Saturday, July 21, 2012

Transcend Diabetes


Most of our lives we are caught up in the moment.  Let’s now take a moment to look at diabetes from 10,000 feet up, where we can see clear patterns and insight emerge from the fog of hypoglycemia, and its opposite, hyperglycemia.  If we plot carbohydrate consumption from low to high on the y-axis, and injected, fast acting (bolus) insulin from low to high on the x-axis, we can see all possible combinations of expected results on the following matrix:


When injected bolus insulin is low or zero, and carbohydrate consumption is high, we are presented with the classical triad of diabetes symptoms: polyuria, polydipsia, and polyphagia: respectively, frequent urination, increased thirst and consequent increased fluid intake, and increased appetite.  Other manifestations will include weight loss (despite normal or increased eating), irreducible fatigue, and changes in the shape of the lenses of the eyes, resulting in vision changes.
When the glucose concentration in the blood is raised beyond the renal threshold, reabsorption of glucose in the proximal renal tubuli is incomplete, and part of the glucose remains in the urine, which is called glycosuria.
Patients may also present with diabetic ketoacidosis (DKA), an extreme state of metabolic dysregulation characterized by the smell of acetone on the patient's breath; a rapid, deep breathing known as Kussmaul breathing; nausea; vomiting and abdominal pain; and any of many altered states of consciousness or arousal (such as hostility and mania or, equally, confusion and lethargy).  In severe DKA, coma may follow, progressing to death.
Surrounding this cell on the matrix is hyperglycemia, both to the right, when carbohydrates consumed are high and injected insulin is moderate, but not enough to cover the load, and below, when a decrease in carbohydrates is consumed, but still not offset enough by injected insulin.
In the middle of the chart, where one eats a moderate amount of carbohydrates and injects a moderate amount of bolus insulin, lies the typical diabetes treatment.  “Eat a balanced diet and learn to adjust your insulin accordingly” is the principal treatment that is followed here.  It is possible to attain near-normal A1c levels with this approach, however, normal levels of cholesterol, weight, and blood pressure may prove unreachable.
Furthermore, this area of the table is fraught with negative consequences at nearly all adjacent and opposite borders.  Not enough insulin puts one in hyperglycemia territory both to the left and above.  Not enough carbohydrates, and one finds themselves hypoglycemic to the right and below.
At the other extreme, when injected insulin is high, and carbohydrates consumed are too low, severe hypoglycemia could result, necessitating a visit from the local paramedics when subsequent low blood glucose causes unconsciousness.  If not attended to quickly, coma and death could occur within minutes.
Too, if carbohydrates and insulin injected are high, the result is a hyper-hypo-glycemic swing—a rollercoaster ride if you will—of great magnitude, where the patient is constantly adjusting carbohydrate and insulin loads to offset their blood sugar.
But look what happens when both carbohydrates consumed and insulin injected are as low as possible.  At the far lower-left cell of the matrix, one doesn’t eat a great many carbohydrates, and, subsequently, does not need to inject much insulin as a result.  In this case, one can achieve a stable and normal blood sugar concentration, and enjoy the benefits of a normal life: lower VLDLs, higher HDLs, stable or decreasing weight, and less anxiety not having to think about whether one has injected the right amount of insulin.  And testing can be reduced to once a day, in the morning, to validate your successful Insulin Glargine dosing, i.e., whether or not your morning BG is in the 70-110 mg/dL range.  This home base is where thriving begins.
At the zero bolus-insulin and near-zero carbohydrate home, you may thrive for a long, long time.  There are three major centenarian studies going on around the world, the New England Centenarian Study, the Georgia Centenarian Study and the Okinawa Centenarian Study.  According to Dr. Ron Rosedale:

They are trying to find the variable that would confer longevity among this group of people who live to be 100 years old.  Why do centenarians become centenarians?  Why are they so lucky?  Is it because they have low cholesterol, exercise a lot and live a healthy, clean life?
What researchers are finding from these major centenarian studies is that there is hardly anything in common among these people.  They have high cholesterol and low cholesterol, some exercise and some don't, some smoke, some don't.  Some are nasty as can be, some nice and calm and some are ornery.  But, they all have relatively low sugar for their age, and they all have low triglycerides for their age.  And, they all have relatively low insulin…The way to treat virtually all of the so-called chronic diseases of aging is to treat insulin itself” (“Insulin and its Metabolic Effects,” Ron Rosedale, Signs for Health Institute’s BoulderFest, August, 1999).

