Thursday, April 19, 2018

The Diabetes Industry is Ripe for Disruption

And it has been for some time.

If we plot carbohydrate consumption from low to high on the y-axis, and pharmaceutical—one or more of the many insulins, metformin, etc.–consumption from low to high on the x-axis, we can see all possible combinations of expected patient results on the following matrix:

When exo- or endogenous insulin—and/or insulin sensitivity—is low, and carbohydrate consumption is high, the patient may present with the classical triad of type one diabetes symptoms: polyuria, polydipsia, and  polyphagia: respectively, frequent urination, increased thirst and consequent increased fluid intake, and increased appetite. Other manifestations may include weight loss despite normal or increased eating, irreducible fatigue, and changes in the shape of the lenses of the eyes or sorbitol accumulation, resulting in vision changes.

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 an altered state 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 exo- or endogenous 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 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 weight, blood pressure, not to mention time and resources spent in the process may prove unsustainable. There must be a better way.

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 carbohydrate, 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 hypo-hyperglycemic 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 and pharmaceuticals consumed are as low as possible. At the far lower-left cell of the matrix, one doesn’t eat a great many non-structural carbohydrates, and, subsequently, does not need to, say, inject much insulin as a result. In this case, one can achieve a normal blood sugar concentration and enjoy the benefits of a normal life, with more energy than previously, stable or decreasing body weight, and less anxiety not having to think about whether one has ingested the correct amount of chemicals. And testing can be reduced to once a day, in the morning, to validate their successful treatment, i.e., whether their 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. See the New England Centenarian Study Website, the Georgia Centenarian Study Article, the Georgia Centenarian Study Youtube Video; and the Okinawa Centenarian Study Website. According to Dr. Ron Rosedale back in 1999:

“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.” See “Insulin and its Metabolic Effects,” by Dr. Ron Rosedale, presented at Designs for Health Institute's BoulderFest, August, 1999. Full online Article.

Although the use of exogenous 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—grotesquely over-prescribed with the knowledge that carbohydrates are non-essential and that, in the case of T2 diabetics, the problem is initially more of insulin resistance than of insulin production.

For more about the non-essentiality of carbohydrates, see Dr. Eric Westman’s article entitled, “Is dietary carbohydrate essential for human nutrition?” here. For more about insulin resistance, see this full online article.

A remarkable picture develops when you take those three yellow-highlighted cells from the above figure and place them on two different axes, one a continuum of complexity from low to high, and the other, a continuum of knowledge, skills, and tools, again, from low to high.

The y-axis, complexity, relates to the treatment—medication and nutrition—and lifestyle a person implements or recommends. Regarding the x-axis, knowledge, skills, and tools, it could be looked at from two perspectives; one, from a diabetic’s perspective, where the focus is on their knowledge and skills 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 and skills, 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 and 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. Patient knowledge 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. Influencers in the medical advice providing supply chain may include:

·       Acquaintances, co-workers, family, friends
·       American Diabetes Association (ADA) and other associations/foundations. See especially the ADA’s 2018 Standards of Medical Care in Diabetes.
·       Educators
·       Endocrinologists. See the Consensus Statement by the American Association of Clinical Endocrinologists and American College of Endocrinology on the Comprehensive Type 2 Diabetes Management Algorithm - 2018 Executive Summary, especially the Disclosures on page 103.
·       Food manufacturers and marketers
·       Medical doctors
·       Medical schools
·       Nurses
·       Nutritionists. Dietetic Associations referred to the public by the USDA include the Academy of Nutrition and Dietetics (FKA the American Dietetic Association), the British Dietetic Association, Dietitians of Canada, Dietitians Association of Australia, the International Confederation of Dietetic Associations, et al. For links see Dietetic Associations.
·       Pharmaceutical companies. See for example Dr. Aseem Malhotra’s appeal to the European Parliament, Brussels, April, 2018. Youtube Video.
·       Popular internet sites, print and TV media
·       Reference media such as the Physician’s Desk Reference, which was formerly a commercially published compilation of manufacturers' prescribing information on prescription drugs, updated annually. While originally designed to provide physicians with the full legally mandated information relevant to writing prescriptions, widely available in libraries and bookstores, widely used by other medical specialists, and in significant part valuable to consumers, it was financially supported in part by pharmaceutical manufacturing corporations which created the drugs listed within its pages. Now it is published only online by ConnectiveRx, and the website is here.
·       Researchers. Most research findings are false for most research designs and for most fields. See Ioannidis JPA. Why Most Published Research Findings Are False. PLoS Medicine. 2005;2(8):e124. doi:10.1371/journal.pmed.0020124. Full online article.
·       United States Department of Agriculture. See USDA Dietary Guidelines.
·       World Health Organization. See their 2016 Global Report on Diabetes.

To the uninitiated, each influencer may seem well-intentioned and sincere; but, by default, advocates of each group act in their own perceived best interests, 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. Or, they may have conflicting interests, having received benefits from other constituencies. For example, surveys conducted in 2004 and again in 2009 showed that more than three-quarters of doctors had at least one type of financial relationship with a drug or medical device company. (See Campbell EG, Rao SR, DesRoches CM, et al. Physician Professionalism and Changes in Physician-Industry Relationships From 2004 to 2009. Arch Intern Med. 2010;170(20):1820–1826. doi:10.1001/archinternmed.2010.383. Full online article.)

And many of the above influencers 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 and pharmaceutical intensive. 

And the results? Perhaps an HbA1c at or below 7%, weight gain, 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 patient; but, for other stakeholders, it may bring and keep customers longer.

Although the science behind pharmaceuticals that may limit the amount of glycogen released from the liver or that bind to receptors allowing channel membranes to open so that glucose may cross is remarkable, it is based upon two assumptions: (1) that carbohydrates are an essential majority part of the diet, and/or (2) 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 and its optimal treatment 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—non-structural carbohydrates—and replacing those carbohydrates in the diet with real food sources of fat and protein, resulting in benefits such as healthy weight loss, 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 or other pharmaceuticals. It is simple. And it should be the first approach in diabetes treatment. See Feinman, Richard, et al. (2014). Dietary carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base. Nutrition. 31. 10.1016/j.nut.2014.06.011. Full online article.

