19thcentury English physician, J.H. Salisbury was free of the shackles of theories, prejudices, and assumptions – the chief one of which was dealing with symptoms as if the symptoms were disease themselves. Not able to help his patients with the drugs and provisions he was privileged with as a physician, Dr. Salisbury was driven to help his patients by any means possible.
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| Dr. Salisbury (Source) |
Dr. Salisbury sought to find real cures for the diseases he encountered (he was sure of, foremost, that the bowels played a central role in disease processes).
With that goal, Dr. Salisbury conducted his own experiments – first on himself and then on others, whom he paid to live with him during the experiments, so that he could have as much control as possible over what his subjects ate.
First, Dr. Salisbury employed baked beans, and after that, oatmeal - both of which were prepared to taste. The subjects were also allowed as much coffee (with milk & sugar) and water as they fancied.
After less than, on average, 3 weeks on the diets, the subjects grew so sick and ill that at this point, the experiments were terminated and the subjects were soon after placed on a recovery diet. The subjects grew more and more bloodless, enervated, and death was likely to warm over at any time. As an illustration of just how weak and sick they were, towards the experiments’ end, many of the subjects couldn't turn in their beds, and in some, paralysis began to set in.
With that goal, Dr. Salisbury conducted his own experiments – first on himself and then on others, whom he paid to live with him during the experiments, so that he could have as much control as possible over what his subjects ate.
First, Dr. Salisbury employed baked beans, and after that, oatmeal - both of which were prepared to taste. The subjects were also allowed as much coffee (with milk & sugar) and water as they fancied.
After less than, on average, 3 weeks on the diets, the subjects grew so sick and ill that at this point, the experiments were terminated and the subjects were soon after placed on a recovery diet. The subjects grew more and more bloodless, enervated, and death was likely to warm over at any time. As an illustration of just how weak and sick they were, towards the experiments’ end, many of the subjects couldn't turn in their beds, and in some, paralysis began to set in.
Once he had amassed enough data, Dr. Salisbury deduced that the chronic consumption of indigestible foods ultimately led to intestinal congestion, inflammation, and, enlargement and swelling. This was attendant to an overgrowth of microbes – especially yeast – and sometimes, ulcers in the intestinal lining would be seen, with blood, mucus, and ropey slime in the stools.
In extreme cases, yeast filaments would be detected in the blood of Dr. Salisbury’s subjects (Though I have doubts whether what Dr. Salisbury saw were, in fact, yeast, and not impurities or artifacts in his samples.)
Dr. Salisbury was especially keen to the fermentative processes that were incited in the bowels by starches, and herein was his greatest insight: diseases came from eating "improper foods" – those that ferment and cause gas.
Soon after his experiments in human subjects, Dr. Salisbury procured 2,000 hogs to which he meticulously fed the same diets, taking bodily samples thereafter as he had before, with the same level of scrutiny. This time – because he could – Dr. Salisbury carried out his experiments to the "end," and permitted some of his hogs to die. He obtained the same disastrous results in the hogs as he did in humans.
We can herein for the remaining discussion employ Dr. Salisbury’s seminal work to provide context for the studies decades later that, in effect, reconfirmed his observations.
In these more recent studies, for instance, it's been established that with starches and cereal grains there is an ever-present concern for rising lipopolysaccharide (LPS) levels, discussed in great detail here.
Intestinal bacteria produce LPS, which, under certain conditions, can slip through the intestinal barrier and into the blood, wherefrom it interacts with a pathogen-recognizing receptors, TLR-4, on the surface of white cells (as well as certain fat cells and endothelial cells) (e.g., Davis, Gabler, Walker-Daniels, & Spurlock, 2008). Briefly, at least a 2-fold rise in blood LPS levels initiates degenerative processes in the liver, fat tissue, skeletal muscles, and dysregulates the secretion of satiety signals – whose actions are executed in the hypothalamus – from the intestines.
Studies show that starches increase levels of TLR-4, LPS, and markers of inflammation in subjects’ blood in contrast to fructose and fruit (namely orange juice).
Take for example this study where healthy subjects were given either a starch-based meal or a fruit-based meal (Ghanim et al., 2009). Blood samples were drawn at baseline and at hours 1, 2, and 3. Here are the results represented graphically by the authors (The starch-based meal had more fat than the fruit-based meal so this could have confounded the results a bit, as fat raises LPS, too.)
In extreme cases, yeast filaments would be detected in the blood of Dr. Salisbury’s subjects (Though I have doubts whether what Dr. Salisbury saw were, in fact, yeast, and not impurities or artifacts in his samples.)
Dr. Salisbury was especially keen to the fermentative processes that were incited in the bowels by starches, and herein was his greatest insight: diseases came from eating "improper foods" – those that ferment and cause gas.