Although the use of exogenous bolus insulin as a treatment to mitigate the effects of carbohydrate consumption was innovative, exciting, and promising nearly a century ago, its use has become—save on the acutely serious hyperglycemic—obsolete with the introduction of Insulin Glargine, and the knowledge that carbohydrates are non-essential.
A remarkable picture develops when you take those three highlighted cells from the previous figure and place them on two different axes, one a continuum of complexity from low to high, and the other, a continuum of knowledge, skill, efficiency, and effectiveness, again, from low to high.


The y-axis, complexity, relates to the treatment—medication & nutrition—and lifestyle a person implements or recommends.  Regarding the x-axis, knowledge, skill, efficiency, and effectiveness, it could be looked at from two perspectives; one, from a diabetic’s perspective, where the focus is on their knowledge & skill as it relates to implementing advice from a third-party or self-directed behavior, and another, from the perspective of a third-party’s knowledge & skill, be it friend, relative, caregiver, nutritionist, nurse, or doctor.  Treatment efficiency and effectiveness in either case is also measured.
The lowest complexity matched with the lowest skill & knowledge, will result in a diabetic on the brink.  It is quite easy for them to eat carbohydrates at will and develop the hyperglycemic symptoms of full-blown diabetes: polyuria, glycosuria, polydipsia, polyphagia, ketoacidosis, weight loss, etc., culminating in shortened life span.  Knowledge for the patient about diabetes may be non-existent, and they will likely seek out medical attention for help, though, unfortunately, some don’t or for many reasons even if they do, helpful advice is not available.  Acquaintances will also most likely notice the change in persona or appearance, and they too will make it a point to tell the person that something is wrong.
“Diabetes Managed” represents a diabetic trying to follow the instructions and advice of his or her general practitioner, though both are influenced by a wide variety of stakeholders with oftentimes divergent self-interests.  A majority of the influencers in the medical advice providing supply chain include:

·        Pharmaceutical companies
·        Researchers
·        Doctors
·        Endocrinologists
·        Nutritionists
·        Educators
·        American Diabetes Association
·        World Health Organization
·        Medical schools
·        Nurses
·        Reference media such as the Physician’s Desk Reference
·        Food manufacturers
·        Food marketers
·        Popular internet sites, print media & the news
·        Friends, family, co-workers & acquaintances

By default, advocates of each group act in their own perceived best interest, based upon their knowledge and skill, which may in turn be based upon the state of information available at their time of training or education.  Many of the above stakeholders, with the exception of the end users themselves—the people with diabetes—have significant power.  In fact, some have a near-absolute advantage in the marketplace—the ability to influence behavior without question or pause—leaving the buyer of an optimal diabetes treatment treating their diabetes sub-optimally, i.e., carbohydrate & bolus-insulin intensive.
And the results?  Perhaps an HbA1c at or below 7%, weight gain, increasing VLDL levels, increasing blood pressure, too much time spent counting carbohydrates and measuring insulin doses, anxiety caused by constantly wondering whether or not too much or too little carbohydrates were eaten or insulin dosed, the ever present chance of hypo- or hyper-glycemia, constant blood sugar testing, and the list goes on.  “Diabetes Managed” may not achieve optimal results for the end user, but, for the other stakeholders, it brings and keeps customers longer.
Although the science behind the drugs that either limit the amount of glycogen released from the liver or that bind and carry glucose from the blood to the receptors that transport it across cell membranes is remarkable, it is based upon two assumptions: (I) that carbohydrates are an essential majority part of the diet, and/or (II) that through education, a patient cannot, will not, or should not keep from consuming them.  Remove those key assumptions, and the house of cards from which that remarkable science is based comes toppling down.
Caveat emptor.  “Diabetes Managed” may be the first natural step for diabetics to enter—a complex medical-advice-providing system—in progression of their self-treatment, but it doesn’t have to be.
As knowledge about diabetes increases, trusted advisers and patients alike will choose a less-complex method, one that transcends diabetes by avoiding the root cause of symptoms and complications—carbohydrates—and replacing those carbohydrates in the diet with fat, resulting in benefits such as healthy weight loss, lowered VLDL levels, increasing HDL levels, reduced mTOR activity, normal blood pressure, etc.; in short, leading to a longer, happier, healthier life.
To transcend diabetes requires reduced carbohydrate consumption to near zero, with emphasis on a combination of fats and protein.  It is orders of magnitude less complex, less worrisome, and less risky than counting carbohydrates and matching it with doses of insulin.  It is simple.