When the blood sugar function is optimized this way, then, a new, refreshing meaning to the words of Frederick G. Banting, largely credited for the idea behind the work which led to the discovery of insulin, becomes evident:

“…with the relief of the symptoms of the disease…the pessimistic, melancholy diabetic becomes optimistic and cheerful.”

This last quote is from the conclusion of Frederick G. Banting, Nobel Lecture, September 15, 1925, The Nobel Prize in Physiology or Medicine 1923. Full online article. That prize for the discovery of insulin was actually divided between Frederick G. Banting and John J. R. Macleod. The choice of this combination of Laureates has been much debated ever since the prize was awarded. Thus, for instance, Banting shared his part of the prize amount with his younger coworker Charles Best. See the article August Krogh and the Nobel Prize to Banting and Macleod.

Tuesday, June 14, 2016

Credit is Due to Uffe Ravnskov, et al. (Updated and Abridged)

“I have lived to see a diffusion of knowledge, which has undermined superstition and error…”
  - Richard Price

[Author’s note: this article is dedicated to the memory of Margaret Heineman Cihocki, kind teacher, mentor, and friend to many, and is an updated and condensed version of an earlier posted article with the same name For background information, see also Cholesterol and the Structure of Scientific Revolutions.]

Although there is a steadily growing number of health providers adhering to and promulgating the benevolent cholesterol paradigm—cholesterol and its protein carriers benefit humanity—few recognize the paradigm’s main proponents.  Credit where credit is due: the foremost proponents of the benevolent cholesterol paradigm are Drs. Uffe Ravnskov, et al.

There have been other proponents of a benevolent cholesterol paradigm that engaged the forming malevolent tradition.  The first was Edward R. Pinckney, M.D., author of The Cholesterol Controversy (1973).  This book was followed up by the compendious Diet, Blood Cholesterol and Coronary Heart Disease, A Critical Review of the Literature (1991) in conjunction with Russell L. Smith, Ph.D.[1]  Other notable advocates include Michael Gurr,[2] George Mann,[3] Thomas Moore,[4] Raymond Reiser,[5] Ray Rosenman,[6] William Stehbens,[7] and Lars Werkö.[8]

John Yudkin, of Pure White and Deadly (1972) fame, was a proponent of the benevolent cholesterol paradigm.[9]  So too were Dr. Robert E. Olson, principal author of a report entitled Toward Healthful Diets by the Food and Nutrition Board of the National Research Council, individual members of that committee, and, the more fervent proponent, Philip Handler, President, National Academy of Sciences.[10]  These proponents, however, were not successful in attracting an enduring group of adherents.

According to the originator of term, Thomas Kuhn, a paradigm serves implicitly to define the legitimate problems and methods of a research field for succeeding generations of practitioners.[11]  Dr. Uffe Ravnskov is the foremost proponent of the benevolent cholesterol paradigm because of two essential characteristics in addition to defining the problems and methods.  His achievements—not only falsifying the lipid hypothesis but creating a new hypothesis that has been severely tested, remains un-falsified and makes better predictions—is sufficiently unprecedented to attract an enduring group of adherents away from competing modes of scientific activity.  Simultaneously, his hypotheses are sufficiently open-ended to leave all sorts of problems for the redefined group of practitioners to resolve.

We can now begin to think about Dr. Uffe Ravnskov’s contributions and the brilliant people that—while they work on their own projects—adhere to, criticize, discuss, refine, and promulgate them.

Drs. Ravnskov, et al., have most recently shown that in free-living populations without pre-existing disease, higher LDL-cholesterol predicts a lower risk of death in those over 60. See, "Lack of an Association or an Inverse Association Between Low-Density Lipoprotein Choleterol and Mortality in the Elderly: a Systematic Review," written by Drs Ravnskov, Diamond, Hama, Hamazaki, Hammarskjold, Hynes, Kendrick, Langsjoen, Malhotra, Mascitelli, McCully, Ogushi, Okuyama, Rosch, Schersten, Sultan, and Sundberg. Note that none of the authors have any competing interests to disclose. For a good summary of that article, please see Professor Grant Schofield's, "The New BMJ Review of High Cholesterol and Mortality in the Elderly."

You can watch and hear about the benefits of cholesterol in two interviews with co-authors Dr. Aseem Malhotra on Sky News here and Dr. Malcolm Kendrick on BBC Breakfast here.

Consider next reviewing, "Vulnerable Plaque Formation from Obstruction of Vasa Vasorum," by Drs. Uffe Ravnskov and Kilmer S. McCully (2009).  Learn here that lipoproteins referred to as good or bad—or even “lousy” by some popular doctors—by anti-rational proponents of the malevolent cholesterol paradigm more likely comprise the body’s secondary immune system. This non-specific immune system binds and inactivates microorganisms and their toxins by complex formation.  Importantly, the article also presents a testable mechanism for developing atherosclerosis and cardiovascular disease more satisfying than inanities such as cholesterol sticks to or penetrates the arteries.

Following up on a problem to solve from that article, Drs. Ravnskov and McCully published “How Macrophages are Converted to Foam Cells” three years later in 2012.  In their view, oxidized LDL is produced inside the macrophages as a side effect of their oxidation of microorganisms or their toxic products.

“Vulnerable Plaque Formation…” was a logical outgrowth of work dating back to 2003, when Dr. Ravnskov published a review of the many studies that have shown LDL to be protective against infections, and put forward the hypothesis that high cholesterol, rather than promoting atherosclerosis, protects against it.  See “High cholesterol may protect against infections and atherosclerosis.”

Supplementing this hypothesis, a leading adherent showed how neither cholesterol nor its carriers are the cause of familial hypercholesterolemia, a misnomer for LDL receptor deficiency.  See  You are a Very Black Swan Indeed,” by Dr. Malcolm Kendrick.

In “Cholesterol Lowering Trials in Coronary Heart Disease: Frequency of Citation and Outcome,” Dr. Ravnskov demonstrated that coronary mortality was not lowered by cholesterol lowering, but total mortality was increased.

