Author's note: the following article first appeared as the chapter entitled "Epilogue" in my second book Essential Diabetes Leadership (2010).
“The known is finite, the unknown infinite; intellectually we stand on an islet in the midst of an illimitable ocean of inexplicability. Our business in every generation is to reclaim a little more land, to add something to the extent and the solidity of our possessions. And even a cursory glance at the history of the biological sciences during the last quarter of a century is sufficient to justify the assertion, that the most potent instrument for the extension of the realm of natural knowledge which has come into men’s hands, since the publication of Newton’s Principia, is Darwin’s Origin of Species.” 
PROFESSOR T.H. HUXLEY, 1887
Diabetes is the relative inability of the body to naturally and effectively process carbohydrates due to an insulin function disturbance; either our bodies are resistant to our own insulin and perhaps we produce too much, or, in the case of type 1s, we do not produce enough, or any. We can buy different types of analog insulin—with a prescription—and take basal plus bolus insulin, consume a balanced diet including 45%-55% carbohydrates, and live with the ever-present chance of hyper- and hypo-glycemia. Or we can forgo the bolus insulin and carbohydrates, and eat just fat and protein. The logical question to then ask is: “Are carbohydrates essential to human life?” If yes, then our hypothesis—forgo the bolus insulin and carbohydrates, and eat just fat and protein to live a healthy, long life—falls on its face. If no, then the simple solution, the trivial solution, the optimal solution, the solution left unharmed sitting atop Occam’s razor is basal insulin, fat and protein, sans bolus insulin and carbohydrates. The ample evidence presented points to the latter.
If carbohydrates are not essential, then, and our diet is based upon fat—and saturated fat at that—will our arteries clog and our destiny manifest itself in heart disease? If yes, then, once again, our hypothesis is moot. If no, then basal plus bolus insulin plus carbohydrates descends down Ocamm’s razor and basal insulin, fat, and protein remain safely perched on top. The overwhelming evidence presented by authors such as Dr. Uffe Ravnskov, Dr. Barry Groves, Dr. Malcolm Kendrick, Dr. Kilmer S. McCully, Gary Taubes, et al., points again to the latter.
And what about a cure? Can type 2’s go under anesthesia and a knife to have a gastric bypass? Yes. Is there a day in the not too distant future when type 1s can have stem cells effectively and efficiently grown to replace our atrophied beta cells? The answer, again, is yes.
And those two treatments simply scratch the surface. There are many other interventions being investigated from metabolic control, i.e., developing an artificial pancreas, to regenerating insulin producing cells, to replacing beta cells with functioning ones from a donor, to artificial preventative treatments, i.e., stopping or reversing the immune system response that causes diabetes.
But, especially in type 1s, then what? Eat normal, balanced meals, burn out the replacement beta cells, and then go in for a refill? Does anyone think that, for example, stem cells implanted in a recipient’s pancreas will somehow not be subjected to the same influencers in the environment that originally triggered the condition, and, overtime, fail too?
I do not know why some people stay slim and healthy throughout life and others develop a deranged metabolism given the same carbohydrate load. When doctors don’t understand a metabolic process, they call it “genetics,” when ethologists can’t pinpoint a reason for an animal’s behavior, they call it “instinct.” You too probably know a slim, healthy person that eats far more than their fair share of cereal with milk in the morning, sandwiches on white bread with potato chips for lunch, ice cream for dessert, and a thousand more calories for dinner made up of those same carbohydrates and a variety more, plus acidic, caffeinated, carbonated, sugar water, and still manage to look good at the beach. Although I must say that I’m happy for them—yes, it all sounds so delicious—it is a disappointment.
But far more disappointing are the health-professionals, health-based organizations, figureheads, and speakers, whether knowledgeable on the subject of diabetes or not, that recommend, prescribe or otherwise espouse the role of carbohydrates as the basis of our diet and treatment. My disappointment culminated when a former favorite author of mine, and, through his books, mentor, Stephen R. Covey, partnered with the American Association of Diabetes Educators, and Bayer Diabetes Care, to write for and distribute free of charge a pamphlet entitled The 7 Habits of Highly Effective People with Diabetes in 2007. Discussing his second habit, “Begin with the end in mind,” he wrote to “Choose one behavior and set a small goal,” and here is one proposed goal:
“For Healthy Eating, I will switch from whole milk to skim milk [my italics].” 
Milk—whole, 2%, 1%, low-fat, skimmed, or skim—contains a considerable amount of the simple sugar lactose and will rapidly raise blood sugar once consumed. Skim milk contains the most lactose per ounce. By his suggestion, Dr. Covey displays support for the “fat antagonizes diabetes” dogma—a diabetic should reduce their consumption of fat, and, instead, increase the amount of carbohydrate. He espouses a dogma on the same par as that of health benefits to lungs from five to ten minute sessions of repeatedly inhaling and exhaling the smoke of burning, rolled-up, dried tobacco particulate.
Recall that memes propagate themselves in the meme pool by leaping from brain to brain via a process which, in the broad sense, can be called imitation. When a credible, respected member of human society helps to spread an idea, from the idea’s perspective it is the idea evolving to become better adapted at spreading itself. So another way to look at it is that Dr. Covey’s well intended but misguided effort is the result of being infected with an evolved strain of the “fat antagonizes diabetes” virus, which may be better stated as the “eat carbohydrates” virus. He too spreads it, but as you read these words now, and those of the preceding chapters, be hopeful that it can be countered by the “don’t eat carbohydrates” meme, of which I am a proud and purposeful carrier.
And there are other noble meme’s to spread.
The Millennium Development Goals  (MDGs) are eight goals commissioned by the UN Secretary General and supported by the UN Development Group to be achieved by 2015, that respond to the world's main development challenges. The MDGs are drawn from the actions and targets contained in the Millennium Declaration  that was adopted by 189 nations-and signed by 147 heads of state and governments during the UN Millennium Summit in September, 2000. Here are the eight goals:
- Eradicate extreme poverty and hunger. 
- Achieve universal primary education.
- Promote gender equality and empower women.
- Reduce child mortality.
- Improve maternal health.
- Combat HIV/AIDS, malaria and other diseases.
- Ensure environmental sustainability. Integrate the principles of sustainable development into country policies and programs and reverse the loss of environmental resources.
- Develop a Global Partnership for Development. Develop further an open, rule-based, predictable, nondiscriminatory trading and financial system, which includes a commitment to good governance, development, and poverty reduction, both nationally and internationally.
Complementing these eight Millennium Development Goals are the 14 Grand Challenges for Engineering in the 21st Century, sponsored by the National Science Foundation.  Here are the 14 Grand Challenges for Engineering in the 21st Century:
- Make solar energy affordable
- Provide energy from fusion
- Develop carbon sequestration methods 
- Manage the nitrogen cycle
- Provide access to clean water
- Restore and improve urban infrastructure
- Advance health informatics
- Engineer better medicines
- Reverse-engineer the brain
- Prevent nuclear terror
- Secure cyberspace
- Enhance virtual reality
- Advance personalized learning
- Engineer the tools for scientific discovery
I never could find answers to life’s questions—nor an optimal solution to our diabetes dilemma, which I had wanted to find first—at, or working my way to, the bottom of a bottle, glass, or can of beer. Although, yes, I have tried. In seeking an optimal solution via paradigms in physics, astronomy, mathematics, cosmology, medicine, ethology, geology, or simple trial and error, I’ve found that the best lens to view the problem comes from Charles Darwin.  As it has been said, nothing in biology makes sense except in the light of evolution.
“Nothing in Biology Makes Sense Except in the Light of Evolution”  is a 1973 essay by the evolutionary biologist and Russian Orthodox Christian Theodosius Dobzhansky,  criticizing anti-evolution creationism and espousing theistic evolution. The essay was first published in the American Biology Teacher. 
Dobzhansky first published the title statement, in a slight variation, in a 1964 article in American Zoologist, “Biology, Molecular and Organismic,” to assert the importance of organismic biology in response to the challenge of the rising field of molecular biology. The term “light of evolution”—or sub specie evolutionis—had been used earlier by biologist Julian Huxley.
Dobzhansky starts with a reductio ad absurdum of the alleged geocentrism of an Arab cleric (identical to or namesake of Shaikh Abdulaziz bin Baz, later the Grand Mufti of Saudi Arabia) who believes the Sun revolves around the Earth because of scripture. Dobzhansky asserts his own belief that scripture and science do not contradict each other. He criticizes creationists for implying that God is deceitful and asserts that this is blasphemous.
Dobzhansky then goes on to describe the diversity of life on Earth, and that the diversity of species cannot be best explained by a creation myth because of the ecological interactions between them. He uses examples of evidence for evolution: the genetic sequence of cytochrome C to show evidence for common descent (citing the work of Emanuel Margoliash & Walter M. Fitch); embryology; and his own work on fruit flies in Hawaii. Dobzhansky concludes that scripture and science are two different things: “It is a blunder to mistake the Holy Scriptures for elementary textbooks of astronomy, geology, biology, and anthropology.”
The central issue of the essay is the need to teach biological evolution in the context of debate about creation and evolution in public education in the United States. The fact that evolution occurs explains the interrelatedness of the various facts of biology, and so makes biology make sense. The concept has become firmly established as a unifying idea in biology education.