Sunday, July 15, 2012

Terrestrial Cause for Obesity, Overweight and Related Chronic, Non-Contagious Diseases (CNCDs)


Author:  Laurence D. Chalem, Independent Researcher

Conflict of Interest:  Nothing to declare

Abstract:  Exogenous, digestible carbohydrates—sugar (sucrose), starch (amylose & amylopectin) and their constituents—have long been considered addictive, obesogenic, diabetogenic and atherogenic.  The mechanism leading to deranged metabolism—perturbation of the insulin-glucose system—has been known for decades.  Little, if any, research, however, has been undertaken to understand why.  This article presents a hypothesis for further study.

Keywords:  Adaptation, Addiction, Carbohydrates, Diabetes Mellitus, Glycosis, Maladaptation, Obesity, Overweight, Sugar


Introduction
The two independent variables most commonly associated with obesity, eating too much food and sloth, have recently been dismissed.[1], [2], [3], [4]
Additional associations recently proffered include: sleep debt, pollution, air conditioning, decreased smoking, medicine, population age, ethnicity, older moms, ancestors’ environment, obesity linked to fertility, unions of obese spouses, and others, including a fat-inducing virus, increases in childhood depression, less consumption of dairy products and hormones used in agriculture.[5]

Francois Magendie
In 1816, Francois Magendie set out to observe the effects of a restricted diet.  He was interested in what role nitrogen played in digestion.  The answer he got, after ten years of painstaking work was none at all.  “As so often in research,” Magendie wrote, “unexpected results had contradicted every reasonable expectation.”  But in the pursuit of this knowledge, Magendie had stumbled upon a striking, if unpleasant discovery: he had found that he was able to starve his experimental dogs to death on diets that should, on the face of it, have given them all the energy they needed for life.
By his own account, Magendie “placed a small dog about three years old upon a diet exclusively of pure refined sugar with distilled water for drink; he had both ad libitum.”  By the third week the animal, already weakened, lost its appetite, and developed small ulcers in the centre of each cornea.  The ulcers spread, and then the corneas liquefied.  Shortly afterwards, the dog died.
Magendie tried other nutritious foods.  “Everyone knows that dogs can live very well on bread alone,” he asserted; but, when he put this to the test, he found that “a dog does not live above fifty days.”  The most calorific foods in Magendie’s pantry—wheat gluten, starches, sugar, olive oil—were not enough for life.  This was totally unexpected.  There was something missing—something available only as part of a varied diet—but what?[6]

No Thrifty Gene
Diabetes confers a significant reproductive disadvantage; yet, populations that James Neel studied had diabetes in such high frequencies that a genetic predisposition to develop diabetes seemed plausible.[7]
The most significant problem for the “thrifty gene” idea is that it predicts that modern hunter gatherers should get fat in the periods between famines.  Yet data on the body mass index of hunter-gatherer and subsistence agriculturalists clearly show that between famines they do not deposit large fat stores.
Neel wrote that modern, very-high levels of obesity and diabetes among formerly native populations were a recent phenomenon most likely caused by dietary changes.  Given that some populations, e.g., the Inuit, experienced a rise in obesity and diabetes in conjunction with a reduction of the proportion of fat and protein in their diets, Neel concluded that the dietary causes of obesity and diabetes lay in carbohydrate consumption.[8]

Emotional States as Addiction
Group identity established by emotional mechanisms requires both a long-lasting negative component and a less stable positive component, the basic elements of an addiction module.[9]  Eating starch- and sugar-based snacks in a social setting entails both positive and negative emotional states.  Positive emotions would include those of pleasure, joy, happiness and contentment.  The stable negative component may not be apparent until after this initial acquisition, when feelings of guilt or unhappiness result from the finding of fat accumulation.  Negative emotional states then might include anxiety, depression and anger.
Although not everyone that consumes sugar is addicted, sugar is implicated in obesity,[10], [11] asthma,[12] and every one of the abnormalities seen in coronary heart disease and in diabetes can be produced by the inclusion of sugar in the diet.[13]
That low carbohydrate diets work best in the treatment of both type 1 and type 2 diabetes,[14], [15], [16], [17], [18], [19], [20], [21], [22] reducing pharmaceutical dependencies, and in weight loss,[23], [24], [25], [26], [27], [28], [29], [30], [31] is the prima fascia case that carbohydrates are the keystone of the obesity, overweight and related CNCDs arch.