For Dr. Ravnskov’s biography and a complete listing of his articles, see “My Life and My Work,” and “The Cholesterol Myths.”  For articles by many of the equally brilliant adherents of Dr. Ravnskov’s paradigm, see “Links,” on the THINCS website.  Dr. Ravnskov has also written three accessible books: The Cholesterol Myths (2000), Fat and Cholesterol are Good for You (2009), and Ignore the Awkward (2010).  You are encouraged to read them all. 

For Edmund Burke—the anti-rationalist author most noted for his 1790 book Reflections on the Revolution in France—resisting the temptation to construct a society from the ground up on the basis of untested rationality was the beginning of political wisdom and the essence of political prudence.  But after reading the works of Ravnskov, et al., perhaps even Burke would say of adherents of the lipid hypothesis—those traditionalists that continue to say artery-clogging cholesterol causes heart disease—that “Their science is presumptuous ignorance.”[12]  You yourself may come to that same conclusion.  Or you may conclude as I have, similar to how Ludwig Wittgenstein quipped about philosophy: “I have learned the jargon as well as anybody.  It is very clever and captivating.  In fact, it is dangerously captivating; for the simple truth about the matter is that it is much ado about nothing—just a lot of nonsense.”

For Further Reading

Burke, Edmund.  Reflections on the Revolution in France.  New Haven and London: Yale University Press, 2003, p. 68.   First published 1790.

Kuhn, Thomas S.  The Structure of Scientific Revolutions.  The University of Chicago Press, Chicago, IL, 2012.  First published 1962.

Popper, Karl.  Conjectures and Refutations.  New York: Routledge Classics, 2002.  First published 1963 by Routlede & Kegan Paul.


[1] For a particularly good historical overview of the developing tradition in the United States, see Smith, Russell L. and Pinckney, Edward R.  Diet, Blood Cholesterol and Coronary Heart Disease, A Critical Review of the Literature.  Sherman Oaks: Vector Enterprises, 1991, V. 2, Chapter 2. 
[2] See, for example, Dietary Lipids and Coronary Heart Disease: Old Evidence New Perspective,” Michael I. Gurr, Prog. Lipid Res. Vol. 31, No. 3, pp. 195-243, 1992.  Article.  For something more recent, see Gurr, Michael I.  Lipids in Nutrition and Health: A Reappraisal.  Isles of Scilly, UK: The Oily Press, 1999, 2009.  Book.
[3] See for example “Dr. George Mann Says Low Cholesterol Diets are Useless, but the ‘Heart Mafia’ Disagrees,” by Kent Demaret and Judith Weintraub, People Magazine, January, 1979.  Article.  See also Mann, George V.  Coronary Heart Disease: The Dietary Sense and Nonsense.  London: Janus, 1993.  He is most known for having said, “The diet-heart hypothesis has been repeatedly shown to be wrong, and yet, for complicated reasons of pride, profit and prejudice, the hypothesis continues to be exploited by scientists, fund-raising enterprises, food companies and even governmental agencies. The public is being deceived by the greatest health scam of the century.” There is also the shorter version of the comment: “Saturated fat and cholesterol in the diet are not the cause of coronary heart disease. That myth is the greatest ‘scientific’ deception of the century, and perhaps any century.”  See Diet-Heart: End of an Era,” George V. Mann, Sc.D., M.D., N Engl J Med 1977; 297;644-850, Sept. 22, 1977.  Article.
[4] Although flawed, see Moore, Thomas J.  Heart Failure.  New York: Touchstone Books, 1989.  A chapter from the book was published in the Atlantic Monthly a few months before the book was published.  See “The Cholesterol Myth,” T.J. Moore, The Atlantic, Vol. 264, September, 1989, p. 37(25), ISSN: 0276-9077.  Article.
[5] Keys’s idea that a high intake of saturated fat raises cholesterol was questioned by Raymond Reiser  in 1973.  In a thorough review of 40 trials he pointed at several types of methodological and interpretational errors.  See Reiser, R.  “Saturated fat in the diet and serum cholesterol concentration: a critical examination of the literature.”  Am J Clin Nutr 1973: 26; 524-555.  Article.
[6] In an extensive review, Rosenman found that serum cholesterol is not strongly related to or primarily regulated by diet. He also cited widespread discordant beliefs about a causal role of diet in coronary artery disease.  See Rosenman, RH, “The Independent Roles of Diet and Serum Lipids in the 20th-CenturyRise and Decline of Coronary Heart Disease Mortality.”  Integr Physiol Behav Sci.  1993 Jan-Mar;28(1):84-98.  Abstract: Risk factors are causally related to coronary heart disease (CHD), but in widely varying historic, geographic, socioeconomic, and individual relationships.  Serum cholesterol is only one of many risk factors that, even when considered together in prospective studies, account for well under half of the CHD incidence. It is neither primarily regulated by the diet nor significantly related to it. Many findings discordant with widespread beliefs about a causal role of the diet in CHD are reviewed. It may be concluded that dietary fats are largely not responsible for relationships of serum cholesterol to CHD, or for its 20th-century rise and decline.  Article.
[7] See for example, “Science, Atherosclerosis and the “Age of Unreason”: A Review,” Stehbens, WE, Integr Physiol Behav Sci. 1993, Oct-Dec;28(4):388-95.  Article.
[8] See for example “Risk factors and coronary heart disease—facts or fancy?”  Werkö, Lars.  American Heart Journal.  Volume 91, Issue 1, Pages 87-98, January 1976.  Article.
[9] See, for example, Dr. Yudkin’s letter published in the British Medical Journal, October 3, 1964, p. 874.  Letter.
[10] For an interesting summary of the issues between Toward Healthful Diets and Diet, Nutrition, and Cancer, see the National Academy of Sciences’ Reports on Diet and Health—Are They Credible and Consistent?   Report by the U.S. General Accounting Office, August 1, 1984.  FullText.
[11] Kuhn, Thomas S.  The Structure of Scientific Revolutions.  The University of Chicago Press, Chicago, IL, 2012, p. 10-11.
[12] Burke, Edmund.  Reflections on the Revolution in France.  New Haven and London: Yale University Press, 2003, p. 68.   Originally published 1790.