The notion of the “light of evolution” came originally from the Jesuit priest Pierre Teilhard de Chardin, whom Dobzhansky much admired. In the last paragraph of the article, de Chardin is quoted as having written the following:
“(Evolution) is a general postulate to which all theories, all hypotheses, all systems must henceforward bow and which they must satisfy in order to be thinkable and true. Evolution is a light which illuminates all facts, a trajectory which all lines of thought must follow—this is what evolution is.”
The phrase “nothing in biology makes sense except in the light of evolution” has come into common use by those opposing creationism or its variant called intelligent design. While the essay argues that Christianity and evolutionary biology are compatible, a position described as evolutionary creationism or theistic evolution, the phrase is also used by those who consider that “in biology” includes anthropology, and those who consider a creator to be unnecessary, such as Richard Dawkins who published The Selfish Gene just three years later. 
And it is Richard Dawkins, one of my favorite authors, that provides answer upon answer to some of life’s greatest questions, e.g., “why are people?”  It is only after understanding the answer to that question that we can begin to grasp the answer to “why is diabetes?”
All his books are seminal in their own right, but most remarkable is The Ancestor’s Tale: A Pilgrimage to the Dawn of Evolution (New York: Houghton Mifflin Company, 2005). In this treatise, Richard Dawkins creatively, eloquently utilizes backward chronology to search out ancestors to “sensibly aim towards a single distant target.” On opposite ends of a small log, he serves as gentle, factual storyteller, bringing us “back to the universal progenitor of all surviving organisms, probably resembling some kind of bacterium.” His lexicon includes “rendezvous,” “confluence,” and, most notably, “concestor.”
“In a backward chronology, the ancestors of any set of species must eventually meet at a particular geological moment. Their point of rendezvous is the last common ancestor that they all share, what I shall call their ‘Concestor’: the focal rodent or the focal mammal or the focal vertebrate, say. The oldest concestor is the grand ancestor of all surviving life.” 
And the oldest concestor, according to Dawkins, before animals and plants, before multicellularity, is the single cell progenitor bacteria.
“The analogy of insect colony to human body is often made, and it is not a bad one. The majority of our cells subjugate their individuality, devoting themselves to assisting the reproduction of the minority that are capable of it: ‘germ-line’ cells in the testes or ovaries, whose genes are destined to travel, via sperm or eggs, into the distant future. But genetic relatedness is not the only basis for subjugation of individuality in fruitful division of labor. Any sort of mutual assistance, where each side corrects a deficiency in the other, can be favored by natural selection on both.” 
In answering our diabetes conundrum, it makes sense to see what, if anything, benefits from diabetes. I’m sure that sounds strange, after all, how could anything benefit from our decline? Well, our environment consists of living things that are themselves adapted to profit at our expense. Although all the evidence isn’t in just yet, it seems that cancer is one example of a beneficiary.
In “Diabetes and Cancer. Epidemiological Evidence and Molecular Links,” (2008), the authors highlighted the following findings:
“…cancer cells growing under hyperglycemic conditions with elevated levels of insulin and other glucose-regulating hormones do have an advantage compared to healthy cells and even over the same cancer cells in a non-diabetic setting.” 
“Numerous studies revealed a direct link between hyperglycemia, high insulin levels and high concentrations of insulin-like growth factor (IGF) and an increased risk of various types of cancer.” 
“Many studies revealed that dietary patterns that accelerate insulin resistance or secretion, including high consumption of sucrose, various sources of starch, a high glycemic index and high saturated fatty acid intake [sic], are associated with a higher risk of colon cancer.” 
“…we discovered that most cancer cell lines display enhanced features of tumor progression when cultured under diabetic conditions. Not only the established stimulus for cell proliferation—insulin—increased the activity of tumor cells, but also hyperglycemic glucose concentrations per se enhanced proliferation and migratory activity of tumor cells.” 
In “The Relationship Between Diabetes and Cancer,” authors Dion Smyth and Theresa Smyth point out the following:
- Insulin and insulin-like growth factor-1 (IGF-1) have been shown to act as growth-promoting hormones that foster cell proliferation and inhibit apoptosis. 
- High circulating levels of IGF-1 increase the risk of breast cancer in premenopausal women. 
- High levels of IGF-1 are also associated with an increased risk of prostate cancer. 
- Various studies have shown that adults with impaired glucose tolerance have a greater risk of cancer mortality. 
- Type 2 diabetes is a risk factor for endometrial cancer. 
- Data from the long-running US Nurses Health Study suggest a slight but significant increased risk of breast cancer in post-menopausal women with type 2 diabetes. 
- Recent reports have suggested that diabetes and high blood glucose levels appear to increase the risk of cancer independent of obesity. 
- A prospective cohort study of almost 1.3 million Koreans, who are typically leaner than their Western counterparts, found that increased levels of fasting serum glucose were strongly linked with an increased risk of pancreatic cancer and significantly associated with an increased risk of cancers of the gullet, liver and colorectum in men and the cervix and liver in women. 
- The Khaw, et al. (2004), study suggested that high blood glucose levels—even levels below those diagnostic of diabetes—could be linked to bowel cancer and people with diabetes could be up to 3 times more likely to get colorectal cancer. 
- The role of medication such as exogenous insulin (that is, the use of therapeutic insulin injections) in the development of cancer has been reported on. The US National Cancer Institute (NCI) highlighted research presented at the most recent American Association for Cancer Research Annual Meeting that men who had diabetes and took medication are at 4 times the risk of developing liver cancer and 2.5 times the risk of developing pancreatic cancer of men who did not have diabetes. 
- Continuous use of insulin for a period of more than 3 years was associated with a significant risk of developing colorectal cancer. 
Validated from another source, patients diagnosed with cancer who have preexisting diabetes are at increased risk for long-term, all-cause mortality compared with those without diabetes. 
In “Abnormal Glucose Tolerance and the Risk of Cancer Death in the United States,” by Saydah SH, Loria CM, Eberhardt MS, and Brancati FL, the authors first stated that “…Although abnormal glucose tolerance is a well-established risk factor for cardiovascular disease, its relation to cancer risk is less certain.” After performing their study, they concluded that “…in the United States, impaired glucose tolerance is an independent predictor for cancer mortality.” 
In “Diabetes Mellitus as a Predictor of Cancer Mortality in a Large Cohort of US Adults,” by S. Coughlin, E. Calle, L. Teras, J. Petrelli, and M. Thun, one of the largest prospective studies worldwide, enrolling 467,922 men and 588,321 women who had no reported history of cancer at the time of enrollment, revealed after 16 years of follow up that:
“…diabetes was significantly associated with fatal colon cancer in men and women, and with prostate cancer in men, and significantly associated with liver cancer and bladder cancer. In addition, diabetes was significantly associated with breast cancer in women. These findings strongly suggest that diabetes is an independent predictor of mortality from these cancer entities.” 
The Västerbotten Intervention Project is a subcohort of the Northern Sweden Health and Disease Cohort, and, in brief, all residents in the county of Västerbotten in northern Sweden were invited to a health survey, in the years in which they became 40, 50, or 60 years old since 1985. The results are detailed in “Prospective Study of Hyperglycemia and Cancer Risk,” (2007), where the authors stated:
“In conclusion, our finding of a statistically significant association of hyperglycemia with overall cancer risk in women and an increase in risk of cancer at many sites in women and men is essentially in accordance with the observations in some other large cohort studies, suggesting that abnormal glucose metabolism is a general risk factor for cancer development. Although the proportion of subjects with hyperglycemia was highest among obese subjects, the absolute numbers of subjects with hyperglycemia were larger among women and men who were overweight or had normal body weight, and plasma glucose levels remained associated with cancer risk after adjustment for BMI. This observation may have considerable implications for public health strategies, as key determinants of hyperglycemia are known and modifiable. A lifestyle that decreases plasma glucose levels may reduce overall cancer risk not only among overweight or obese subjects but most likely also among subjects with normal body weight. At the same time, current evidence suggests that such a strategy also would contribute to the prevention of diabetes and cardiovascular disease.” 
Cancer, according to the National Cancer Institute, US National Institutes of Health (www.cancer.gov), is a term used for diseases in which abnormal cells divide without control and are able to invade other tissues. Cancer cells can spread to other parts of the body through the blood and lymph systems.  Cancer is a class of diseases in which a group of cells display uncontrolled growth (division beyond the normal limits), invasion (intrusion on and destruction of adjacent tissues), and sometimes metastasis (spread to other locations in the body via lymph or blood). These three malignant properties of cancers differentiate them from benign tumors, which are self-limited, and do not invade or metastasize. Most cancers form a tumor but some, like leukemia, do not. Leukemia is a cancer of the blood or bone marrow and is characterized by an abnormal proliferation of blood cells, usually white blood cells (leukocytes). 
In short, cancer is the abnormal proliferation of cells.
With our above discussion on diabetes, cancer and that specific definition of cancer in mind, then, at best, diabetes enables cancer. If we relax the above definition, however, from “abnormal proliferation of cells,” to “abnormal proliferation of cells or substances, e.g., hormones,” and we recall the essence of untreated diabetes, that it is:
- the abnormal proliferation of insulin (type 2)
- the abnormal proliferation of glucose
- the abnormal proliferation of glycosylated hemoglobin
- the abnormal proliferation of triglycerides
- the abnormal proliferation of complications
then we see that, at worst, diabetes is cancer. Sans any tumor(s).