Obesity Today
2.7% of UK men and women were obese in 1972.  Fewer than three decades later, in 1999, 22.6% of men and 25.8% of women were obese.[32]  Two-thirds of UK citizens are now overweight or obese.
70% of Americans are currently overweight or obese.  Animals inhabiting human influenced environments haven’t fared much better.[33]


Figure 1.  US Overweight & Obesity.  Centers for Disease Control and Prevention, 2006.

Evidence accumulated since 1917 has indicated that eat less, do more does not work;[34], [35] in fact, those that implement the advice fail 98% of the time.[36]  Calorie restriction results in a disproportionate reduction in energy expenditure and metabolic activity.[37], [38]

Carbohydrates
Carbohydrates are defined by two criteria.  First, they usually contain only of carbon, hydrogen, and oxygen, although a few carbohydrates contain nitrogen or sulphur.  Second, the ratio of hydrogen to oxygen is close to 2:1, the same ratio as in water; the generalized chemical formula is (CH2O)n.[39]
Carbohydrates are divided into four groupings.  Oligosaccharides and polysaccharides, commonly referred to as complex carbohydrates, can further be classified either as non-structural carbohydrates (NSCs) or structural carbohydrates.  Amylose and amylopectin—starch—are polysaccharide NSCs.  Cellulose, hemicellulose and lignin (wood), are structural polysaccharides.[40], [41]
Polysaccharide NSCs—complex carbohydrates—reduce to simple carbohydrates during human digestion.  But humans can’t digest structural polysaccharides; we don’t produce cellulase, the necessary enzyme for breaking them down.  Wood-rotting fungi and bacteria have cellulose-degrading enzymes, but even termites, cockroaches and cattle can live on cellulose only because their digestive tracts contain microorganisms with the proper enzymes that then convert it to short-chain fatty acids for energy.[42], [43]
Monosaccharides and disaccharides are referred to as simple sugars, of which all are NSCs.  Blood sugar is the monosaccharide glucose and table sugar is the disaccharide sucrose, consisting of glucose and fructose.
Starch serves as a long-term storage chemical for energy.  Although sugars are excellent for storing energy because they are not very reactive, cells cannot store large amounts of sugars.  Sugars absorb and hold water, causing cells to swell; starch does not.[44]


Figure 2.  US Dept. of Commerce reports and the USDA: continuous yearly sweetener sales from 1822 to 2005.  Stephan Guyenet, Ph.D. & Jeremy Landen, 2012.

Figure 2 presents added sweeteners such as cane sugar, high-fructose corn syrup and maple syrup, but not naturally occurring sugars in fruit and vegetables.  It’s a remarkably straight line, increasing steadily from 6.3 pounds per person per year in 1822 to a maximum of 107.7 lb/person/year in 1999.  In 1822, we ate the amount of added sugar in one 12 ounce can of soda every five days; today, every seven hours.
Figure 3 presents the consumption of the three macronutrients from 1971 to 2000.


Figure 3.  Percent kilocalories from macronutrient intake among men aged 20-74 years (NHANES).