Wednesday, June 17, 2015

Essential Diabetes Leadership


“Why in this stultifying and needless conflict between reason and tradition, it should be so easy to believe the incredible and so difficult to accept the obvious, is a riddle which is not flattering to contemplate.”[1]
F. J.  COLE, 1944

In ESSENTIAL DIABETES LEADERSHIP (2011), the hypothesis and proof that a ketogenic—high fat, adequate protein, low-carbohydrate—diet for diabetics, as part of an overall BG optimization model, supports a long, happy, healthy life in general, I included specifics from six of the twelve total systems: the (1) circulatory, (2) digestive, (3) endocrine, (4) excretory, (5) nervous, (6a) skeletal (teeth), and (7a) integumentary (gingiva: the gums).[2]

Regarding the (5) nervous system, which includes the sense organs and vestibular system, the last endnote of the “Epilogue” provided supporting evidence for the use of a ketogenic diet in the successful treatment of epilepsy.  Since there’s more to the nervous system, and to the diseases of, than forty different kinds of epilepsy, this blog suggests a couple other information sources.

Reminiscent of Dr. Weston Price, we find a brave treatise written by another dentist.  First published in 2001, then condensed in 2005, ALZHEIMER’S SOLVED, by Dr. Henry Lorin, proffers a thoroughly researched theorem—his book references over 2,500 scientific articles—that better explains the data and observations than any other work on the subject: “It is indeed possible for a person to have blood cholesterol levels that are too low.”[3]  Reading through his manuscript, that conclusion is inescapable.

From aging to xanthomas, Dr. Lorin’s theorem in ALZHEIMER’S SOLVED unifies seemingly diverse conditions such as AIDS, Alzheimer’s disease, brain surgery, Cushing’s disease, dementia, depression, Down syndrome, epilepsy, head injury, HIV, osteoporosis, Parkinson’s disease, vasculitis, and others, with his remarkably simple deduction that amyloid—beta amyloid plaques—“is the body’s temporary substitute for cholesterol molecules.  Amyloid is to be used as a short-term ‘bandage’ for cell membranes until more cholesterol is provided.”[4]  Should that cholesterol, for whatever reason, be withheld, nearly all the aforementioned diseases inevitably become terminal.  Dr. Lorin summarizes his diet—beyond important micronutrients such as vitamin D—quite eloquently in one sentence: “The easiest and most natural way to do this [preventing and treating most of the described diseases] is by eating foods that contain cholesterol, while minimizing the consumption of foods that are primarily carbohydrates (starches).”[5]

You may also be interested in reading THE BRAIN TRUST PROGRAM (2007), by Larry McCleary, MD, which accessibly describes the important component parts of the nervous system, then delivers a striking contrast to all the also-ran diet-brain books published on how to best support them through diet.  Although he doesn’t outright advocate a low-carbohydrate diet, his 7-day menu plan sure does resemble one.[6]  A person with diabetes would simply need to skimp further on the fruit and minimal multigrain bread and crackers mentioned.

Here I could discuss the (8) muscular system in detail, but so much data exists on low-carbohydrate diets and exercise physiology, overlapping some with the (9) respiratory system—and I reprinted with permission much of the material written by Professor Emeritus Robert S. Horn on the subject in my first book—that, although tempting, I shall not rehearse the subject here, other than to say that Stephen D. Phinney provides great additional insight.

In “Ketogenic Diets and Physical Performance,” which contains many good sources for further reading, Dr. Phinney states in the Abstract that “impaired physical performance is a common but not obligate result of a low carbohydrate diet.  Lessons from traditional Inuit culture indicate that time for adaptation, optimized sodium and potassium nutriture, and constraint of protein to 15–25 % of daily energy expenditure allow unimpaired endurance performance despite nutritional ketosis.”[7]

And he concludes:

“Both observational and prospectively designed studies support the conclusion that submaximal endurance performance can be sustained despite the virtual exclusion of carbohydrate from the human diet.  Clearly this result does not automatically follow the casual implementation of dietary carbohydrate restriction, however, as careful attention to time for keto-adaptation, mineral nutriture, and constraint of the daily protein dose is required.  Contradictory results in the scientific literature can be explained by the lack of attention to these lessons learned (and for the most part now forgotten) by the cultures that traditionally lived by hunting.  Therapeutic use of ketogenic diets should not require constraint of most forms of physical labor or recreational activity, with the one caveat that anaerobic (i.e., weight lifting or sprint) performance is limited by the low muscle glycogen levels induced by a ketogenic diet, and this would strongly discourage its use under most conditions of competitive athletics.”[8]

Based upon Dr. Phinney’s work, my blood glucose model, of which I proudly presented in the chapter entitled “The Way Things Ought To Be (Part I),” recommended frequent, light exercise.

If you were thinking that I would now go over each of remaining five human organ systems (five because I’m including the skeletal system proper, the bones, and the integumentary system proper, the skin, hair and nails), I have a shocker for you: the medical literature world is predominantly data- and theorem-light—more, ignorant—about how macronutrients, not just vitamins and minerals, but how macronutrients—fats, proteins, and carbohydrates—and, specifically, a low-carbohydrate, medium-protein, high-fat diet, affect all but one of the remaining systems.

True, we know how the use of sugar per se affects nearly every organ system; two accessible books on the subject that you may find interesting are LICK THE SUGAR HABIT (2001) and SUICIDE BY SUGAR (2009), both by Nancy Appleton, PhD.[9]  By the way, these books remind me of an experiment on dogs performed by an ex-physician about two hundred years ago.  Let me share this brief story.

“In 1816, in an attempt to understand the biological value of certain foodstuffs, Francois Magendie—a child of revolutionary Paris and a former physician—set out to observe the effects of a restricted diet.  He was particularly interested in what role nitrogen has to play in digestion.  The answer he got back, after ten years of painstaking work was none at all: ‘As so often in research,’ Magendie wrote, with what bitterness we may imagine, ‘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 confidently 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?”[10]

Turns out that it was vitamin A, isolated a hundred years later by two American teams, that was needed to keep the eyes from liquefying, though not enough to save the life.  The addition of whole milk to the diet saved the life; no, not of the dog, but of children, soldiers, waifs and strays suffering from xerophthalmia in the years preceding the isolation of vitamin A.  Of course, even then, experiments—on dogs, children, waifs, or strays—were not performed in the reverse to prove that you don’t need the sugar.  Carbohydrates have been considered essential since the dawn of agriculture.