Soon after his experiments in human subjects, Dr. Salisbury procured 2,000 hogs to which he meticulously fed the same diets, taking bodily samples thereafter as he had before, with the same level of scrutiny. This time – because he could – Dr. Salisbury carried out his experiments to the "end," and permitted some of his hogs to die. He obtained the same disastrous results in the hogs as he did in humans.
We can herein for the remaining discussion employ Dr. Salisbury’s seminal work to provide context for the studies decades later that, in effect, reconfirmed his observations.
In these more recent studies, for instance, it's been established that with starches and cereal grains there is an ever-present concern for rising lipopolysaccharide (LPS) levels, discussed in great detail here.
Intestinal bacteria produce LPS, which, under certain conditions, can slip through the intestinal barrier and into the blood, wherefrom it interacts with a pathogen-recognizing receptors, TLR-4, on the surface of white cells (as well as certain fat cells and endothelial cells) (e.g., Davis, Gabler, Walker-Daniels, & Spurlock, 2008). Briefly, at least a 2-fold rise in blood LPS levels initiates degenerative processes in the liver, fat tissue, skeletal muscles, and dysregulates the secretion of satiety signals – whose actions are executed in the hypothalamus – from the intestines.
Studies show that starches increase levels of TLR-4, LPS, and markers of inflammation in subjects’ blood in contrast to fructose and fruit (namely orange juice).
Take for example this study where healthy subjects were given either a starch-based meal or a fruit-based meal (Ghanim et al., 2009). Blood samples were drawn at baseline and at hours 1, 2, and 3. Here are the results represented graphically by the authors (The starch-based meal had more fat than the fruit-based meal so this could have confounded the results a bit, as fat raises LPS, too.)
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| Open triangles: data points from fruit-based diet (Ghanmin et al., 2009) |
The same group of authors then provided further clarity on the matter in an experiment where healthy human subjects were given, either water or 300 calories of cream, glucose, or orange juice after an overnight fast. Again blood samples were drawn like before. At each time point analyzed, LPS, TLR-4, and markers of inflammation were the highest in the cream-fed subjects, next was glucose, and, finally, orange juice and water – whose curves were nearly identical (Deopurkar et al., 2010).
Other studies have confirmed that orange juice, in healthy individuals and diabetics, decreases the generation of ROS, CRP, and NF-κB activation.
Other studies have confirmed that orange juice, in healthy individuals and diabetics, decreases the generation of ROS, CRP, and NF-κB activation.
Another issue, established by more recent studies (and somewhat related to LPS) is a phenomenon called "persorption."
First noted over 150 years ago, persorption describes the paracellular movement of solid microparticles (0.1 of a millimeter) through the intestinal wall via tight junctions on intestinal villa or Peyer’s patches (among other minor routes), wherefrom they are drained into lymph nodes, and finally into the lymph and blood vessels, through which they are dispersed throughout the body.
Found in starchy vegetables and unripened fruit, starch granules meet the criteria for persorption processes. Indeed, it's been confirmed, via electron microscopy, that these starch granules persorb, and are found in every place in the body that’s been checked.
One of the earliest investigators of persorption, Gerhard Volkheimer found that persorbed microparticles persisted in the blood for up to 24 hours (Volkheimer, 1974).
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| Illustration of persorption processes in the intestinal villa (Volkheimer, 1974) |
There are a few ways to decrease the persorption of starch granules, one of which involves boiling starches in water to gelatinize and burst their starch granules. Because it doesn’t contain starch granules (as long as it is fully ripened) persorption processes are not a concern with fruit.
In addition to not contributing fodder for persorption processes, and not adding to the burden of inflammation, oxidative stress, or metabolic endotoxemia, fruit contains flavonoids that protect against the damages caused by starches. Hesperetin and naringenin, for instance, are flavonoids, in oranges, that are beneficial in this regard (e.g., Ghanim et al., 2007).
The graph below represents data from an in vitro study where the components of oranges were tested individually for their ability to curtail the generation of ROS from a type of white blood cell – something that starches promote. It’s clear that hesperetin and narinenin significantly decreased ROS generation (while fructose and acorbic acid were neutral).
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| (Ghanim et al., 2007) |
Starch could lead to weight gain, more than fruit, because of the rate and intensity with which it stimulates insulin secretion. On average, fruit contains equal amounts of glucose and fructose. So fruit leads to a steadier rise in blood glucose levels because, for one, fructose slows the rate of gastric emptying of glucose, and two, via GLUT-5, fructose is slowly absorbed from the intestines, wherefrom it is drained into the liver, and therein converted to glucose (Mayes, 1993). The secretion of insulin as a result is slow and controlled with fruit, and so drastic decreases in blood glucose levels (and thus the rapid return of hunger) are buffered against.
