“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: Bartleby.com, 2000) is available online at
http://www.bartleby.com/107/.
“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 http://www.nutritionandmetabolism.com/content/1/1/2. Retrieved on 12/10/09.
[8] Ibid.
[9] Dr. Appleton lists “146 Reasons Why
Sugar Is Ruining Your Health,” on her website at
http://www.nancyappleton.com/NA144reasons.html.
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
http://www.ncbi.nlm.nih.gov/pubmed/19710517?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=43. 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
http://www.springerlink.com/content/0195rt84xr947wvt/fulltext.pdf. 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
http://www.talkorigins.org/faqs/dover/kitzmiller_v_dover_decision.html. Retrieved on 12/10/09. For good background information and further
references, see http://en.wikipedia.org/wiki/Kitzmiller_v._Dover_Area_School_District. 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
http://www.wilsonelser.com/files/repository/Nextrounddietlit_FallWinter20042005.pdf
and http://www.wilsonelser.com/files/repository/LeghornAtkins_Dec2006.pdf. 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 http://en.wikipedia.org/wiki/Butler_Act. 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
http://www.nutritionandmetabolism.com/content/2/1/35. 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: 1398–1403. doi:
10.1007/s00198-006-0134-x. Available
online at http://www.springerlink.com/content/ej54l85238623l57/. 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 http://content.healthaffairs.org/cgi/content/full/22/3/224. 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 http://www.mdpi.com/1660-4601/6/10/2626/pdf. 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.”
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