Just as Copernicus showed that the universe does not revolve around the earth, Darwin showed that the natural world does not revolve around humans; we are no more unique than any other species. In his own words:
“I view all beings not as special creations, but as the lineal descendants of some few beings which lived long before the first bed of the Silurian system was deposited, they seem to me to become ennobled.” 
And all species—all memes—struggle to survive, reproductively, at the level of the individual. 
Nothing is alone in the universe. The possibilities for organisms, cells, organelles, proteins, etc., to interact in the universe, include, and are on a continuum of, altruism to exploitation, antagonism to synergism, attraction to repulsion, catabolism to anabolism, catalyst to anti-catalyst, stimulator to repressor, and mutualism through commensalism to parasitism; with specific roles, whether one to one, one to many, or many to many, such as brother to sister, cell wall to environment, enzyme to reactant, friend to friend, husband to wife, manipulator to submitter, master to slave, parasite to host, parent to child, predator to prey, signaler to receiver, et al. And in the rivalrous, predator-prey and parasite-host relationships, arms races explain the relative increasing strength of sides in the struggle for fitness. 
Cancer does not appreciate any of our discoveries or advancements, whether we can travel to or populate distant stars and ocean depths, or whether our deep thinking scientists are working to tie—let alone succeed in tying—the forces of gravity, weak, strong, and electromagnetic into a theory of everything. It does not care about our civilization, our cultures, our libraries, languages, Betts or Cassavetti Stradivarii. It does not sit in awe listening to Dufay, Palestrina, de Prez, Gesualdo, Monteverdi, Bach, Albinoni, Handel, Haydn, Mozart, Beethoven, Paganini, Schubert, Berlioz, Mendelssohn, Chopin, Schumann, Liszt, Verdi, Wagner, Bruckner, Brahms, Saint-Saëns, Bizet, Mussorgsky, Tchaikovsky, Dvořák, Grieg, Rimsky-Korsakov, Puccini, Mahler, Debussy, Strauss, Sibelius, Rachmaninoff, Schoenberg, Ravel, Bartók, Stravinsky, Webern, Berg, Villa-Lobos, Prokofiev, Orff, Gershwin, Copland, Khachaturian, Shostakovich, Messiaen, Barber, Cage, Britten, Bernstein, Xenakis, Ligeti, Penderecki, Glass, and many, many more. It, better stated, they, are content siphoning our blood, glucose, and, eventually, our lives. 
Once cancer manifests itself in daughter cells that further divide, it may not even care about itself. It certainly doesn’t care about its host. Cancer works toward its own end, an unintended yet deeply troubling double entendre, emphasizing the difficulty we humans have placing it in the universal schema. And killing it before it kills us is the central problem in cancer treatment:
“The mutations that benefit the survival and reproduction of cells in a tumor are the things that drive it towards malignancy. Evolution is also driving therapeutic resistance. When you apply chemotherapy to a population of tumor cells, you're quite likely to have a resistant mutant somewhere in that population of billions or even trillions of cells. This is the central problem in oncology. The reason we haven't been able to cure cancer is that we're selecting for resistant tumor cells. When we spray a field with pesticide, we select for resistant pests. It's the same idea.” 
Returning to the question that started this discussion, why is diabetes? Well, having lived with it for so many years, I can answer that question first by saying that it is certainly not here to benefit us, unless a prompt leading to self-development and enlightenment can be thought of as a benefit. Yes, diabetes is related to stress—stress from injury, surgery, infection, pregnancy, mental anguish and the like—or it could be a natural consequence of aging. It may simply be attributed to metabolic error or miscommunication between cells, imposed on a random selection of unlucky individuals in the human population, though that doesn’t explain why some populations have a higher incidence than others.  Nor does it explain why other substances or cells are able to thrive in its environment. Obesity, inflammation, and immunosuppression can lead to a myriad of complications, not the least of which is diabetes; but, we’re left wondering why some with the former conditions do not develop the latter. 
Diabetes may exist due to faulty genes, though that doesn’t explain why some with the “genes for diabetes” don’t express the disease and some do.  It may exist for the benefit of health-providers, though that is hopefully a tenuous explanation for a disease that has been around longer than a profession. It could be that its purpose is to benefit itself, i.e., that diabetes is its own meme, and that it too is struggling for lineage-based reproductive survival against the odds of a solitary, poor, nasty, brutish, and short existence.  The Coxsackie B4 virus is strongly associated with the development of insulin dependent diabetes mellitus.  Conversely, it appears that bacterial phyla normally present in the human gut may provide protection against developing diabetes. 
There are cases of chemicals, environmental toxicants and drugs causing temporary or permanent type 1 or type 2 diabetes documented in the medical literature. High serum selenium concentrations are associated with higher prevalence of diabetes.  The atypical antipsychotic drugs clozapine, olanzapin, risperidone, quetiapine and ziprasidone are known to induce insulin resistance, hyperglycemia, and even diabetic ketoacidosis (DKA).  The biologic plausibility of a diabetogenic effect of exposure to persistent organic pollutants, e.g., dioxins, polychlorinated biphenyls, and organophosphate insecticides, e.g., chlordane, is supported by numerous studies.  Alloxan, synthesized by the oxidation of uric acid by nitric acid, and the antibiotic streptozocin, produced by the soil bacterium Streptomyces achromogenes, are two of the best known toxins capable of damaging the pancreatic beta cells.  Vacor, a rat poison derived from the waste product urea, also has been reported to cause insulin dependent diabetes in humans who survived the exposure. 
The existence of naturally occurring toxins produced by many species of fungi capable of causing diabetes is also deeply troubling. Fungi are living things in our environment adapted to profit at our expense, though other microorganisms are probably the “intended” victims.  According to A.V. Costantini, M.D., Head (retired) of the World Health Organization Collaborating Center For Mycotoxins In Food:
“Fungi are masters at producing a wide array of biologically active substances which serve the producing fungus extremely well. These biological metabolites are anti-predatory, i.e., territory-protective, and exist to ensure that the fungus will survive as long as possible in this quite hostile world. These metabolites are anti-viral, anti-bacterial, anti-protozoan, anti-insect, anti-animal and, of course, anti-human. These metabolites are referred to as mycotoxins. The term is derived from the Greek mykes, meaning fungus, and toxicum, meaning toxin or poison. Fungi and mycotoxins are present in variable amounts in the food products of Western civilization such as the stored grains, particularly corn, fat-ladened meat of stored grain-fed animals, yeast-fermented beer, wine, bread, cheeses, coffee, and cured (fermented) meats and tobacco leaf.” 
Others too, such as Doug Hoffman and David Holland, M.D.,  and Laurens Maas,  each extensively drawing from Dr. Costantini’s works, emphasize, perhaps better stated as reiterate, that the link between diabetes and fungi is not entirely from the “utterly rotten fabric of guess and speculation.”  Although I agree that it is disconcerting to think that we are mere fodder for some other form, these authors do make a strong case.
What I do know with much certainty is that eliminating carbohydrates from the diet halts the abnormal proliferation of all five of the aforementioned items: insulin, glucose, glycosylated hemoglobin, triglycerides, and complications. If the relaxed definition makes sense to you, and you prefer to collectively call those five items cancer, then carbohydrate consumption is the proximate cause and ingesting near-zero of the same is the cure. 
Diabetes manifests itself in the body as ineffective carbohydrate processing; the corollary is that diabetes is a disease of insulin derangement. Too much insulin ought to be treated with too few carbohydrates. Not enough, or any, insulin ought to be treated similarly, with the addition of just enough exogenous, long-acting, basal insulin. Fat and protein only, as diet for both.
No, it’s not easy; nothing worthwhile ever is. But it is simple. And it works without enabling ischemic heart disease, cancer, or any other parasitoid, from any biota or mineralia, more, from any category—kingdom, chemical, compound, name, form, or idea—providing the great escape from our prisoner’s dilemma.
 Huxley, Professor T.H., “On the Reception of the Origin of Species,” 1887. In Darwin, Francis. The life and letters of Charles Darwin, including an autobiographical chapter. London: John Murray. Volume 2, ed. 1887. Available online at http://darwin-online.org.uk/converted/published/1887_Letters_F1452/1887_Letters_F1452.2.html.
“If T.H. Huxley (May 4, 1825 to June 29, 1895) is known at all, it is as “Darwin’s bulldog.” This self-imposed nickname recognizes the collegiate defense and enthusiastic offense—he undertook in support of the theory of evolution. In November of 1859, after reading the newly-published Origin of Species, he warned Charles Darwin that there would be mischief from anti-evolutionists, and that he himself, T.H. Huxley, was sharpening up his claws preparing to annihilate these creationist critics. He devoted himself for most of his career defending Darwinism and related notorious subversive subjects.” See The Huxley File online at http://aleph0.clarku.edu/huxley/.
 See Covey, Stephen R. The 7 Habits of Highly Effective People with Diabetes. Tarrytown, NY: Bayer Healthcare, LLC Diabetes Care, 2007, Habit No 2.
 For more information about the UN’s Millennium Development Goals, see http://www.unmillenniumproject.org/goals/index.htm.