In the late 1980s, it was noted that as obesity rates in this country increased, sugar consumption stayed constant, more or less. What’s changed since? First, high fructose corn syrup replaced, one for one, sucrose as the principle sweetener used (And with this change, the consumption of starches increased slightly because HFCS contains small amounts of starch molecules.) Second, the consumption of carbohydrates, as a whole, increased substantially – mostly from starches. And third, the consumption of fructose – from added and natural sources – decreased slightly.
It's safe to say, I think, that the consumption of starches and cereal grains is coming to a head, and we now have a basis for predicting what some of the consequences may be/are.
A corollary of this awareness has been an increasingly growing movement to recommending whole food starches in placed of refined starches on the basis of the former's nutritional superiority – even though differences are actually negligible, in effect.
Take for example the comparison between isocaloric servings of potatoes, rice, and wheat (refined). Flours of each will be compared to provide the fairest comparison.
Wheat contains more vitamin B1, vitamin B2, iron, and selenium than rice and potatoes; potatoes contain more vitamin B6 than wheat and rice; and rice contains more manganese than wheat and potatoes. Nonetheless the nutritional profiles of these three starch sources are still a wash.
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| From left to right: refined wheat, brown rice, and potato (cronometer) |
Asians are usually used as an example of people who live on starches without suffering health consequences. I have a few issues with this.
For one, despite the presumptions, Asians (especially Koreans) don’t eat massive amounts of rice. Actually, compared to other foods, rice is more of a side dish. Two, Asians don’t prosper from incredible longevity (especially of late due to the progressive encroachment of processed foods). And three, Asians are small in stature, physically weak, and lacking in the stamina department. Why then are Asians help up as a paradigm of health of sorts?
Fruit can be taken in large quantities daily without adverse effects. The same can’t be said for starches, however, the overconsumption of which will lead to bowel problems, a drain on our energies, and a feeling of heaviness and sluggishness.
Regardless of which an individual chooses to eat, fruit or starches, each should be consumed in accordance with one's appetite, habits, stress, and physical activity level. I’ve found that eating no more than what's absolutely needed is easy and intuitive with fruit – but not with starches.
Starches aren’t eaten alone because alone they'd be dry and tasteless. So extra moisture, seasoning, fat, etc., are usually added make them palatable. Conversely, fruit can be relished without any preparation.
Dr. Salisbury was incredibly prescient in that he recognized the importance of having clean and clear bowels. As such, he created a program in which his patients would eat only fully digestible foods: meat trimmed of its fat and connective tissue, coffee with sugar, hot water, and scant amounts of vegetables and fruit (if any). And of course starches and cereal grains were not allowed.
The fermentative quality of starches, however, is not the only concern, as we know now, and Dr. Salisbury’s diet plan is far from perfect. Still, I think it provides us with a foundation for creating an ideal diet – one that first eradicates "improper foods," which is what Dr. Salisbury called them.
Part 2
References
Davis, J. E., Gabler, N. K., Walker-Daniels, J., & Spurlock, M. E. (2008). Tlr-4 deficiency selectively protects against obesity induced by diets high in saturated fat. Obesity (Silver Spring, Md.), 16(6), 1248–55. doi:10.1038/oby.2008.210
Deopurkar, R., Ghanim, H., Friedman, J., Abuaysheh, S., Sia, C. L., Mohanty, P., Viswanathan, P., et al. (2010). Differential effects of cream, glucose, and orange juice on inflammation, endotoxin, and the expression of Toll-like receptor-4 and suppressor of cytokine signaling-3. Diabetes care, 33(5), 991–7. doi:10.2337/dc09-1630
Ghanim, H., Abuaysheh, S., Sia, C. L., Korzeniewski, K., Chaudhuri, A., Fernandez-Real, J. M., & Dandona, P. (2009). Increase in plasma endotoxin concentrations and the expression of Toll-like receptors and suppressor of cytokine signaling-3 in mononuclear cells after a high-fat, high-carbohydrate meal: implications for insulin resistance. Diabetes care, 32(12), 2281–7. doi:10.2337/dc09-0979
Ghanim, H., Mohanty, P., Pathak, R., Chaudhuri, A., Sia, C. L., & Dandona, P. (2007). Orange juice or fructose intake does not induce oxidative and inflammatory response. Diabetes care, 30(6), 1406–11. doi:10.2337/dc06-1458
Mayes, P. A. (1993). Intermediary metabolism of fructose. The American journal of clinical nutrition, 58(5 Suppl), 754S–765S. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/8213607
Volkheimer, G. (1974). Passage of particles through the wall of the gastrointestinal tract. Environmental health perspectives, 9, 215–25. Retrieved from http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1475370&tool=pmcentrez&rendertype=abstract