Before you read, check out this quick video which Harvard psychologists shot in the ’90’s.
Did you see the gorilla?! Half of the students originally shown the video had no idea it was even there.
This video demonstrates the attention bias, a cognitive bias which illustrates that while we think we see everything happening before us, in fact we only notice what we’re focusing on.
What has this got to do with nutrition?
The focus of our attention on the rise of diet-induced disease emphasises increases in dietary saturated fat, animal meat (in particular red meat) consumption, and refined sugars in the Western diet over the past 50 years.
This emphasis on simple scapegoats has made it easy to miss the finer details. There is, however, a common thread that weaves through all of them which has escaped notice, primarily because it is absent the modern diet.
I’m talking about fibre.
There is no one specific cause of our ill health crisis: disease processes are multifactorial. This makes fibre particularly interesting in that its absence from the modern diet is a consistent common factor in many different disease states.
By looking at the Western health crisis from the perspective of fibre intake, we can see fibre associated with each of the following:
It’s not the breakfast cereal-bagel-fruit juice Western diet that lacks fibre. Eating a better diet doesn’t necessarily guarantee an adequate fibre intake, depending on food choices.
The question is, does fibre warrant unique attention in your diet? This two-part post will answer that question.
What is fibre?
Fibre is a component of the edible part of plant foods that are resistant to digestion and absorption in the small intestine. It can be broadly broken down into two main forms, soluble fibre and insoluble fibre.
In addition to this broad categorisation, resistant starch has emerged to be defined as a third type of fibre, and encompasses a variety of starches that resist digestion in the small intestine, and are fermented by bacteria in the large intestine into short-chain fatty acids. 
Soluble fibre dissolves in water to form a viscous gel, which also passes undigested through the small intestine to be fermented by bacteria of the large intestine. In this respect, resistant starch and soluble fibre are similar in their mechanism of action; the difference is that, unlike soluble fibre, resistant starch does not dissolve in water.
This process of fermentation results in the production of short-chain fatty acids, which have numerous important functions in the body including energy production, lowering circulating blood cholesterol levels and prevention of colon cancer. 
Insoluble fibre doesn’t dissolve in water, and is not subject to fermentation to the same extent as soluble fibre. Food sources of fibre generally contain a mix of soluble and insoluble, in a ratio of one-third soluble to two-thirds insoluble fibre.
Resistant starch is present in food as five subtypes. For present considerations, the most important are types R1, R2 and R3. R1 is found in seeds, grains, and certain legumes; RS2 is found in unripe bananas and legumes; RS3, known as retrograde starch, forms after starch has been physically modified, such as in cooking and cooling a food. Ever boil potatoes and let them cool, and notice that stickiness that forms after cooling? That’s resistant starch.
Soluble fibre slows down the transit time through the gastrointestinal tract, by slowing the rate of food leaving the stomach, while insoluble fibre increases transit time and keeps bowel movements regular. 
To keep things simple, for the most part I’m going to refer to all three types only as fibre. There is enough reductionist thinking in nutrition, and it doesn’t make sense to me to be telling you to eat soluble or insoluble fibre: just eat food. The rights foods, which we’ll cover in the follow-up, will have you eating enough fibre of all types.
Fibre rich diets have been shown to increase satiety and reduce calorie intake, without increases in hunger . In one study, each 1g increase in fibre in the diet corresponded to a decrease in weight and body fat, independent of confounding variables like age, activity level and fat intake. 
Fibre supports weight loss efforts because the increase in satiety and decrease of hunger facilitate a significant decrease in overall calorie intake over time. 
By increasing fibre intake, you in turn decrease the energy that is available from the diet, as fibre cannot be metabolised as a direct source of energy . For example, take two diets each consisting of 200g carbohydrates per day. Diet A consists of 200g of glucose, and Diet B consists of 150g glucose with 50g fibre: the available energy from Diet B is confined to the glucose, notwithstanding that the total carbohydrate content is the same.
This concept is often referred to as “net carbs”, as any fan of Quest bars will gleefully tell you.
Fibre directly increases circulating levels of satiety hormones, a vital factor in regulating energy intake. [7, 8]
The net effect of fibre in relation to weight loss and obesity is to allow for a reduction in overall calorie intake over time. [4, 5]
Decreased overall energy intake, increased production of satiety hormones, decreased metabolizable energy, and the influence of fibre-rich food choices on diet composition are all factors in the weight loss effects of a high dietary fibre intake.
Metabolic syndrome, characterised by high blood pressure, high blood sugar levels and excessive abdominal body fat (along with other conditions like abnormal cholesterol) is inversely related to fibre intake: the higher the fibre, the lower the incidence of metabolic syndrome. 
Fibre has been shown to significantly reduce blood glucose in Type-1 diabetics . Increased dietary fibre intake is associated with a decreased risk of Type-2 diabetes, with an increased risk from low fibre, high rapidly absorbed carbohydrate diets. [11, 12]
Soluble fibre, particularly beta-glucan found in oats and barley, have consistently proven to lower the blood sugar response to meals . Insoluble fibre has proven to have the same effect, whilst also reducing appetite and food intake. 
Of all the associations between lack of fibre and modern disease, however, I think the most compelling is the relationship with cholesterol, given the witch-hunt to burn saturated fats at the stake since the 1960’s as the primary causative agent in heart disease.
A brief primer on circulating cholesterol: bile salts produced and secreted by the gallbladder are responsible digesting dietary fats, and for binding to cholesterol for excretion from the intestinal tract.