“That transition from hunting and gathering to agriculture is generally considered a decisive step in our progress, when we at last acquired the stable food supply and leisure time prerequisite to the great accomplishments of modern civilization.  In fact, careful examination of that transition suggests another conclusion: for most people the transition brought infectious diseases, malnutrition, and a shorter life span.  For human society in general it worsened the relative lot of women and introduced class-based inequality.  More than any other milestone along the path from chimpanzeehood to humanity, agriculture inextricably combines causes of our rise and our fall.”[11]

Back to organ systems.  As I was saying, we know how sugar by itself negatively affects many organs and organ systems, but little is known about how any specific diet permutation affects the (7b) integumentary (skin, hair and nails), (9) respiratory, (10) lymphatic, (11) immune,[12] or (12) reproductive system.  Now, it surely can be inferred that, if we forgo the bolus insulin and carbohydrates, and eat just fat and protein, with type 1s only adding basal insulin, and we live a long, happy, healthy life, then all other organ systems must be doing just fine.  But such circumstantial evidence doesn’t necessarily prove that they’re healthy in the court of public opinion, let alone in science.  Unlike in evolution versus creationism, where, thankfully, evolution has been upholded,[13] no action has been brought against any carbohydrate-espousing proponent, by any low-carbohydrate proponent, in any jurisdiction.  Thus, we have no precedent, no ruling, no adjudication, based upon any evidence, for or against any diet, from any court of law.  Not that the vegans haven’t tried.[14]

We live today in an environment similar to that initially championed by John Washington Butler,[15] except, instead of its realization deriving from a law forbidding public school teachers from denying the Biblical account of man’s origin, we now navigate through an environment emotionally charged by a low-fat dogma; those that pray to it and live by its code do so influenced by the trinity of politics—playing into the public perceptions that they themselves or their forebearers created—faith and commerce, not science, serving it best by ensuring its promulgation into clinical practice guidelines, research, education, news and fixed media.  This dogma, however, unlike the Butler Act, is enforced not just in public schools, but across nearly all demographics.  Maybe by the time the 18th edition of this book is published, a precedent will be set upholding low-carbohydrate diets in a court of law, the above organ systems will be covered in more detail, and I will be able to provide a robust summary.

There is some information about how diet affects the (12) reproductive system, but most sources highlight the role of calories, not how any specific combination of macronutrients affects the reproductive system.  At first glance, learning that a low-carbohydrate, ketogenic diet led to significant improvement in weight, percent free testosterone, and fasting insulin in women with obesity and Polycystic Ovary Syndrome (PCOS) over a 24 week period, it sounds like we can put one in the win column for a low-carbohydrate diet best supporting the reproductive system.  Alas, PCOS is considered an endocrine disorder.[16]

Which really leaves only one organ system that I didn’t cover.  Well, half of one.

The (6b) Skeletal (bone) system, beyond studies about the correlation between osteoporosis and calcium, is supported by a low-carbohydrate diet in “The Effect of a Low-Carbohydrate Diet on Bone Turnover,” by J. D. Carter, F. B. Vasey, and J. Valeriano.  Here, the authors set out to determine whether or not a low-carbohydrate diet would lead to increased bone turnover.  Thirty patients (15 study subjects and 15 controls) were recruited for this 3-month study.  The 15 patients on the diet were instructed to consume less than 20 g of carbohydrates per day for the 1st month and then less than 40 g per day for months 2 and 3.  Control subjects had no restrictions on their diet.  And the conclusion?  “Although the patients on the low-carbohydrate diet did lose significantly more weight than the controls did, the diet did not increase bone turnover markers compared with controls at any time point. Further, there was no significant change in the bone turnover ratio compared with controls.”[17]

In what could be classified as the only compendium devoted to the relationship between the skeletal system and diet, NUTRITION AND BONE HEALTH (2004) doesn’t advocate any particular diet, although it does include an article—the book is a collection of independently written articles—describing both the plate model of the UK and the pyramid model of the US.[18]  The authors used these models as an assumption of diet; that, and a reference to fat leading to heart disease, without quoting any specific, credible evidence in defense of either.  As you read more and more health, diet, medical, reference books and articles, you’ll find support of those two concepts without evidence common faults.[19]  Mark Twain understated it best when he said “Be careful about reading health books.  You could die of a misprint.” 

However, if I could choose one quote from the book to best embody its entirety, it is that “bone health is not a mononutrient issue.”[20]  Some specific examples include:

·      “An inadequate intake of calcium and an inadequate level of vitamin D, alone and in combination, influence calcium-regulating hormone levels.  Deficiency of either nutrient results in reduced calcium absorption and a lower circulating ionized concentration.  The latter stimulates the secretion of parathyroid hormone (PTH), a potent bone-resorbing agent.  Over time, a small increase in the circulating level of PTH leads to measurable and significant bone loss and increased risk of fracture.”[21]

·     “Vitamin A deficiency is characterized by xerophthalmia, night blindness, cessation of growth, and increased susceptibility to infections.  On the other side, very vitamin A intake might affect, among others, bone and bone metabolism, as it has long been known.  High vitamin A intake seems to accelerate bone loss.”[22]

·  “Fluorine is an indispensable trace element and plays a role in normal development and maintenance of the skeleton and teeth.  As is true for other essential trace elements, deficiency or excess has clinical consequences: intakes below the recommended daily dose result in growth and development retardation, whereas long-term high intake leads to hyperostosis or even severe skeletal sclerosis.”[23]

Low-fat endorsing as it may be perceived, one article clearly supports the use of fat in promoting bone health: “Dairy products are complex, containing many essential nutrients, and thus their effects on bone health are likely more that can be accounted for by any single constituent and the totality of their effects may be more than the sum of parts.”[24]

But more interesting is the book’s discussion on fruits and vegetables:

·     “The approach of using food groups to examine the relationship between diet and disease is an appropriate and logical approach to examining the relationship between diet and osteoporosis.  There is somewhat remarkable agreement among countries as to the proportions with which we should be eating food groups.  The data suggest that milk and milk products (as providers of more than 50% of total dietary calcium) and fruit and vegetables are beneficial to bone health across the age ranges, although clearly more work on fracture reduction is required.”[25]