 To see the online Resolution adopted by the General Assembly, [without reference to a Main Committee (A/55/L.2)], 55/2, United Nations Millennium Declaration, see http://www.un.org/millennium/declaration/ares552e.htm.
 A common, often altruistic, theme amongst many is to be able to solve world hunger via some method that may produce more food. However, often missed is the relationship between poverty and hunger. Hunger is an effect of poverty and poverty is largely a political issue (While manifesting itself as an economic issue, conditions causing poverty are political and end up being economic.). People are hungry not due to lack of availability of food, but because people do not have the ability to purchase food and because distribution of food is not equitable. In addition, there is also a lot of politics influencing how food is produced, who it is produced by (and who benefits), and for what purposes the food is produced (such as exporting rather than for the hungry, feedstuff, etc.). See, for example, http://www.globalissues.org/TradeRelated/Poverty/Hunger/Solutions.asp. Of particular interest to a diabetic, is how to get the right food, i.e., less emphasis on carbohydrates, and more on essential proteins and fats, to the right people.
 A diverse committee of experts from around the world, convened at the request of the National Science Foundation (NSF), and announced 14 grand challenges for engineering in the 21st century that, if met, would improve how we live.
“Tremendous advances in quality of life have come from improved technology in areas such as farming and manufacturing,” said committee member and GOOGLE co-founder Larry Page. “If we focus our effort on the important grand challenges of our age, we can hugely improve the future.”
The panel, some of the most accomplished engineers and scientists of their generation, was established in 2006 and met several times to discuss and develop the list of challenges. Through an interactive Web site, the effort received worldwide input from prominent engineers and scientists, as well as from the general public, over a one-year period. The panel's conclusions were reviewed by more than 50 subject-matter experts.
The final choices fall into four themes that are essential for humanity to flourish: sustainability, health, reducing vulnerability and increasing joy of living. The committee did not attempt to include every important challenge, nor did it endorse particular approaches to meeting those selected. Rather than focusing on predictions or gee-whiz gadgets, the goal was to identify what needs to be done to help people and the planet thrive.
“We chose engineering challenges that we feel can, through creativity and commitment, be realistically met, most of them early in this century,” said committee chair and former U.S. Secretary of Defense William J. Perry. “Some can be, and should be, achieved as soon as possible.”
The National Science Foundation (NSF) is an independent federal agency that supports fundamental research and education across all fields of science and engineering, with an annual budget of $5.92 billion. NSF funds reach all 50 states through grants to over 1,700 universities and institutions. Each year, NSF receives about 42,000 competitive requests for funding, and makes over 10,000 new funding awards. The NSF also awards over $400 million in professional and service contracts yearly. The NSF website is http://www.nsf.gov/index.jsp.
The National Academy of Engineering website is located at: http://www.nae.edu/nae/naehome.nsf. Retrieved on 3/4/08. The Grand Challenges site features a five-minute video overview of the project along with committee member interview excerpts.
 Although this meme is highly visible in nearly every industrialized nation, this challenge may be the least important of the 14 grand challenges.
“Claimed human-caused warming of the Earth to dangerous and unprecedented levels by human-related emissions of carbon dioxide is contradicted by a non-correlation of carbon dioxide levels with warming.
The Anthropogenic Global Warming Hypothesis states that sunlight radiation warms the Earth by being absorbed at its surface. Then some of the absorbed heat is reradiated into the atmosphere. Some gases in the atmosphere, called “greenhouse gases,” absorb much of this heat, and then reradiate it, some toward the surface of the Earth, making the Earth warmer than it would be without a heat-absorbing atmosphere. The primary “greenhouse gases” by far is said to be carbon dioxide, with some hints about methane, ozone, and traces of halocarbons.
Many serious scientists cite evidence that it’s the variations in solar output, solar distance and number of sunspots that are primarily responsible for temperature changes on Earth. This makes up the Solar Output Variation Hypothesis.
The predominant greenhouse gas is water vapor, not carbon dioxide. More water vapor also limits the day/night temperature range. This should not be construed as condoning wasteful use of hydrocarbon fuels. For the obvious economic reasons, not an unthreatening global warming, hydrocarbon fuels should be conserved or substituted when possible.”
See “Climate Change Reexamined,” by Joel M. Kauffman, Emeritus, Department of Chemistry & Biochemistry, University of the Sciences in Philadelphia, PA. Available online at http://www.scribd.com/doc/14299932/Climate-change-reexamined-joel-m.
 Perhaps no one has influenced our knowledge of life on Earth as much as the English naturalist Charles Robert Darwin (1809-1882). His theory of evolution by natural selection, now the unifying theory of the life sciences, explained where all of the astonishingly diverse kinds of living things came from and how they became exquisitely adapted to their particular environments. His theory reconciled a host of diverse kinds of evidence such as the succession of fossil forms in the geological record, the geographical distribution of species, recapitulative appearances in embryology, homologous structures, vestigial organs and nesting taxonomic relationships. No other explanation before or since has made sense of these facts.
In further works Darwin demonstrated that the difference between humans and other animals is one of degree not kind. In geology, zoology, taxonomy, botany, paleontology, philosophy, anthropology, psychology, literature and theology Darwin's writings produced profound reactions, many of which are still ongoing. Yet even without his evolutionary works, Darwin's accomplishments would be difficult to match. His brilliantly original work in geology, botany, biogeography, invertebrate zoology, psychology and scientific travel writing would still make him one of the most original and influential workers in the history of science. Darwin's writings are consequently of interest to an extremely wide variety of readers.
In further works Darwin demonstrated that the difference between humans and other animals is one of degree not kind. In geology, zoology, taxonomy, botany, paleontology, philosophy, anthropology, psychology, literature and theology Darwin's writings produced profound reactions, many of which are still ongoing. Yet even without his evolutionary works, Darwin's accomplishments would be difficult to match. His brilliantly original work in geology, botany, biogeography, invertebrate zoology, psychology and scientific travel writing would still make him one of the most original and influential workers in the history of science. Darwin's writings are consequently of interest to an extremely wide variety of readers.
For more on Darwin, see The Complete Work of Charles Darwin Online (or Darwin Online) at http://darwin-online.org.uk/. The site contains over 79,000 pages of searchable text and 190,000 electronic images.
 To read the article “Nothing in Biology Makes Sense Except in the Light of Evolution,” see http://www.pbs.org/wgbh/evolution/library/10/2/text_pop/l_102_01.html.
 Theodosius Grygorovych Dobzhansky, also known as T. G. Dobzhansky, and sometimes Anglicized to Theodore Dobzhansky (Ukrainian—January 24, 1900 - December 18, 1975) was a noted geneticist and evolutionary biologist, and a central figure in the field of evolutionary biology for his work in shaping the unifying modern evolutionary synthesis. Dobzhansky was born in Ukraine (then part of Imperial Russia) and emigrated to the United States in 1927.
Dobzhansky was born on January 24, 1900 in Nemyriv, Ukraine (then in the Russian Empire). An only child, his father Grigory Dobzhansky was a mathematics teacher, and his mother was Sophia Voinarsky. In 1910 the family moved to Kiev, Ukraine. At high school, Dobzhansky collected butterflies and decided to become a biologist. In 1915, he met Victor Luchnik who convinced him to specialize in beetles instead. Dobzhansky attended the University of Kiev between 1917 and 1921, where he then studied until 1924. He then moved to Leningrad, Russia, to study under Yuri Filipchenko, where a Drosophila melanogaster lab had been established.
In 1937 he published one of the major works of the modern evolutionary synthesis, the synthesis of evolutionary biology with genetics, entitled Genetics and the Origin of Species, which amongst other things defined evolution as “a change in the frequency of an allele within a gene pool.” Dobzhansky's work was instrumental in spreading the idea that it is through mutations in genes that natural selection takes place. Also in 1937, he became a naturalized citizen of the United States. During this time he had a very public falling out with one of his Drosophila collaborators, Alfred Sturtevant, based primarily in professional competition.
Dobzhansky returned to Columbia University from 1940 to 1962. He was one of the signatories of the 1950 UNESCO statement The Race Question. He then moved to the Rockefeller Institute (shortly to become Rockefeller University) until his retirement in 1971.
On June 1, 1968 it was discovered that Dobzhansky was suffering from lymphocytic leukemia, a chronic form of leukemia, and given a few months to a few years to live. Natasha died of coronary thrombosis on February 22, 1969. In 1971 he retired but continued working as an emeritus professor, moving to the University of California, Davis where his student Francisco Jose Ayala was made assistant professor.
Meanwhile, he continued working and published a famous essay “Nothing in Biology Makes Sense Except in the Light of Evolution.” A loyal defender of Darwinian evolution, Dobzhansky, according to Francisco J. Ayala “was a religious man.” Dobzhansky himself spoke of God as creating through evolution, and considered himself a communicant of the Eastern Orthodox Church.
His leukemia became more serious in the summer of 1975; on November 11 he made a trip to San Jacinto, California where he died of heart failure on December 18. He was cremated and his ashes were scattered in the Californian wilderness.
Abridged biography courtesy of the Wikipedia article entitled “Theodosius Dobzhansky.” Available online at http://en.wikipedia.org/wiki/Theodosius_Dobzhansky.
 American Biology Teacher, volume 35, pages 125-129.