This is a two-way street, known as entero-hepatic circulation, in which the hepatic portal vein provides direct access from the liver to the intestine, and vice versa.
Fibre is the key to making this system work: fibre binds to metabolites, including cholesterol and free fatty acids in order to excrete them from the body . In the absence of fibre, these metabolites are reabsorbed via entero-hepatic circulation, and return to circulation in the body.
In providing the means for cholesterol excretion, fibre improves cholesterol profiles and fat distribution in subjects with metabolic syndrome. 
Consuming a high dose fibre supplement with a meal reduces circulating blood levels of triglycerides (fats) in obese subjects, which lowers the exposure of arteries to higher blood triglyceride levels. 
And high fibre intake has been directly compared to a low saturated fat and cholesterol intake in determining which has more of a relationship to metabolic syndrome: high fibre intake is related to lower incidences of metabolic syndrome, while low saturated fat and cholesterol intake is not. 
This has been repeatedly demonstrated in the literature in recent years. With blood cholesterol as the primary risk factor for determining risk for heart disease, it has been an assumption impervious to rebut that the cause of elevated blood cholesterol was dietary saturated fat and cholesterol intake.
This core tenet of conventional dietary wisdom has held notwithstanding the conspicuous absence of evidence that dietary saturated fat and cholesterol have any significant relationship with risk of heart disease. [15, 19, 20]
In contrast, increases in dietary fibre of 10g per day are associated with 32% decreased risk of cardiovascular disease. 
And while I’m not disputing elevated blood cholesterol levels as an appropriate risk factor, I’m saying the cause of elevated levels would appear now to be more related to the amount of refined carbohydrate in the diet, the excess of which convert to saturated fatty acids. 
The more persistent evidence points the finger at lack of fibre (and excess refined carbohydrate), which deprives the body of its mechanism to ensure proper cholesterol metabolism: fibre modulates the expression of the enzyme HMG-CoA reductase (the rate-limiting step in cholesterol synthesis, and the target of statin drugs), which decreases cholesterol synthesis and increases the excretion of cholesterol in the bile. 
It appears that we’ve had the wrong party on trial for 60 years, and it may be time to shift the charges to an act of omission (dietary fibre), rather than commission (saturated fats) in relation to heart disease.
Dietary fibre has been shown to inhibit the development of colon cancer, by inhibiting colon carcinogenesis and modifying the bacterial enzymes involved in promoting the development of cancerous colonic tumours. 
The association here is again something I think needs to be emphasised, because it goes to the heart of another core tenet of modern dietary conventional wisdom: red meat and cancer.
Red meat is primarily associated with colorectal cancer. It is true that certain metabolites of red meat are associated with overexpression of cancer genes in the colon. 
What doesn’t make the headlines is that eating your veg can neutralise this risk.
The expression of cancer genes is observed with consumption of meat alone: when resistant starch fibres are added, colon cancer gene expression is inhibited. 
Fermentation of fibre in the colon results in the production of short-chain fatty acids, which suppress the expression of tumour genes. 
It is important to note that cancer is characterised by uncontrolled cell growth. Short-chain fatty acids regulate the apoptosis (programmed cell death) of colorectal mucosal cells and reduce cell proliferation, protecting against unregulated expression of these cellular pathways in colon cancer. 
This is why context and the nuances in the dietary discussion are so important.
Can we really pinpoint red meat as the cause, when it would appear that the greater factor in the progression of colon cancer is the absence of fibre, not the presence of meat?
Fibre plays a vital role in gut health, with soluble and insoluble fibres providing different benefits.
The human gut is its own ecosystem, comprised of over 100 trillion bacteria, which are strongly associated with the health of the individual: the healthier the population of bacteria, the healthier the host individual. [23, 24]
Dietary fibre alters intestinal bacteria to a more positive composition, by providing substrate for fermentation by bacteria . As we have seen, this fermentation process results in the production of short-chain fatty acids, which have a range of important roles including prevention against colon cancer, reduced fatty acid synthesis and fat storage, reduced free fatty acids and circulating cholesterol. [23, 15, 16, 17]
Altered gut bacterial composition has far reaching implications: obese individuals have different gut bacterial populations than lean and non-obese people. 
Certain types of fibre, known as prebiotics, are so called because they have the ability to stimulate the growth of select strains of bacteria . In particular, prebiotics are observed to stimulate the Bifidobacterium strains of bacteria, which play a specific role in preventing immune-mediated disruption of the intestinal lining, improve intestinal barrier function, and increase immune function (26, 27).
Dietary fibre also has a direct role in immune system function, by decreasing biomarkers of inflammation and interacting with immune cells . Beta-glucans found in oats, for example, can bind directly to immune cells and decrease immune system inflammatory compounds. 
Stimulation of the Lactobacilli and Bifidobacterium strains by dietary fibre can modulate the immune system, reducing gastrointestinal symptoms and frequency of colds and flu. 
Fermentation of fibre into short-chain fatty acids may provide yet another benefit: SCFA’s down-regulate pro-inflammatory compounds and communicate directly with the immune system. 
While research is still emerging, the role of fibre in influencing immunity appears to result from altering blood concentrations of key inflammatory substances, by modulating the gut bacterial populations. 
There is ample reason here to ensure that fibre is a core part of your diet. In the follow up to this, we’ll look at strategies to increase your fibre intake, regardless of what kind of diet you follow.
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