·  “Only two large population-based studies have examined the specific impact of dietary “quality”/food groups directly on indices of bone health, namely, the Aberdeen Prospective Osteoporosis Screening Study (APOSS) and the Framingham Offspring Study.  Cluster analysis on 904 women (mean age 54 yr.), pre-, peri-, and postmenopausal, showed that a number of food groups, including fried foods, cakes, processed meats, and puddings, were associated with worsening hip bone loss…”[26]

·   “These data support the findings of both the original APOSS baseline study and the older Framingham cohort and indicate that a high fruit and vegetable intake is protective to the skeleton, whereas high candy consumption is associated with lower bone mass, regardless of gender.  These data also suggest that a high intake of fatty, sugary foods is detrimental to bone health around the time of menopause.”[27]

This last quote conflicts with one of the most interesting cohort studies I’ve seen on the subject.  In “Food Choices and Coronary Heart Disease: A Population Based Cohort Study of Rural Swedish Men with 12 Years of Follow-up,” by Sara Holmberg, Anders Thelin, and Eva-Lena, the authors concluded: “Daily intake of fruit and vegetables was associated with a lower risk of coronary heart disease when combined with a high dairy fat consumption, but not when combined with a low dairy fat consumption.  Choosing wholemeal bread or eating fish at least twice a week showed no association with the outcome.”[28]

As with other nutritional controversies, we find the unifying answer to whether or not it’s fruits and vegetables per se or in combination with other foods that reduces heart or bone disease risk from Gary Taubes, and here he delivers the last words: “As a matter of logic, though, it doesn’t necessarily imply that the lack of vitamins are caused by the lack of fresh fruits and vegetables…It’s possible that eating easily digestible carbohydrates and sugars increases our need for vitamins that we would otherwise derive from animal products in sufficient quantities.”[29]  There is an increased need for these vitamins when more carbohydrate in the diet is consumed.”[30]

[1] In its original context, this quote refers to the 17th century comparative anatomist Tyson, who “Nevertheless after carefully reviewing the evidence which demonstrated conspiculously that the porpoise must be a mammal, Tyson nowhere has the courage to declare that it is not a fish, for once attaching more importance to habitat than to structure.  He says he should like to think it was a mammal, but further than that he did not go.”  See Cole, F.J.  A History of Comparative Anatomy: From Aristotle to the Eighteenth Century.  London: Macmillan & Co. Ltd., 1944, p. 202.

[2] There are three main approaches to studying anatomy: systemic, regional, and clinical.  Systemic anatomy is the study of the body as a series of organ systems. Although systemic anatomy textbooks typically cover all the human organ systems, they may group them differently, into from six to many more organ systems.  This grouping difference is based on writers’ specialty, preference and style, and editors’ formatting concerns.  Complicating the issue, some organ systems share significant functional overlap.  For instance, the nervous and endocrine system both operate via a shared organ, the hypothalamus; thus the two systems are sometimes combined and studied as the neuroendocrine system.  And the vestibular system, in fact all sense organs, are often covered in sections on the nervous system.  The musculoskeletal system combines two as one; textbooks frequently include the immune with the lymphatic system.

The publication of Andreas Vesalius’s De Humani Corporis Fabrica in 1543 ushered a new era in the history of medicine and marked the beginning of modern anatomy.  This first anatomy book of 659 pages detailed six human systems: (1) skeletal, (2) muscles and ligaments, (3) circulatory, (4) cerebral and peripheral nerves, (5) abdominal and thoracic organs, and (6) brain and organs of special senses.  See Persaud, T.V.N.  A History of Anatomy: The Post-Vesalian Era.  Springfield, IL: Charles C. Thomas Publisher, Ltd., 1997.

In the classic work Anatomy of the Human Body (Philadelphia: Lea & Febiger, 1918), Henry Gray (1827-1861, smallpox) posthumously grouped the various systems of the human body into the following six headings: “(1) Osteology—the bony system or skeleton, (2) Syndesmology—the articulations or joints, (3) Myology—the muscles.  With the description of the muscles it is convenient to include that of the fasciæ which are so intimately connected with them, (4) Angiology—the vascular system, comprising the heart, blood vessels, lymphatic vessels, and lymph glands, (5) Neurology—the nervous system.  The organs of sense may be included in this system, and (6) Splanchnology—the visceral system.  Topographically the viscera form two groups, viz., the thoracic viscera and the abdomino-pelvic viscera.  The heart, a thoracic viscus, is best considered with the vascular system.  The rest of the viscera may be grouped according to their functions: (a) the respiratory apparatus; (b) the digestive apparatus; and (c) the urogenital apparatus.  Strictly speaking, the third subgroup should include only such components of the urogenital apparatus as are included within the abdomino-pelvic cavity, but it is convenient to study under this heading certain parts which lie in relation to the surface of the body, e.g., the testes and the external organs of generation.”  The work, thoroughly revised and re-edited by Warren H. Lewis (New York:, 2000) is available online at

“The shortcomings of existing anatomical textbooks probably impressed themselves upon Henry Gray when he was still a student at St. George’s Hospital Medical School, near London’s Hyde Park Corner, in the mid 1840’s.  He began thinking about creating a new anatomy textbook a decade later, while war was being fought in the Crimea.  New legislation was being planned which would establish the General Medical Council (1858) to regulate professional education and standards.

Gray shared the idea for the new book with a gifted artistic colleague on the teaching staff at St. George’s, Dr. Henry Vandyke Carter, in November, 1855.  Neither was interested in producing a pretty book, or an expensive one.  Their purpose was to supply an affordable, accurate teaching aid for students like their own, who might soon be required to operate on soldiers injured at Sebastopol or on some other battlefield.  The book they planned together was a practical one, designed to encourage youngsters to study anatomy, help them pass exams, and assist them as budding surgeons.

The book Gray and Carter created, Anatomy: Descriptive and Surgical, published by JW Parker & Son, appeared in August, 1858, to immediate acclaim.”  (Condensed from Stranding, 2005, p. xvii).