 Abridged description courtesy of the Wikipedia article entitled “Nothing in Biology Makes Sense Except in the Light of Evolution.” Available online at http://en.wikipedia.org/wiki/Nothing_in_Biology_Makes_Sense_Except_in_the_Light_of_Evolution.
 “Why Are People?” is the title of the first chapter of Richard Dawkin’s book The Selfish Gene (New York: Oxford University Press, 30th Anniversary edition, 2006).
 Dawkins, Richard. The Ancestor’s Tale: A Pilgrimage to the Dawn of Evolution. New York: Houghton Mifflin Company, 2005, page 7.
 Ibid, page 530.
 Masur K, Thévenod F, Zänker KS (eds): Diabetes and Cancer. Epidemiological Evidence and Molecular Links. Frontiers in Diabetes. Basel; Karger, 2008, Vol 19, page 50.
 Ibid, page 51.
 Ibid, page 44.
 Calle EE, Kaaks R (2004) Overweight, obesity and cancer: epidemiological evidence and proposed mechanisms. Nature Reviews: Cancer 4(8): 579-91. Op cit. Smyth D, and Smyth T., “The Relationship Between Diabetes and Cancer,” Journal of Diabetes Nursing, July-August, 2005. Available online at http://findarticles.com/p/articles/mi_m0MDR/is_7_9/ai_n15727529/?tag=content;col1.
 Shi R, Yu H, McLarty, J, Glass J (2004) IGF-I and breast cancer: a meta-analysis. International Journal of Cancer 111(3): 418-23. Op cit. Smyth D, and Smyth T. (2005).
 Stattin P, Rinaldi S, Biessy C, Stenman UH, Hallmans G, Kaaks R (2004) High levels of circulating insulin-like growth factor-1 increase prostate cancer risk: a prospective study in a population-based nonscreened cohort. Journal of Clinical Oncology 22(15): 3104-12. Op cit. Smyth D, and Smyth T. (2005).
 Richardson LC, Pollack LA (2005) Therapy Insight: influence of type 2 diabetes on the development, treatment and outcomes of cancer. Nature Clinical Practice Oncology 2(1): 48-53. Op cit. Smyth D, and Smyth T. (2005).
 Anderson KE, Anderson E, Mink PJ, Hong CP, Kushi LH, Sellers TA et al (2001) Diabetes and endometrial cancer in the lowa women's health study. Cancer Epidemiology, Biomarkers & Prevention 10(6): 611-6. Op cit. Smyth D, and Smyth T. (2005).
 Michels KB, Solomon CG, Hu FB, Rosner BA, Hankinson SE, Colditz GA et al (2003) Type 2 diabetes and subsequent incidence of breast cancer in the Nurses' Health Study. Diabetes Care 26(6): 1752-8. Op cit. Smyth D, and Smyth T. (2005).
 Khaw KT, Wareham N, Bingham S, Luben R, Welch A, Day N (2004) Preliminary communication: glycated hemoglobin, diabetes, and incident colorectal cancer in men and women: a prospective analysis from the European prospective investigation into cancer-Norfolk study. Cancer Epidemiology, Biomarkers & Prevention 13(6): 915-9. See also Jee SH, Ohrr H, Sull JW, Yun JE, Ji M, Samet JM (2005) Fasting serum glucose level and cancer risk in Korean men and women. Journal of the American Medical Association 293(2): 194-202. Op cit. Smyth D, and Smyth T. (2005).
 Jee SH, Ohrr H, Sull JW, Yun JE, Ji M, Samet JM (2005) Fasting serum glucose level and cancer risk in Korean men and women. Journal of the American Medical Association 293(2): 194-202. Op cit. Smyth D, and Smyth T. (2005).
 Khaw KT, Wareham N, Bingham S, Luben R, Welch A, Day N (2004) Preliminary communication: glycated hemoglobin, diabetes, and incident colorectal cancer in men and women: a prospective analysis from the European prospective investigation into cancer-Norfolk study. Cancer Epidemiology, Biomarkers & Prevention 13(6): 915-9. Op cit. Smyth D, and Smyth T. (2005).
 National Cancer Institute: Diabetes increases men's risk of liver, pancreatic cancer, study finds. NCI Cancer Bulletin. NCI, Bethesda, MD. Available online at http://www.cancer.gov/NCICancerBulletin/NCI_Cancer_Bulletin_102604/page4. Retrieved on 5/20/09. Op cit. Smyth D, and Smyth T. (2005).
 Yang YX, Hennessy S, Lewis JD (2004) Insulin therapy and colorectal cancer risk among type 2 diabetes mellitus patients. Gastroenterology 127(4): 1044-50. Op cit. Smyth D, and Smyth T. (2005).
 Having diabetes when given a cancer diagnosis increases the risk of death by 41%, researchers here said. That finding comes from the first systematic assessment of long-term, all-cause mortality in newly diagnosed cancer patients with or without diabetes, according to Frederick Brancati, M.D., and colleagues at Johns Hopkins University.
All told, they found 48 articles that evaluated the effect of pre-existing diabetes on cancer outcome, including 23 that could be combined in a meta-analysis.
Possible explanations include interactions between the two disease types, treatment effects, poorer response to therapy, and sub-optimal cancer screening that leads diabetic patients to be diagnosed later, the researchers said.
It's even possible that the observed increase in risk of death is just a result of the effect of diabetes on cardiovascular health and has nothing to do with cancer at all, Dr. Brancati and colleagues said.
See the online article “Diabetes Increases Cancer Death Risk,” By Michael Smith, North American Correspondent, MedPage Today, Published: December 16, 2008. Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston. Available online at http://www.medpagetoday.com/Endocrinology/Diabetes/12177.
The above source comments on the original article by Barone BB, et al., “Long-term all-cause mortality in cancer patients with preexisting diabetes mellitus: a systematic review and meta-analysis,” JAMA 2008; 300(23): 2754-2764. Available online at http://jama.ama-assn.org/cgi/content/short/300/23/2754.
 The authors performed a prospective cohort study using data from the Second National Health and Nutrition Examination Survey and the Second National Health and Nutrition Examination Survey Mortality Study to determine this relation.
This analysis focused upon a nationally representative sample of 3,054 adults aged 30-74 years who underwent an oral glucose tolerance test at baseline (1976-1980). Deaths were identified by searching national mortality files through 1992. Adults were classified as having either previously diagnosed diabetes (n = 247), undiagnosed diabetes (n = 180), impaired glucose tolerance (n = 477), or normal glucose tolerance (n = 2250). There were 195 cancer deaths during 40,024 person-years of follow-up. Compared with those having normal glucose tolerance, adults with impaired glucose tolerance had the greatest adjusted relative hazard of cancer mortality (relative hazard = 1.87, 95% confidence interval (CI): 1.06, 3.31), followed by those with undiagnosed diabetes (relative hazard = 1.31, 95% CI: 0.48, 3.56) and diabetes (relative hazard = 1.13, 95% CI: 0.49, 2.62).
See “Abnormal glucose tolerance and the risk of cancer death in the United States,” by Saydah SH, Loria CM, Eberhardt MS, Brancati FL. Am J Epidemiol. 2003 Jun 15;157(12):1092-100. Available online at http://www.ncbi.nlm.nih.gov/pubmed/12796045?ordinalpos=87&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum.
 Coughlin SS, Calle EE, Teras LR, Petrelli J, Thun M, “Diabetes Mellitus as a Predictor of Cancer Mortality in a Large Cohort of US Adults,” Am J Epidemiol, 2004;159:1160-1167. Available online at http://aje.oxfordjournals.org/cgi/content/full/159/12/1160.
 See “Prospective Study of Hyperglycemia and Cancer Risk,” by Pär Stattin, MD, PHD, Ove Björ, BSC, Pietro Ferrari, BSC, Annekatrin Lukanova, MD, PHD, Per Lenner, MD, PHD, Bernt Lindahl, MD, PHD, Göran Hallmans, MD, PHD and Rudolf Kaaks, PHD. Diabetes Care, March, 2007, vol. 30, no. 3, 561-567. doi: 10.2337/dc06-0922. Available online at http://care.diabetesjournals.org/content/30/3/561.full.
 See http://www.cancer.gov/cancertopics/what-is-cancer.
 Abridged from the Wikipedia article entitled “Cancer,” available online at http://en.wikipedia.org/wiki/Cancer.
 Darwin, Charles. On the Origin of Species by Means of Natural Selection, or The Preservation of Favoured Races in the Struggle for Life. London: John Murray, Albemarle Street, 1859. In Darwin: The Indelible Stamp. Four Essential Volumes in One. Edited, with commentary, by James D. Watson. Philadelphia: Running Press, 2005, page 600. Please note that this is not a first edition quote, as preferred by more scholarly writers, but the gist of the message is just as clear in any edition.
 I had originally written “…at a level much higher than the individual,” however, after further reading, most notably, Richard Dawkins’s Unweaving the Rainbow, I came to realize that evolution, whether through domestication, sexual selection, or natural selection, unfolds gradually from the level of the individual. Being American, most of my knowledge was shaped by the American-based writer Stephen Jay Gould. “Ironically, Gould is one of the few Darwinians who still think of natural selection as working at levels higher than the individual organism.” See Dawkins, Richard. Unweaving the Rainbow. Boston & New York: A Mariner Book, Houghton Mifflin Company, 1998, p. 199.