Ancestor’s Diet
The best benchmark to use is what we ate before the agricultural revolution. But it is difficult to accurately determine the nature of past hominid diets because survival of organic materials is very rare.  The morphological changes—based on analogies with living primates—increasing gracilization of the mandible and increasing brain size, have been interpreted as the move from plants to higher-quality, more digestible, animal meat, although this explanation is debated.  Artefacts, such as stone tools which are likely to be used for hunting, and animal bones with evidence of human processing and butchering, do indicate that hunting did occur at many times in the past; but, it is impossible to judge the frequency.  Direct evidence from bone chemistry, such as the measurement of the stable isotopes of carbon and nitrogen, provide direct evidence of past diet and indicates the importance of animal protein in diets.  There is a rapid increase in population associated with domestication of plants, and in many cases a general decline in health and stature and the appearance of new nutritional disorders.[45]
Present-day hunter-gatherer societies, on average, consume a diet of 65% animal food and 35% plant food.[46]  Contrast that with the fact that 72% of the total daily energy consumed by people in the United States is made up of dairy products, cereals, refined sugars, refined vegetable oils, and alcohol, all items that didn’t exist until about ten-thousand years ago.[47]  According to Dr. Loren Cordain, the word for the difference between what we evolved to eat and what we currently eat is “discordance,” and is due to the fact that our cultural evolution has paced faster than our biological evolution.  Our biology has not caught up with the nutritional, cultural, and activity patterns of contemporary western populations, and thus, many of the so-called diseases of civilization have emerged.[48]
Most of those diseases are related to the glycemic load of our diets.  Within the past two decades, substantial information has accumulated showing that long-term consumption of high glycemic load carbohydrates can adversely affect metabolism and health.  Specifically, chronic hyperglycemia and hyperinsulinemia, induced by high glycemic load carbohydrates may elicit a number of hormonal and physiological changes that promote insulin resistance.  Diseases of insulin resistance include obesity, coronary heart disease, type two diabetes, hypertension, acne, gout, some cancers, and many others.  Diseases of insulin resistance are rare or absent in hunter-gatherer and other less-westernized societies living and eating in their traditional manner.[49]

Strategies
The sugar first formed as a result of photosynthesis was discovered in the early 20th century to be glucose; part of it was then converted into fructose.  Condensation converts both into sucrose, and it is as sucrose that translocation takes place to the bulbs.[50]
Plant organs that provide resources to other tissues in the same plant are termed sources, and those that receive the resource are called sinks.  Sucrose from a source cell is loaded into the phloem for long-distance transport.  Then, the sucrose is unloaded from the phloem at a sink, such as a root, where it is used for storage, growth or respiration.  When plants are defoliated, storage organs become sources and the growing shoots are sinks.[51]
Among many strategies, plants produce fruit or nectar to entice animals to disperse their seeds or pollen.  In seed dispersal known as endozoochory, an animal eats the fruit and the seeds inside it; the seeds survive the digestive process of the animal, and, later, are deposited when the animal defecates.  When an animal feeds on nectar, however, plants deposit their pollen—mobile, single-use sperm production and delivery devices—on them.  On its quest for more nectar, the animal moves pollen from male anthers of one flower to female stigma of another.
Although sucrose is the main sugar found in nectar, other carbohydrates, including arabinose, galactose, mannose, gentiobiose, lactose, maltose, melibiose, trehelose, melezitose, raffinose, and stachyose have been identified in nectars of some flowers.[52]  The various types of nectars can be ordered into three groups according to sugar content: sucrose prevalent, glucose and fructose prevalent, and equal amounts of sucrose, glucose, and fructose.[53]
Some animals remove nectar without contacting anthers or stigma.  These nectar robbers include a small number of species of ants, bees, birds, bats and others.  But, contrary to the pure sucrose humans obtain from sugar cane, all twenty of the amino acids found in protein have been identified in various nectars, with alanine, arginine, serine, proline, glycine, isoleucine, threonine, and valine, most prevalent.[54]
H. sapiens does not obtain sugar via pollination or nectar robbery; but, through two operations separated in space time.  We methodically depredate croplands then cultivate them back again.
There are other depredating species.  The Asian giant hornet Vespa mandarinia is especially adapted to raid bee hives.  A single giant hornet can kill tens of bees a minute and only a few can decimate an entire bee colony of 30,000 in just a few hours.  The hornets depredate bees to satiate the hunger of their demanding young.  Swarm-raiding army ants Eciton burchelli devastate the arthropod fauna on the ground and low vegetation over which they conduct their daily forays.[55]
Leafcutter ants consume far more vegetation than any other group of animals of comparable taxonomic diversity.  The amount of vegetation cut from tropical forests by Atta alone has been calculated to lie between 12%-17% of leaf production.  Because of the catholicity of the diets of the fungus that they eat, leafcutters have an extraordinary diverse impact on agriculture; loss to human interests is estimated in the billions of dollars.[56]
Members of the myrmicine tribe Attini share with macrotermitine termites and certain wood-boring beetles the sophisticated habit of culturing and eating fungi.[57]  But no other animal depredates-cultivates palatable, non-essential food.  Although it’s true that humans manipulate the plants, the opposite is equally true.  We increase their fecundity; they, in turn, reduce our fitness.
“They” refer to a number of plants containing accessible NSCs.  Included is sugar cane (Saccharum spp.) and corn (Zea mays)—grasses—and beet sugar (Beta vulgaris), a tuber.  Corn is an annual; that is, it germinates, flowers and dies in one year or season.  So too are the grasses wheat (Triticum spp.) and rice (Zizania spp. & Oryza spp.).  Beet sugar is biennial, taking two years to complete its lifecycle, and the sugar canes are all perennial, living for years.
Unlike an angiosperm that uses sweetness to entice an animal to pollinate it or disperse its seeds, sugar cane attracts humans to raid its stem, for it is there that phloem contain significant, translocating sucrose.  H. sapiens has diverged into consumers and producers, members of the latter doing much more work than any bat, bee, butterfly, hummingbird or moth.
Think how much of these organisms we depredate-cultivate each year.  Worldwide, Homo sapiens—referred to by some as Homo ludens, yet by others as H. stultus—produce two-billion metric tons of sugar cane, a billion metric tons of corn and about a half-billion metric tons of beet sugar to meet demand.[58]
Beet sugar and sugar cane have a high water content, about 75% of the total weight of the plants.  The sugar content of sugar cane ranges from 10%-15% of the total weight, while that of beet sugar is between 13%-18%.  Assuming seven billion people worldwide, that’s more than a quarter-pound of sugar produced per day per person, not including the high fructose corn syrup which is now nearly equal to sugar consumption.  Add in the billion metric tons of corn—a large portion goes to produce ethanol—and a billion metric tons each of wheat and rice, and we have well over a pound of edible, non-essential carbohydrate production per person per day.  Although rice and wheat provide some protein—the mysterious, life-sustaining component of food that Magendie the dog killer would eventually find—the protein and fat content of sugar is zero.
Some that try to eat just a little sugar are surprised and discouraged when they crave more.  It’s no coincidence that sugar is sweet; sweetness is a powerful bribe.  Once ensnared in the taste, humans demand more, driving further cultivation and depredation.  We wind up favoring the plant’s interests at the expense of our own because we have uncoupled food intake from functional needs.  Animals that must flap their wings fifty times a second in order to feed have a hard time staying fat and do not develop diabetes, at least as we know it.[59]
Still, why can some people eat all the NSCs they want and remain fit?  Richard Lenski provides a prescient template.