The thirty-ninth edition of Gray’s Anatomy: The Anatomical Basis of Clinical Practice (Edited by Susan Stranding, et al., New York: Elsevier Churchill Livingstone, 2005), an enormous reference book consisting of 1,627 pages, “…is radically different from earlier editions because the body is described in regions rather than in systems.  In the real world, the editorial team for the 39th edition decided that a book which would be of the greatest benefit to practicing clinicians should mirror their daily practice and describe anatomy in the way in which they use it, i.e., regionally.”  However, it too describes six systems: the (1) nervous, (2) blood, lymphoid tissues and haemopoiesis (red and white blood cells), (3) musculoskeletal, (4) smooth muscle and the cardiovascular and lymphatic, (5) skin and its appendages, and (6) endocrine.  Basic structure and function of cells, integrating cells into tissues, embryogenesis, prenatal and neonatal growth are also covered.  Following the systemic overview, this compendium then describes seven sections: (1) neuroanatomy, (2) head and neck, (3) back and macroscopic anatomy of the spinal cord, (4) pectoral girdle and upper limb, (5) thorax, (6) abdomen and pelvis, and (7) pelvic girdle and lower limb.

A recent textbook, Principles of Anatomy and Physiology, by Professors Gerard J. Tortora and Bryan Derrickson (New Jersey: John Wiley & Sons, Inc., 12th edition, 2009) describes eleven systems of the human body: the (1) integumentary, (2) skeletal, (3) muscular, (4) nervous, (5) endocrine, (6) cardiovascular, (7) digestive, (8) urinary, (9) lymphatic and immunity, (10) respiratory, and (11) reproductive system.  In what seems like the authors proudly going the extra mile, this textbook advocates a high-carbohydrate, low-fat diet in support of optimum health: “…many experts recommend the following distribution of calories: 50-60% from carbohydrates, with less than 15% from simple sugars; less than 30% from fats (triglycerides are the main type of dietary fat), with no more than 10% as saturated fats; and about 12-15% from proteins.” (See page 1006).

[3] See Lorin, Henry.  Alzheimer’s Solved (Condensed Edition).  South Carolina: BookSurge, LLC, 2005, p. 5.

[4] Ibid, p. 94.

[5] Ibid, p. 225.

[6] See McCleary, Larry.  The Brain Trust Program.  New York: Penguin Group (USA) Inc., 2007, pages 97-93.

[7] See “Ketogenic Diets and Physical Performance,” by Stephen D Phinney.  Nutrition & Metabolism 2004, 1:2.  doi: 10.1186/1743-7075-1-2.  Available online at  Retrieved on 12/10/09.

[8] Ibid.

[9] Dr. Appleton lists “146 Reasons Why Sugar Is Ruining Your Health,” on her website at  Retrieved on 12/10/09.

[10] See Ings, Simon.  A Natural History of Seeing: The Art & Science of Vision.  New York: W.W. Norton & Company, 2008, p. 65.

[11] See Diamond, Jared.  The Third Chimpanzee: The Evolution and Future of the Human Animal.  New York: Harper Perennial, 1992, p. 139

[12] “Whether diet may influence autoimmunity has been the subject of many unsolved debates.  Interestingly, growing evidence indicates a large overlap between the mechanisms controlling tolerance to dietary antigens and autoimmunity.  See “Autoimmunity and Diet,” by Cerf-Bensussan N.  Nestle Nutr Workshop Ser Pediatr Program. 2009;64:91-9; discussion 99-104, 251-7. Available online at  Retrieved on 12/11/09.

The use of omega-3 polyunsaturated fat—fish oil—has been known in small doses to aid the immune system.  See “Dietary Fatty Acids and the Immune System,” by Calder PC.  Lipids 1999; 34:S137-S140.  Available online at  Retrieved on 12/13/09.

[13] As of 2009, proponents of evolution are 18-0 in US court cases.  Although State v. Scopes (1925), the first and most famous court case, resulted in a loss for Scopes, who was then fined $100, the verdict was eventually set aside due to a technicality on appeal to the Supreme Court of Tennessee.  The most recent case, Tammy Kitzmiller, et al. v. Dover Area School District, et al. (2005) was the first direct challenge brought in the United States federal courts against a public school district that required the presentation of intelligent design as an alternative to evolution as an “explanation of the origin of life.”  The plaintiffs successfully argued that intelligent design is a form of creationism, and that the school board policy thus violated the Establishment Clause of the First Amendment to the United States Constitution.  The Decision of the Court in the matter of Kitzmiller, et al. v. Dover Area School District, et al., is available online at  Retrieved on 12/10/09.  For good background information and further references, see  Retrieved on 12/10/09.

[14] In 2006, Wilson Elser attorneys won a significant victory in US District Court, Southern District of New York, by securing the dismissal of a case charging the Atkins book and food products were defective and dangerous under product liability laws.  The case involved a Florida man, and the lawsuit was commensed on the plaintiff’s behalf by the Physicians Committee for Responsible Medicine, which publically advocates a vegan (no meat, no dairy, no fish) lifestyle and has long been an opponent of the Atkins diet, attacking it as unhealthy.  Southern District Judge Denny Chin said the suit must be dismissed because the Atkins book and food products are not defective or dangerous under product liability law.  See the archives of the Wilson Elser Moskowitz Edelman & Dicker LLP law firm online at and  Both retrieved on 12/14/09.

[15] John Washington Butler (1875 – 1952) was an American farmer and a member of the Tennessee House of Representatives.  He is most noted for introducing the Butler Act, which prohibited teaching of evolution in public, i.e., state, schools, and which was challenged in the Scopes Trial.  The Butler Act was a 1925 Tennessee law forbidding public school teachers from denying the Biblical account of man’s origin.  It was enacted as Tennessee Code Annotated Title 49 (Education) Section 1922.  The law also prevented the teaching of the evolution of man from lower orders of animals in place of the Biblical account.  However, the law did not prohibit the teaching of evolutionary theory for other species of plants or animals.  The Butler Act was Introduced in the Tennessee House of Representatives as House Bill No. 185 by John Washington Butler on January 21, 1925; it passed the House on January 28, 1925 (Yeas: 71; Nays: 5); it passed the Senate on March 13, 1925 (Yeas: 24; Nays: 6); signed into law by Governor Peay on March 21, 1925; repealed on September 1, 1967 by Chapter No. 237, House Bill No. 48.  See the Wikipedia article titled “Butler Act,” available online at  Retrieved on 12/15/09.