For two great, recent overviews of the fact of evolution, see Dawkins, Richard. The Greatest Show on Earth: The Evidence for Evolution. New York: Free Press, 2009; and Coyne, Jerry A. Why Evolution is True. New York: Viking, the Penguin Group, 2009. According to Coyne, “Life on Earth evolved gradually beginning with one primitive species—perhaps a self-replicating molecule—that lived more than 3.5 billions years ago; it then branched out over time, throwing off many new and diverse species; and the mechanism for most (but not all) of evolutionary change is natural selection.” (Page 3)
 For a good discussion of arms races, manipulation, and descriptions of the five different types of fitness, see the chapters entitled “Arms Races and Manipulation,” and “An Agony in Five Fits,” in Dawkins, Richard. The Extended Phenotype: The Long Reach of the Gene. New York: Oxford University Press, 2008.
Note that all these concepts, namely, parasitism, symbiosis, conflict, cooperation, and co-evolution—which were developed with reference to whole organisms—are relevant to genes within an organism. See Ibid, page 178.
 For a fascinating article detailing how cancer is not an “it” but a “they,” see “Evolution of Cooperation Among Tumor Cells,” by Robert Axelrod, David E. Axelrod, and Kenneth J. Pienta. Published online before print August 28, 2006, doi: 10.1073/pnas.0606053103. Proceedings of the National Academy of Sciences of the United States of America (PNAS), September 5, 2006 vol. 103 no. 36 13474-13479. Available online at http://www.pnas.org/content/103/36/13474.full#sec-3.
“…We marshal evidence that tumor cells overcome certain host defenses by means of diffusible products. Our original contribution is to raise the possibility that two nearby cells can protect each other from a set of host defenses that neither could survive alone. Cooperation can evolve as by-product mutualism among genetically diverse tumor cells. Our hypothesis supplements, but does not supplant, the traditional view of carcinogenesis in which one clonal population of cells develops all of the necessary genetic traits independently to form a tumor. Cooperation through the sharing of diffusible products raises new questions about tumorigenesis and has implications for understanding observed phenomena, designing new experiments, and developing new therapeutic approaches.”
 See The Wistar Institute (2006, November 17). Does Natural Selection Drive The Evolution Of Cancer? ScienceDaily. Available online at http://www.sciencedaily.com/releases/2006/11/061117114616.htm.
 For percentage breakdown by geography, see the Disease Control Priorities Project online at http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=dcp2.table.4313.
For actual numbers of diabetics worldwide, see the World Health Organization’s diabetes pages online at http://www.who.int/diabetes/facts/world_figures/en/index.html.
“The reasons for the uneven worldwide distribution of Type 1 diabetes mellitus have yet to be fully explained. Epidemiological studies have shown a higher prevalence of Type 1 diabetes in northern Europe, particularly in Scandinavian countries, and Sardinia. Recent animal research has uncovered the importance of the generation of elevated levels of glucose, glycerol and other sugar derivatives as a physiological means for cold adaptation. High concentrations of these substances depress the freezing point of body fluids and prevent the formation of ice crystals in cells through supercooling, thus acting as a cryoprotectant or antifreeze for vital organs as well as in their muscle tissue. In this paper, we hypothesize that factors predisposing to elevated levels of glucose, glycerol and other sugar derivatives may have been selected for, in part, as adaptive measures in exceedingly cold climates.”
See “The sweet thing about Type 1 diabetes: a cryoprotective evolutionary adaptation,” by Moalem S, Storey KB, Percy ME, Peros MC, Perl DP. Med Hypotheses, 2005;65(1):8-16. Available online at http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=15893109.
 Over the last decade, an abundance of evidence has emerged demonstrating a close link between metabolism and immunity. It is now clear that obesity is associated with a state of chronic low-level inflammation. In the below cited article, the authors discuss the molecular and cellular underpinnings of obesity-induced inflammation and the signaling pathways at the intersection of metabolism and inflammation that contribute to diabetes. They also consider mechanisms through which the inflammatory response may be initiated and discuss the reasons for the inflammatory response in obesity. The authors put forth for consideration some hypotheses regarding important unanswered questions in the field and suggest a model for the integration of inflammatory and metabolic pathways in metabolic disease.”
See “Inflammation, stress, and diabetes,” by Kathryn E. Wellen and Gökhan S. Hotamisligil. J. Clin. Invest. 115(5): 1111-1119 (2005). doi: 10.1172/JCI25102. Available online at http://www.jci.org/articles/view/25102/version/1.
 “…genes are named after the conditions and abnormalities that led to their discovery. This, inevitably, means that their name commemorates what happens when they don’t work. The gene that triggers the development of eyes in fruit flies—discovered in 1915—is called ‘eyeless’.” See Ings, Simon. A Natural History of Seeing: The Art and Science of Vision. New York: W.W. Norton & Company, 2008, p. 83.
Researchers have found nearly 20 different genes that can affect one’s risk for developing diabetes. See GeneticHealth online at http://www.genetichealth.com/dbts_genetics_of_type_1_diabetes.shtml.
There are hundreds, more, thousands of articles in the medical literature pertaining to the genetic associations with diabetes. Here I’ll provide just two such recent articles that you may find interesting:
Regarding type 2 diabetes, see for example “Genetic Basis of Beta-Cell Dysfunction in Man,” by Groop L and Lyssenko V. Diabetes Obes Metab 2009 Nov;11 Suppl 4():149-58. “Although the genetic causes of monogenic disorders have been successfully identified in the past, the success in dissecting the genetics of complex polygenic diseases has until now been limited. With the introduction of whole genome wide association studies (WGAS) in 2007, the picture has been dramatically changed. Today we know of about 20 genetic variants increasing the risk of type 2 diabetes (T2D). Most of them seem to influence the capacity of beta-cells to increase insulin secretion to meet the demands imposed by an increase in body weight and insulin resistance. This probably represents only the tip of the iceberg, and over the next few years refined tools will provide a more complete picture of the genetic complexity of T2D. This will not only include the current dissection of common variants increasing the susceptibility of the disease but also rare variants with stronger effects, copy number variations and epigenetic effects like DNA methylation and histone acetylation. For the first time, we can anticipate with some confidence that the genetics of a complex disease like T2D really can be dissected.” Available online at http://www.ncbi.nlm.nih.gov/pubmed/19817797?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=3. PMID: 19817797; doi: 10.1111/j.1463-1326.2009.01117.x.
Regarding type 1 diabetes, see for example “Genetic Basis of Type 1 Diabetes: Similarities and Differences between East and West,” by Ikegami H, Noso S, Babaya N, Hiromine Y, and Kawabata Y. Rev Diabet Stud 2008 Summer;5(2):64-72. “Type 1 diabetes is a multifactorial disease caused by a complex interaction of genetic and environmental factors. The genetic factors involved consist of multiple susceptibility genes, at least five of which, HLA, INS, CTLA4, PTPN22 and IL2RA/CD25, have been shown to be associated with type 1 diabetes in Caucasian (Western) populations, as has recently been confirmed by genome-wide association studies. It has been proposed, however, that the contribution of these genes to type 1 diabetes susceptibility may be different in Asian (Eastern) populations.” Available online at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2556443/?tool=docline. PMID: 18795209; doi: 10.1900/RDS.2008.5.64.
 The famous quotation describing life in the state of war of every man against every man: “…the life of man, solitary, poor, nasty, brutish, and short,” is from Chapter XIII “Of the Natural Condition of Mankind, as concerning their Felicity, and Misery,” from Leviathan, The Matter, Forme and Power of a Common Wealth Ecclesiasticall and Civil, commonly called Leviathan, a book written by Thomas Hobbes which was published in 1651. It is titled after the biblical Leviathan. The book concerns the structure of society and legitimate government, and is regarded as one of the earliest and most influential examples of social contract theory. Adapted from the Wikipedia article entitled “Leviathan (book),” available online at http://en.wikipedia.org/wiki/Leviathan_(book).
 See “Diabetes induced by Coxsackie virus: Initiation by bystander damage and not molecular mimicry,” by Horwitz, et al. Nature Medicine 4, 781 - 785 (1998), doi: 10.1038/nm0798-781. Available online at http://www.nature.com/nm/journal/v4/n7/abs/nm0798-781.html. Retrieved on 6/13/09. For the first prospective study, see “A prospective study of the role of coxsackie B and other enterovirus infections in the pathogenesis of IDDM. Childhood Diabetes in Finland (DiMe) Study Group,” by Hyöty, et al. Diabetes June, 1995, vol. 44, no. 6, 652-657. doi: 10.2337/diabetes.44.6.652. Available online at http://diabetes.diabetesjournals.org/content/44/6/652.abstract.
 See “Innate immunity and intestinal microbiota in the development of Type 1 diabetes,” by Li Wen, et al. Nature. 2008, October 23; 455(7216): 1109–1113. Published online 2008, September 21. doi: 10.1038/nature07336. PMCID: PMC2574766; NIHMSID: NIHMS67288. Available online at http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2574766.
“Humans consist of about a trillion cells, but there are some 10 trillion bacterial cells on or in us at any given time. Bacteria digest our food, make our vitamins, educate our immune system to keep harmful antigens out. But there are also notorius and harmful bacteria.” See http://www.ted.com/talks/bonnie_bassler_on_how_bacteria_communicate.html.