Richard E. Lenski
Michigan State University biologist Richard Lenski, his colleagues and students started off with a single bacteria of E. coli; after it divided a few times into identical clones, he started twelve colonies, each in its own flask.  Each day he and his colleagues provided the bacteria with a little glucose, which the bacteria ate by the afternoon.  The next morning, the scientists took a small sample from each flask and put it in a new one with fresh glucose.  They did this for more than twenty years and it’s still running today.[60]
Lenski expected that the bacteria would experience natural selection in their new environment.  In each generation, some of the microbes would mutate.  Most of the mutations would be harmful, killing the bacteria or making them grow more slowly.  Others would be beneficial allowing them to breed faster in their new environment.  They would gradually dominate the population, only to be replaced when a new mutation arose to produce an even fitter sort of microbe.
Over the generations, the bacteria did indeed evolve into faster breeders.  The bacteria in the flasks today breed seventy-five percent faster on average than their original ancestor.  Lenski and his colleagues have pinpointed some of the genes that have evolved along the way; in some cases, for example, the same gene has changed in almost every line, but it has mutated in a different spot in each case.  Lenski and his colleagues have also shown how natural selection has demanded trade-offs from the bacteria; while they grow faster on a meager diet of glucose, they’ve gotten worse at feeding on some other kinds of sugars.
But that’s not all.  In addition to becoming faster breeders, they also became larger.[61]  And then the bacteria had abandoned their glucose-only diet and had evolved a new way to eat.[62]
After 33,127 generations, Lenski and his students noticed something strange in one of the colonies.  The flask started to turn cloudy.  This happens sometimes when contaminating bacteria slip into a flask and start feeding on a compound in the broth known as citrate.  Citrate is made up of carbon, hydrogen, and oxygen; our own cells produce citrate in the long chain of chemical reactions that lets us draw energy from food.  Many species of bacteria can eat citrate, but in an oxygen-rich environment like Lenski’s lab, E. coli can’t.  The problem is that the bacteria can’t pull the molecule in through their membranes.  In fact, their failure has long been one of the defining hallmarks of E. coli.
If citrate-eating bacteria invade the flasks, however, they can feast on the citrate, and their exploding population turns the flask cloudy.  This has only happened rarely in Lenski’s experiment, and when it does, he and his colleagues throw out the flask and start the line again from its most recently frozen ancestors.
So in one remarkable case, they discovered that a flask had turned cloudy without contamination.  It was E. coli thriving on the citrate.  The researchers found that when they put the bacteria in pure citrate, the microbes could use it as their sole source of nutrition and energy.
What was going on?  What was it that suddenly happened to that one tribe?  If a mutant could discover how to deal with citrate, a bonanza would open up for it.  This is exactly what happened with that one tribe.  This tribe, and this tribe alone, suddenly acquired the ability to eat citrate as well as glucose, rather than just glucose.  The amount of available food in each successive flask in the lineage therefore shot up.  The only explanation was that this one line of E. coli had evolved the ability to eat citrate on its own.[63]