[16] See “The Effects of a Low-Carbohydrate, Ketogenic Diet on the Polycystic Ovary Syndrome: A Pilot Study,” by John C Mavropoulos, William S Yancy, Juanita Hepburn, and Eric C Westman.  Nutrition & Metabolism 2005, 2:35.  doi: 10.1186/1743-7075-2-35.  Available online at  Retrieved on 12/10/09.

[17] See “The Effect of a Low-Carbohydrate Diet on Bone Turnover,” by J. D. Carter, F. B. Vasey, and J. Valeriano.  Osteoporos Int (2006) 17: 13981403.  doi: 10.1007/s00198-006-0134-x.  Available online at  Retrieved on 12/10/09.

[18] See “Food Groups and Bone Health,” by Susan A. New. In: Nutrition and Bone Health.  Edited by M.F. Holick and B. Dawson-Hughes.  New Jersey: Humana Press Inc., 2004.

[19] For a summary of the issues involved, see “Toward A Policy Agenda On Medical Research Funding: Results Of A Symposium,” by Robert I. Field, Barbara J. Plager, Rebecca A. Baranowski, Mary Anne Healy and Margaret L. Longacre.  Health Affairs, 22, no. 3 (2003): 224-230.  doi: 10.1377/hlthaff.22.3.224.  Available online at  Retrieved on 12/13/09.

[20] See “Sodium, Potassium, Phosphorous, and Magnesium,” by Robert P. Heany.  In: Nutrition and Bone Health.  Edited by M.F. Holick and B. Dawson-Hughes.  New Jersey: Humana Press Inc., 2004, p. 327.

[21] See “Calcium and Vitamin D for Bone Health in Adults,” by Bess Dawson-Hughes.  In: Nutrition and Bone Health.  Edited by M.F. Holick and B. Dawson-Hughes.  New Jersey: Humana Press Inc., 2004, p. 197.

[22] See “Vitamin A and Bone Health,” by Peter Burckhardt.  In: Nutrition and Bone Health.  Edited by M.F. Holick and B. Dawson-Hughes.  New Jersey: Humana Press Inc., 2004.

[23] See “Fluoride and Bone Health,” by Johann D. Ringe.  In: Nutrition and Bone Health.  Edited by M.F. Holick and B. Dawson-Hughes.  New Jersey: Humana Press Inc., 2004, p.345.

[24] See “Food Groups and Bone Health,” by Susan A. New. In: Nutrition and Bone Health.  Edited by M.F. Holick and B. Dawson-Hughes.  New Jersey: Humana Press Inc., 2004, p. 237.

[25] Ibid, p. 245.

[26] Ibid, pages 236-237.

[27] Ibid, p. 237.  See also the following: Macdonald HM, New SA, Grubb DA, Goloden MHN, Reid DM.  “Impact of Food Groups on Perimenopausal Bone Loss.”  In: Burckhardt P, Dawson-Hughes B, Heaney RP, eds.  Nutritional Aspects of Osteoporosis 2000 (4th International Symposium on Nutritional Aspects of Osteoporosis, Switzerland, 1997).  Challenges of Modern Medicine.  Ares-Serono, Academic, New York, 2001, pp. 399-408; Tucker KL, Chen H, Hannan MT, et al.  “Bone Mineral Density and Dietary Patterns in Older Adults: the Framingham Osteoporosis Study.”  Am J Clin Nutr 2002; 76:245-252; New SA, Bolton-Smith C, Grubb DA, Reid DM.  “Nutritional Influences on Bone Mineral Density: a Cross-Sectional Study in Premenopausal Women.”  Am J Clin Nutr 1997; 65:1831-1839; New SA, Robins Sp, Campbell MK, et al.  “Dietary Influence on Bone Mass and Bone Metabolism: Further Evidence of a Positive Link Between Fruit and Vegetable Consumption and Bone Health?”  Am J Clin Nutr 2000; 71:142-151; & Tucker KL, Hannan MT, Chen H, Cupples A, Wilson PWF, Kiel DP.  “Potassium and Fruit & Vegetables are Associated with Greater Bone Mineral Density in Elderly Men and Women.”  Am J Clin Nutr 1999; 69:727-736.  Op cit. ”Food Groups and Bone Health,” by Susan A. New. In: Nutrition and Bone Health.  Edited by M.F. Holick and B. Dawson-Hughes.  New Jersey: Humana Press Inc., 2004, p. 237.

[28] The authors followed coronary heart disease morbidity and mortality in a cohort of rural men (N = 1,752) participating in a prospective observational study.  Dietary choices were assessed at baseline with a 15-item food questionnaire.  138 men were hospitalized or deceased owing to coronary heart disease during the 12 year follow-up.  See “Food Choices and Coronary Heart Disease: A Population Based Cohort Study of Rural Swedish Men with 12 Years of Follow-up,” by Sara Holmberg, Anders Thelin, and Eva-Lena Stiernström.  Int. J. Environ. Res. Public Health 2009, 6, 2626-2638; doi: 10.3390/ijerph6102626.  Available online at  Retrieved on 12/13/09.

[29] See Taubes, Gary.  Good Calories, Bad Calories.  First Anchor Books Edition.  New York: Anchor Books, 2008, p. 322.

[30] Ibid, p. 325.  As it relates specifically to vitamin C, Gary Taubes states: “The vitamin C molecule is similar in configuration to glucose and other sugars in the body.  It is shuttled from the bloodstream into the cells by the same insulin-dependent transport system used by glucose.  Glucose and vitamin C compete in this cellular-uptake process, like strangers trying to flag down the same taxicab simultaneously.  Because glucose is greatly favored in the contest, the uptake of vitamin C by cells is “globally inhibited” when blood sugar levels are elevated.  In effect, glucose regulates how much vitamin C is taken up by the cells…In other words, there is significant reason to believe that the key factor determining the level of vitamin C in our cells and tissues is not how much or little we happen to be consuming in our diet, but whether the starches and refined carbohydrates in our diet serve to flush vitamin C out of our system, while simultaneously inhibiting the use of what vitamin C we do have.”