Bonnie Bassler discovered that bacteria “talk” to each other, using a chemical language that lets them coordinate defense and mount attacks. The find has stunning implications for medicine and industry. See http://www.molbio.princeton.edu/index.php?option=content&task=view&id=27.
For more on quorum sensing see the Wikipedia article entitled “Quorum Sensing,” online at http://en.wikipedia.org/wiki/Quorum_sensing.
 In summary, high serum selenium concentrations were associated with higher prevalence of diabetes in a representative survey of US adults conducted in 2003-2004. These findings are consistent with an earlier National Health and Nutrition Examination Survey (NHANES) survey conducted in 1988-1994. See “Serum Selenium Concentrations and Diabetes in US Adults: National Health and Nutrition Examination Survey (NHANES) 2003-2004,” by Martin Laclaustra, Ana Navas-Acien, Saverio Stranges, Jose M Ordovas, and Eliseo Guallar. Environmental Health Perspectives, doi: 10.1289/ehp.0900704. Aavailable online at http://ehp.niehs.nih.gov/docs/2009/0900704/abstract.html.
 American Diabetes Association; American Psychiatric Association; American Association of Clinical Endocrinologists; North American Association for the Study of Obesity (February 2004). “Consensus development conference on antipsychotic drugs and obesity and diabetes.” Diabetes Care 27 (2): 596–601. doi: 10.2337/diacare.27.2.596. PMID 14747245. Available online at http://care.diabetesjournals.org/cgi/content/full/27/2/596.
 See “Incident Diabetes and Pesticide Exposure among Licensed Pesticide Applicators: Agricultural Health Study, 1993–2003,” by M. P. Montgomery, F. Kamel, T. M. Saldana, M. C. R. Alavanja, and D. P. Sandler. American Journal of Epidemiology, March 14, 2008. doi: 10.1093/aje/kwn028. Available online at http://www.toxfree.net/chlordane/Education/Healthrisk/Applicators.pdf.
“The authors’ aim was to investigate the relation between lifetime exposure to specific agricultural pesticides and diabetes incidence among pesticide applicators. The study included 33,457 licensed applicators, predominantly non-Hispanic White males, enrolled in the Agricultural Health Study. Incident diabetes was self-reported in a 5-year follow-up interview (1999–2003), giving 1,176 diabetics and 30,611 nondiabetics for analysis. Lifetime exposure to pesticides and covariate information were reported by participants at enrollment (1993–1997). Using logistic regression, the authors considered two primary measures of pesticide exposure: ever use and cumulative lifetime days of use. They found seven specific pesticides (aldrin, chlordane, heptachlor, dichlorvos, trichlorfon, alachlor, and cyanazine) for which the odds of diabetes incidence increased with both ever use and cumulative days of use. Applicators who had used the organochlorine insecticides aldrin, chlordane, and heptachlor more than 100 lifetime days had 51%, 63%, and 94% increased odds of diabetes, respectively. The observed association of organochlorine and organophosphate insecticides with diabetes is consistent with results from previous human and animal studies. Long-term exposure from handling certain pesticides, in particular, organochlorine and organophosphate insecticides, may be associated with increased risk of diabetes.
This study is to our knowledge the largest study to evaluate the potential effects of pesticides on diabetes incidence in adults. The prospective design of the study ensures that exposures were reported prior to the diagnosis of diabetes and reduces the potential for recall bias. Of the 50 pesticides evaluated, seven displayed evidence suggesting an association with diabetes incidence in both ever-use and cumulative days-of-use models: aldrin, chlordane, heptachlor, dichlorvos, trichlorfon, alachlor, and cyanazine. It is noteworthy that all of these pesticides are chlorinated compounds, while only half of the pesticides investigated were chlorinated. Few studies, if any, have considered the potential diabetogenic effects of alachlor and cyanazine, which both showed a dose-response association with diabetes in the present study. However, the biologic plausibility of a diabetogenic effect of exposure to persistent organic pollutants (e.g., dioxins, polychlorinated biphenyls, and organochlorine insecticides) and organophosphate insecticides is supported by numerous studies.”
See also “Treatment of Homes for Termites Decades Ago May Cause Diabetes Today,” by Dr. Richard Cassidy, DiabetesHealth, Mar 13, 2009. Available online at http://www.diabeteshealth.com/read/2009/03/12/6117/treatment-of-homes-for-termites-decades-ago-may-cause-diabetes-today/.
“Recently, the Centers for Disease Control mapped the incidence of diabetes by state. There is a striking correlation between the incidence of diabetes and the use of chlordane for termite control in these states. Southern states with the highest temperatures and humidity have not only the highest rates of termite infestations and chlordane use, but also the highest rate of diabetes. States from the midsection of the United States, with moderate temperatures and humidity and lower chlordane applications, have lower rates of diabetes. In northern states such as Minnesota, where chlordane was rarely used, the incidence of diabetes is less than 50 percent that of southern states.”
Because of concern about damage to the environment and harm to human health, the United States Environmental Protection Agency (EPA) banned all uses of chlordane in 1983 except termite control. The EPA banned all uses of chlordane in 1988.
 See, for example, “Blood levels of alloxan in children with insulin-dependent diabetes mellitus,” by A. Mrozikiewicz, D. Kielstrokczewska-Mrozikiewicz, Z. Lstrokowicki, E. Chmara, K. Korzeniowska and P. M. Mrozikiewicz. Acta Diabetologica, Volume 31, Number 4, December, 1994, pages 236-237. doi: 10.1007/BF00571958. Available online at http://www.springerlink.com/content/r001211h96j18266/.
The mechanisms underlying alloxan and streptozotocin diabetes are a major research topic of the Institute of Clinical Biochemistry of Hannover Medical School. For the full list of publications addressing this topic, which can all be downloaded via PubMed, see http://www.mh-hannover.de/8750.html.
 See “Diabetes mellitus and orthostatic hypotension resulting from ingestion of Vacor rat poison: endocrine and autonomic function studies,” by K S Peters, T G Tong, K Kutz, and N L Benowitz. West J Med. 1981 January; 134(1): 65–68. Available online at http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1272465.
 According to Nicholas P. Money, in Mr. Bloomfield’s Orchard, “In England in 1960, 100,000 turkeys died following loss of appetite, lethargy, and liver failure. It was discovered that they had been fed aflatoxin-contaminated peanut meal, and the name turkey X-disease was coined for their plague…It is unlikely that turkeys, or any other animals, are the targets for aflatoxins in an evolutionary sense. It has been suggested that animals compete with fungi for the same food—harvested grain, for example—and that aflatoxins would reduce the number of these rivals. But I’m not convinced; other microorganisms are probably the “intended” victims. While fungi produce mycotoxins in minute quantities in the soil and in plant tissues, local concentrations may be high enough in the immediate vicinity of the growing hyphae to clear the territory for the mold.” See Money, Nicholas P. Mr. Bloomfield’s Orchard: The Mysterious World of Mushrooms, Molds, and Mycologists. New York: Oxford University Press, 2002, Page 162.
Regarding another mycotoxin, amatoxin, Dr. Money writes: “Insects and fungi have interacted with one another for 400 million years or more, an expanse of time that has offered ample opportunity for the evolution of defense and counter-defense mechanisms in both groups of organisms. If insect larvae are the real targets of amatoxins, then human casualties were “unintended” by evolution. In every sense, then, mushrooms couldn’t care less about Homo sapiens.” See page 156.
Interestingly, in this book he wrote about Curtis Gates Lloyd, one of Cincinnati’s most eligible bachelors, and a millionaire obsessed with fungi. Mr. Lloyd became a self-taught expert in fungal identification and had undertaken the publication of his own mycological work. “Mr. Lloyd had suffered from diabetes for many years, and with little in the contemporary pharmacopia to prolong his life, he died of complications from the disease in 1926.” See page 102.
See also Money, Nicholas P. Carpet Monsters and Killer Spores: A Natural history of Toxic Mold. New York: Oxford University Press, 2004.
“Fungi never intended to inflame or poison humans. After all, black molds spent hundreds of millions of years rotting dead plants before the evolution of wheezing authors and bleeding babies. Their spores were designed for drifting in air, not for swimming in lung mucous, so problems with molds are rooted in our insistence on breathing rather than any microbial malevolence.” See page 58.
“Fungi produce hundreds of different kinds of toxins, a few of proven harm to humans, most of dubious significance. Everyone is familiar with poisonous mushrooms. A single fruiting body of a death cap or a destroying angel contains a few thousandths of a gram of amatoxins, which is adequate to kill an adult. Amatoxins are peptides that block protein synthesis in cells. The reason that the mushroom accumulates these poisonous molecules is unclear, but the most satisfying answer is that they defend the fruiting body against insect grubs.” See page 59.
 See The Garden of Eden Longevity Diet Antifungal/Antimycotoxin,Anti-Cancer, Anti-Atherosclerosis; see also The Fungal/Mycotoxin Etiology of Breast Cancer Foods That Cause & Foods that Prevent; see also The Fungal/Mycotoxin Etiology of Prostate Cancer Foods That Cause & Foods That Prevent; and The Fungal/Mycotoxin Etiology of Atherosclerosis Foods That Cause & Foods that Prevent all written by A.V. Costantini, M.D., H. Wieland, M.D., and Lars Qvick, M.D. For excerpts, see http://www.fungalbionicbookseries.com/index.htm.