Glycosis (glī-kō’sĭs)
Why are there some people who consume quite a lot of sugar but are not overweight?  John Yudkin in Pure, White and Deadly (1988) proposed that some lucky people have the facility of burning off surplus calories.[64]  That may or may not be true; but, why should some be luckier than others?  In all likelihood it is because they are better adapted to that fare than others.
Adaptedness is the morphological, physiological, and behavioural equipment of a species or of a member of a species that permits it to compete successfully with other members of its own species or with individuals of other species and that permits it to tolerate the extant physical environment.  Adaptation, as measured by evolutionary success, consists of a greater ecological-physiological efficiency of an individual than is achieved by most other members of the population or at least by the average.  Adaptation is achieved by the greater survival or higher reproductive success of certain individuals owing to the fact that they possess ecological-physiological traits not, or only partially, shared by other individuals of their population, traits that are useful in the struggle for existence.[65]
Surely every fish is adapted for its life in water and yet in the history of the vertebrates, ten thousands of species of fish have become extinct, either because they were not sufficiently well-adapted to some component of the environment or because they lost in the competition with some “better adapted” other species.  The same is true for individuals within a species.  All have the same species-specific adaptations and yet only a small minority will survive into the next generation.  Thus, it is evident that we have “adapted” and “better adapted.”  This is precisely the process of natural selection, which, on average, favors those that are “better adapted.”[66]
Proposed is a word to indicate relative maladaptedness to carbohydrates: glycosis.  It is defined as the quantifiable maladaptation to one or more specific carbohydrates in a given species.  For example, if a species that uses glucose as its sole food source is fed a different carbohydrate, the survival rate would serve as the measure of adaptation or maladaptation to that carbohydrate, depending on whether the value was high or low.  If a hundred percent of the population survives, then there is no adaptational benefit to any select few and the species as a whole is adapted.  If they all die out, then they are completely maladapted.
Quantifying adaptation in humans is complex because carbohydrates are not essential macronutrients.  Homo sapiens need exogenous amino acids, DHA and EPA fatty acids, energy, water, vitamins, electrolytes and minerals; but, we never need to eat carbohydrates.[67]  Although we get all the glucose we need endogenously from our livers, adaptation to carbohydrates as an energy source can theoretically be calculated.
Population glycosis could be depicted as the percent of people suffering from CNCDs related to NSC consumption such as obesity, overweight, diabetes mellitus, some types of heart disease, some cancers, gout, etc.  Diseases related to the use of tobacco (Nicotiana spp.) and alcohol—ethanol, the product of carbohydrate fermentation—could be included.  Thus, the higher the consumption of NSCs, the higher the prevalence of CNCDs, the higher the maladaptation to those NSCs, the higher the glycosis.
Although there may be a lag between NSC consumption levels and CNCD presentation, that 63% of the global population expire as a result of CNCDs[68] implies that the current limit of glycosis in Homo sapiens is the same, given current NSC consumption.  In sub-populations with known overweight rates of two-thirds or more, that’s an underestimation.
Like psychosis—abnormal condition of the mind—the word glycosis at the individual level could be defined as the abnormal condition of glucose in the blood.  People with diabetes mellitus of any type are most demonstrably glycotic.
An analogy might be helpful.  In an old TV commercial for “Off!,” a name-brand mosquito repellent, two bare arms, each connected to a live human, were placed consecutively into a glass tube full of hungry mosquitoes.  The first arm, which can be thought of as the experimental arm, was sprayed with a generous amount of “Off!,” and the second arm, the control, wasn’t sprayed with anything.  Not surprisingly, the first arm, the one sprayed with “Off!,” suffered fewer, if any, mosquito bites than that of the bare arm.  This commercial is analogous to diabetes mellitus if you imagine that the mosquito bites represent complications and the “Off!” represents insulin.  Carbohydrates are equivalent to the actual placing of an arm into the mosquito-filled glass container.
Ideally, one probably shouldn’t be placing their arm into a container full of hungry mosquitoes.  Similarly, for the obese and overweight too—because insulin is the main hormone that stores fat and carbohydrates are the most significant secretagogue of insulin—doesn’t it make sense to reduce carbohydrate intake?  That would be congruent with recent research indicating that anything enabling the reproduction and growth of microbial parasites—carbohydrates, nicotine, mental stress, and low vitamin B, C and D levels, are primary risk factors for cardiovascular disease.[69]

