates and high FODMAPs with complex sugars provide a lot of energy and fermentation. FODMAP vegetables aren't toxic in themselves. The toxic foods are man-made starches.


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