In describing the strength of mycotoxins, the above authors wrote the following:
“As many as 1,000 compounds, classifiable as mycotoxins, were studied by the pharmacology industry as potential antibiotics in the 1930s and 1940s only to be discarded as being too toxic for higher life forms to be of value in treating bacterial diseases in humans. Little, if any of the discarded data was published. Yet what these toxicity studies actually documented was the existence of a large number of fungal-derived toxins which caused serious target organ injury in various animal models. Obviously, in retrospect, what was being seen was the pathology produced by the mycotoxins. In order to understand this toxicity, one only has to look at what some of these mycotoxins, used as medications, causes in humans: The mycotoxin cyclosporin used for transplantation causes cancer and atherosclerosis, complete with hyperlipidemia, in ALL humans who have received it. Many others develop gout and other diseases.”
Prof. Dr. A.V. Costantini, MD was the keynote speaker at the 1993 conference of the American Academy of Environmental Medicine held in Reno, Nevada, where he stated the following:
“Auto-immune diseases are characterized by the finding of so-called auto-antibodies. It is a most popular concept but biologically fatally defective in that no species of life can make an antibody against itself; particularly causing fatal disease such as scleroderma. Scleroderma is considered to prove the validity of the auto-immune concept with the presence of auto-antibodies. However these are now documented to be antibodies against ubiquitin which is present in many species including fungi. Scleroderma responds well to the antifungal agent griseofulvin. Against whose ubiquitin is the host raising antibodies to, its own, or fungal-derived, in a disease state which responds to an antifungal drug? The auto-immune diseases appearing to have a fungal and mycotoxin origin are: scleroderma, diabetes mellitus, HLA-related disease, rheumatoid arthritis, Sjogren’s syndrome, psoriasis & systemic lupus erythematosus. All of the drugs effective in the treatment of these diseases possess antifungal or anti-mycotoxin activity. This includes all NSAIDs [Non-Steroidal Anti-Inflammatory Drugs].”
From the Chesser-Naugle International Lectureship Grant: The Fungal/Mycotoxin Connections: Autoimmune Diseases, Malignancies, Atherosclerosis, Hyperllpldemias, and Gout, October 11, 1993. Twenty-eighth annual meeting entitled “New horizons in Chemical Sensitivities: State of the Art Diagnosis and Treatment. Available online at http://www.arthritistrust.org/Articles/Fungal-Mycotoxin%20Connection/index.htm.
 See Kaufmann, Doug and Holland, David. The Fungus Link to Diabetes: A Cutting-Edge Approach to Stopping One of America’s Fastest Growing Epidemics in Its Tracks. Rockwall, Texas: MediaTrition, Inc., 2003.
 See Maas, Laurens. The Hidden Cure: The Five Laws of Perfect Health. Wheatmark: Tuscan, Arizona, 2009.
 The most outraged and formidable opponent of Charles Darwin was Richard Owen, Hunterian Professor at the Royal College of Surgeons, who examined the fossil bones Darwin had had brought back from South America. Owen acted largely behind the scenes, and was the one who provided material for Bishop Wilberforce’s scathing review in the Quarterly Review, where Wilberforce referred to Darwin’s ideas as “his utterly rotten fabric of guess and speculation.” See “Commentary: On the Origin of Species,” in Darwin: The Indelible Stamp. Four Essential Volumes in One. Edited, with commentary, by James D. Watson. Philadelphia: Running Press, 2005, page 342.
The four volumes include: The Voyage of the Beagle (no publication information given); On the Origin of Species by Means of Natural Selection (London: John Murray, Albemarle Street, 1859); The Descent of Man, and Selection in Relation to Sex (Second Edition, London: John Murray, Albemarle Street, 1882); and The Expression of the Emotions in Man and Animals (London: John Murray, Albemarle Street, 1872).
The Voyage of the Beagle is a title commonly given to the book written by Charles Darwin published in 1839 as his Journal and Remarks, which brought him considerable fame and respect. The title refers to the second survey expedition of the ship HMS Beagle, which set sail from Plymouth Sound on December 27, 1831, under the command of captain Robert FitzRoy.
 Appendix C of the book ESSENTIAL DIABETES LEADERSHIP (2010) contains scores of low-carbohydrate, ketogenic diet articles, including several on point to ketogenic diet and cancer. See for example:
· Implementing a ketogenic diet based on medium-chain triglyceride oil in pediatric patients with cancer. Nebeling LC, Lerner E., J Am Diet Assoc. 1995 Jun;95(6):693-7. Available online at http://www.ncbi.nlm.nih.gov/pubmed/7759747.
· Effects of a ketogenic diet on tumor metabolism and nutritional status in pediatric oncology patients: two case reports. Nebeling LC, Miraldi F, Shurin SB, Lerner E., J Am Coll Nutr. 1995 Apr;14(2):202-8. Available online at http://www.ncbi.nlm.nih.gov/pubmed/7790697.
· The calorically restricted ketogenic diet, an effective alternative therapy for malignant brain cancer. Weihua Zhou, Purna Mukherjee, Michael A Kiebish, William T Markis, John G Mantis, and Thomas N Seyfried, Nutr Metab (Lond). 2007; 4: 5. Published online 2007 February 21. doi: 10.1186/1743-7075-4-5. Available online at http://www.ncbi.nlm.nih.gov/pubmed/17313687.
· The Effects of Varying Dietary Carbohydrate and Fat Content on Survival in a Murine LNCaP Prostate Cancer Xenograft Model. Mavropoulos JC, Buschemeyer WC 3rd, Tewari AK, Rokhfeld D, Pollak M, Zhao Y, Febbo PG, Cohen P, Hwang D, Devi G, Demark-Wahnefried W, Westman EC, Peterson BL, Pizzo SV, Freedland SJ, Cancer Prev Res (Phila Pa). 2009 May 26. Available online at http://www.ncbi.nlm.nih.gov/pubmed/19470786.
· Targeting energy metabolism in brain cancer with calorically restricted ketogenic diets. Seyfried TN, Kiebish M, Mukherjee P, Marsh J, Epilepsia. 2008 Nov;49 Suppl 8:114-6. Available online at http://www.ncbi.nlm.nih.gov/pubmed/19049606.
The ketogenic diet has also been used successfully in the treatment of epilepsy.
The biggest modern study with an intent-to-treat prospective design was published in 1998. As with most studies of the ketogenic diet, there was no control group, which would be patients who were denied the treatment. A team from the Johns Hopkins Hospital studied 150 children for at least 12 months. By three months, 25 patients had dropped out, 26% had a good reduction in seizures (50–90% reduction), 31% had an excellent reduction (90–99% reduction) and 3% became seizure free. By twelve months, 67 patients had dropped out, 23% had a good reduction, 20% had an excellent reduction and 7% were seizure free. See Freeman JM, Vining EP, Pillas DJ, Pyzik PL, Casey JC, Kelly LM. The efficacy of the ketogenic diet–1998: a prospective evaluation of intervention in 150 children. Pediatrics. 1998 Dec;102(6):1358–63. PMID 9832569. Available online at http://www.ncbi.nlm.nih.gov/pubmed/9832569.
In the same year, a multi-center study of 51 children showed similar efficacy, and proved that the results could be repeated by other institutions. See Vining EP, Freeman JM, Ballaban-Gil K, Camfield CS, Camfield PR, Holmes GL, et al. A multicenter study of the efficacy of the ketogenic diet. Arch Neurol. 1998 Nov;55(11):1433–7. PMID 9823827. Available online at http://www.ncbi.nlm.nih.gov/pubmed/9823827. Retrieved on 5/28/09. See also Hartman AL, Vining EP. Clinical aspects of the ketogenic diet. Epilepsia. 2007 Jan;48(1):31–42. PMID 17241206. doi: 10.1111/j.1528-1167.2007.00914.x. Available online at http://www.ncbi.nlm.nih.gov/pubmed/17241206.
The first randomised controlled trial was published in 2008, which had an intent-to-treat prospective design, but no blinding. It studied 145 children, half of whom were randomly selected to start the ketogenic diet immediately, and half to start after a three-month delay. The children who were delayed treatment acted as a control, which is particularly important for medical conditions where patients may get better or worse regardless of treatment. Of the children in the diet group, 38% had at least a 50% reduction in seizure frequency, 7% had at least a 90% reduction; one child became seizure-free. Only 6% of the control group saw a greater than 50% reduction in seizure frequency and no children had a 90% reduction. The mean seizure frequency of the diet group fell by a third; the control group's mean seizure frequency actually got worse. See Neal EG, Chaffe H, Schwartz RH, Lawson MS, Edwards N, Fitzsimmons G, et al. The ketogenic diet for the treatment of childhood epilepsy: a randomised controlled trial. Lancet Neurol. 2008 Jun;7(6):500–6. PMID 18456557. doi: 10.1016/S1474-4422(08)70092-9. Available online at http://www.ncbi.nlm.nih.gov/pubmed/18456557.
Abridged from the Wikipedia article entitled “Ketogenic Diet,” available online at http://en.wikipedia.org/wiki/Ketogenic_diet.