A New Found Path
Once deranged metabolism manifests, the simple way to proceed is to eat natural foods made up of mostly fat and protein.  Without carbohydrates in the diet, the brain and central nervous system will run on ketone bodies, converted from dietary fat and from the fatty acids released by the adipose tissue; on glycerol, also released from the fat tissue with the breakdown of triglycerides into free fatty acids; and on glucose, converted from the protein in the diet.  Since a carbohydrate-restricted diet, unrestricted in calories, will, by definition, include considerable fat and protein, there will be no shortage of fuel for the brain.[70]
Every fat is part saturated, part mono-unsaturated and part polyunsaturated.[71]  All “saturated” means is that every carbon has a hydrogen attached to it; intake of saturated fat is associated with reduced progression of coronary atherosclerosis.  Greater NSC intake is linked to increased progression.[72], [73]
Of the many vertebrate protein sources available, one necessitates clarity.  “Grass-fed beef” is a peculiar expression because cattle naturally eat grass; they’re graminivores.  The problem becomes clear after considering three arguments: (1) grass stems are higher in NSCs than leaves; but, (2) lush grass is much lower in NSCs than dry grass or fruit, and, (3) the content of NSCs is higher when sampled closer to the ground.  Cattle and their bacteria are best adapted to eat structural carbohydrates.[74]
For grass, high levels of NSCs enable them to be more persistent under drought conditions.  Moreover, the distribution of NSCs being higher the lower they are in the stem is an adaptive advantage.  It allows plants to maintain reserves for re-growth after the tops have been consumed by grazing animals.[75]  Hence, feeding cattle corn—which although is fruit from a grass, it contains a higher proportion of NSCs than their natural diet of lush grass tops—is the bane of some cattle, not to mention in some people that eat their beef.
While ruminant livestock enterprises benefit from higher levels of NSCs in grass, various forms of carbohydrate intolerance are recognized in horses.  Obesity, laminitis, insulin resistance, developmental orthopedic disease, polysaccharide storage myopathy, all involve excess dietary NSC in their etiology.[76]
In those with diabetes, obesity, overweight, etc., or the propensity to become so, risk may be mitigated by avoiding carbohydrate intake.  No, it’s not easy; but, it is simple.  For those free of CNCDs, it’s also good policy.  As there used to be only one way to distinguish between edible and poisonous mushrooms, so too might learning of one’s own maladaptedness to carbohydrates: it will be in retrospect of having become less fit.
And that fits nicely into nature’s scheme.  Stephan Jay Gould eloquently stated it at the conclusion of Wonderful Life: “We are the offspring of history, and must establish our own paths in this diverse world, one indifferent to our own suffering, and therefore offering us maximal freedom to thrive, or to fail, in our own chosen way.”[77]

--------------------------------------------------------------------------------


Acknowledgements
The section "Obesity Today" was adapted from the work of Zoe Harcombe and many of the cited articles were made available by Lt. Col., Dr. Luca Mascitelli.  The author is grateful to both.


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Figure 1.  US Overweight & Obesity.  Centers for Disease Control and Prevention, 2006.
Figure 2.  US Dept. of Commerce reports and the USDA: continuous yearly sweetener sales from 1822 to 2005.  Stephan Guyenet, Ph.D. & Jeremy Landen, 2012.   http://wholehealthsource.blogspot.com/2012/02/by-2606-us-diet-will-be-100-percent.html
Figure 3.  Percent kilocalories from macronutrient intake among men aged 20-74 years.  (NHANES).