small intestine, the means by which 60 per cent of all B12 is absorbed.24 Grain consumption can also trigger antibodies against the intrinsic factor or against the stomach parietal cells that produce intrinsic factor.25
Severe B12 deficiency has serious implications, including pernicious anaemia (fatal if untreated) or macrocytic anaemia, describing the abnormally large red blood cells that develop as a result of this condition. Abdominal pain, an enlarged liver and a characteristic cherry red tongue develop with B12 deficiency. Lesser degrees of deficiency have health and performance implications, too, as they can lead to diminished concentration and learning ability. Typical of the silliness of modern nutritional thinking, the solution often offered is increased B12 supplementation in grains to compensate for these effects.26
Because dietary B12 is obtained mostly from animal-sourced products, such as meat, liver and eggs, vegans and vegetarians who consume grains are especially likely to develop a deficiency. People with inflammatory bowel diseases (Crohn’s disease and ulcerative colitis) are also especially prone to vitamin B12 deficiency.
FOLATE DEFICIENCY is less common than deficiencies of iron, zinc and vitamin B12. It is, however, known to occur in people with coeliac disease and gluten intolerance.27 People with inflammatory bowel diseases also suffer from impaired folate absorption sufficient to cause deficiency. Also, situations in which greater folate needs develop, especially pregnancy, can magnify the severity of deficiency. In all these situations, assessment of folate levels should be performed and supplementation instituted. (See here for more information.) Folate deficiency has serious implications, including birth defects in children born from folate-deficient mothers and increased potential for gastrointestinal cancers. Many of the same phenomena that develop with vitamin B12 deficiency are caused by folate deficiency, since folate and B12 participate in many similar processes.
Folate is the form that occurs naturally in foods, while folic acid is the synthetic form added to foods or taken in supplement form. Because modern diets dependent on processed grains and sugar are potentially deficient in folate, manufacturers in the United States and Canada have been required to add synthetic folic acid to grain products since 1998 to decrease the incidence of birth defects. This has indeed improved the folate status of most people, but it is proving to be a double-edged sword: Folate levels increased more than intended, and increased reliance on synthetic folic acid has also been associated with increased colon and prostate cancers.28
VITAMIN D DEFICIENCY is a widespread phenomenon with significant implications for health. Vitamin D deficiency is the rule, rather than the exception. While we can blame more severe cases of deficiency on grains, it also commonly occurs independent of grain consumption. Various other modern habits have served to worsen our vitamin D status, including inhabiting cold climates deprived of year-round sunlight, wearing clothes that cover skin surface area (since vitamin D is activated in our skin by sunlight), increasingly indoor lifestyles, aversion to organ consumption, especially liver (they contain vitamin D), and ageing, which is associated with a progressive loss of the ability to activate vitamin D in the skin.29 Living in the tropics is no guarantee of adequate vitamin D status, though; a recent assessment of elderly males living in a tropical climate, for instance, revealed that 66.7 per cent were deficient.30 Vitamin D status is such a crucial factor for health that we discuss it at greater length later in the book (see here).
People with coeliac disease are especially prone to vitamin D deficiency, which also contributes to low bone mineral density. In one clinical study, only 25 per cent of people showed normal bone density at the time of their coeliac disease diagnosis.31 Bone demineralization (loss of calcium) that weakens bones is also worsened by the impaired calcium absorption characteristic of coeliac disease.
Gut Flora: Don’t Get Your Bowels in an Uproar
You can view bacterial flora that inhabit the intestinal tract like a garden: if you fertilize it properly, provide sufficient water and nutrients, and avoid herbicides and pesticides that disrupt the natural balance, your garden will yield a bounty of vigorous, healthy crops. If you fail to water or fertilize it properly, you will probably have a lousy yield of stunted crops, not to mention lots of weeds. Bowel flora operate on similar principles.
We know that diet plays an important role in shaping the composition of bowel flora, even in the absence of disease. For example, bowel flora of children living in rural Africa and eating traditional diets, when compared with European children eating a modern diet, demonstrate striking differences. The African children have higher than expected numbers of Bacteroidetes, an adaptation theorized to enhance efficiency in digesting plant matter.32 I’ve discussed how the adoption of grains changed the composition of mouth and gut flora in humans. Changes in oral flora have clear implications for dental disease; changes in gastrointestinal flora have less clear implications, but it should come as no surprise that there could be such changes, given the toxic effects grains have on the intestines. The composition of bacteria in the gastrointestinal tract, concentrated in the colon, varies from individual to individual, shifts with age and hormonal status, and is modified by exposure to antibiotics and components of diet. When factors that allow healthy bacteria to survive are altered, bowel flora species change and microorganisms can extend above the normal furthest segment of the small intestine, a situation called small intestinal bacterial overgrowth, or SIBO. That’s when nasty things can happen: bloating, diarrhoea, nutritional deficiencies and inflammation. (See ‘Small Intestinal Bacterial Overgrowth: The Case of the Human Petri Dish’.)
It is estimated that more than 1,000 different species of bacteria dwell in our intestines. Unfortunately, most of our understanding of the composition of bowel flora involves comparing people with various diseases, such as ulcerative colitis, to people without the same disease. It is not clear whether the changes in bowel flora composition are part of the cause or simply a consequence of the disease. People without disease are also assumed to be normal, but this may not be true, since ‘normal’ ignores potentially disruptive factors such as prior antibiotic use, emotional stress and unnatural distortions of diet, such as grain and sugar consumption. Nobody quite knows what normal or ideal bowel flora look like yet.
A number of health conditions have been associated with changes of bowel flora, including multiple sclerosis, fibromyalgia, diabetes (both type 1 and type 2), irritable bowel syndrome, gallstones, acid reflux and oesophagitis, irritable bowel syndrome, ulcerative colitis, Crohn’s disease and food allergies.33 Funny thing: each and every one of these conditions has also been associated with grain consumption, especially consumption of wheat, rye and barley.
Changes in the composition of our bacteria develop as quickly as days to weeks after a change in diet.34 Right now, our understanding of bowel flora remains limited, but it is rapidly yielding to study. I believe that in the next few years we will know with confidence how to assess an individual’s bowel flora status and how to know when it has been fully corrected. In the meantime, the steps required to reestablish what we currently believe represents an ideal composition of bowel flora will be discussed in Chapter 9.
Small Intestinal Bacterial Overgrowth: The Case of the Human Petri Dish
Put a petri dish out in the open air and, over just a few days, it will be ripe with bacteria and fungi. Likewise, mess up the health of the human intestine by allowing undesirable bacteria and fungi to gain an advantage and reducing normal bacterial species, and you have the equivalent of a human petri dish. Such a situation is common, and it’s called small intestinal bacterial overgrowth (SIBO), or dysbiosis, an abnormal overabundance of bacteria in the normally sparsely populated upper small intestine, or jejunum, along with changed species in other parts of the intestinal
