Home > Nutrition in Prevention and Treatment of Disease
Nutrition and Health
Rima E. Laibow, MD
Medical Director
Natural Solutions Foundation
www.HealthFreedomUSA.org
healthfreedom@optonline.net
With special thanks to
Arline McDonald, PhD, Assistant Professor, Adjunct
For her permission to use portions of the
Preventive Medicine Lectures
Feinberg School of Medicine
Northwestern University, Chicago Illinois
Lauren Congo
Andrew Saul,
PhD
Nutrition is nothing less than the foundation of medicine, the cornerstone of all medical therapeutics.
A Forum on Nutrition and Health, JON 2(4),
1993
Prevention cannot start too early. Neither can it start too late.
Rima E. Laibow, MD 2005
Introduction
Nutrition brings together the goals and objectives of public health policy planners, medical/health systems and consumers. Global health policy experts know that health, itself, is a great bargain since people who are robustly well:
Robust individual and family
health objectives thus become goals that are shared between people and
society.
The core of robust health is
a level of nutritional abundance which supports and meets the global
right and the unique personal nutritional requirements of each individual
to optimal nutritional status and health. This is, however, a
challenging goal to achieve in a world in which the degradation of the
quality of the food supply is an increasingly severe problem in both
the developing and the developed world.
A 2003 WHO/FAO joint expert
consultation report, Diet, Nutrition and the Prevention of Chronic
Diseases 1 states that chronic diseases are preventable
and that the developing world is facing the medical consequences of
a nutritionally compromised food supply.. It goes on to identify
the consequences of under-nutrition on the development of what it refers
to as a ��non communicable epidemic,�� noting that increasingly sedentary
lifestyles, sharp decreases in the nutritional adequacy of food and
globally produced, commercially prepared food are in stark contradistinction
to local and national food supplies and trading economies supportive
of access to fresh and local food and sustainable economic and agricultural
practices.
The non-communicable epidemic
to which the WHO/FAO refers is in fact a global pandemic, one marked
by a growth in the prevalence of widespread chronic illness which is
impacting heavily the developing nations of the world. The pandemic
is, by contrast, already well established in the developed world and
is now worsening in both economic sectors of the world.
This WHO/FAO report identifies
obesity, type 2 diabetes mellitus, cardiovascular disease, hypertension
and stroke and some types of cancer as increasingly significant causes
of premature death and disability in both developing and developed countries.
These diseases place additional burdens on already overtaxed medical
systems.2
��Nutrition is coming
to the fore as a major, modifiable determinant of chronic disease with
scientific evidence increasingly supporting the view that alterations
in diet have strong effects, both positive and negative, on health throughout
life,�� adds the WHO/FAO report. ��Most importantly, dietary adjustments
may not only influence present health, but may determine whether or
not an individual will develop such diseases
��. In many developing countries,
food policies remain focused only on under nutrition and are not addressing
the problem of chronic disease��3 and overall long-term health
status, including immune capacity to resist infectious diseases, parasitic
infestations and other health assaults dependant upon an optimally and
healthy underlying nutritional matrix in each individual.
In fact, that nutritional matrix
is crucial. To illustrate this point, it is useful to examine
the importance, and dangers, of saturated fat. It has become a
matter of axiomatic truth that saturated fat is a component of an unhealthy
diet and that intake is correlated strongly with elevated LDL-cholesterol
and the resulting increase in cardiovascular disease. However,
the biochemical and nutritional picture does not support that well-held
belief without significant qualification.
In the context of the modern
nutrient-depleted diet which most urban and urbanizing people consume
saturated fat (SFA) is the strongest dietary predictor of LDL-cholesterol
levels in the presence of inadequate antioxidant levels.
In the presence of adequate nutritional components (i.e., unmodified
saturated fat from healthy plant and animal sources including free range,
naturally fed animal protein) SF not a health threat; rather, it is
of great benefit. Dietary recommendations and strategies must
take into account the nutritional context of the person being nourished,
supported and advised. Single findings of depletion or depression
of nutrients usually have concomitant significance far beyond the specific
nutrient profile or symptom associated with that finding and should
be addressed as part of a total nutritional picture which involves the
biochemical, dietary and physiological matrix of that individual.
Attention should be paid to that person��s relationship with food and
supplements as well as the production, preparation, preference and consumption
of food for optimal health.,
Weston Price4,
an American dentist, carried out decades of observation and examination
of people living on native and modern diets all over the world over
many decades. His conclusion was that when native foods were replaced
by the "displacing foods of modern commerce��5
—sugar, white flour, condensed milk, canned foods, chocolate, jams
and pastries—results were not only serious dental abnormalities, but
the development of the diseases of modern civilization��s diet, including
the epidemic development of diabetes, obesity and cardiovascular disease.6
This global exploration of
diet and health found that universally, healthy people eat saturated
fat in the context of optimal nutritional intake of vitamins and minerals
along with co-factors found both in meat and in fats. Optimal nutrition
is supported by a complex and complete relationship between intake of
fats and nutrients. It is important to note that dietary SF, recently
vilified in Western science, play many critical roles in human health
and biochemistry.
Saturated fatty acids:
Perhaps even more important,
animal fats are carriers for vital fat-soluble vitamins A and D which
are needed for a host of processes, from prevention of birth defects
to health of the immune system to proper development and maintenance
of bones and teeth. In fact, Price was convinced that these "fat-soluble
activators" were key to the beautiful facial development, freedom
from dental caries and absence of chronic degenerative diseases that
characterized the people he studied.
The diets of traditional groups
noted for longevity are rich in animal fats: The people of Hunza consume
large quantities of fermented goat milk products. Goat��s milk is higher
in fat, and contains more SF, than cow��s milk; the inhabitants of
Vilcabamba in Ecuador consume fatty pork and whole milk products; and
the long-lived inhabitants of Soviet Georgia also eat liberally of pork,
whole milk yoghurt and cheeses. In fact, a Soviet study
found that longevity was greatest
in rural communities where people ate the most fatty meat, compared
to town dwellers who ate more carbohydrates.21, 22
Dr Price found that healthy, disease free people eating their native diets which, without exception, contained, compared to the processed Western diet:
Price found in the diets of healthy isolated populations.
It is vitally important to
note that the so-called laboratory ��norms�� and population definitions
of ��nutritional adequacy�� and ��health�� upon which our understandings
of levels and limits of nutrients are built may not express normal
findings but, rather, normative ones for an unhealthy population.
Our conventional definitions of nutritional adequacy may be, in reality,
standards developed from populations eating a compromised diet (ours)
and prone to develop preventable diseases (and, on a statistical basis,
already in the process of developing them at the time that any lab value
might have been drawn or other data gathered). Thus, the concept
of limitation of nutrients to a supposed standard of normality drawn
from the most disease-prone population the world has ever known, a population
which habitually eats foods depleted in nutrients and whose genetic
potential for health is manifestly not supported by that diet is not
based in either science or sense, despite its familiarity.
This fully flawed premise leading
to nutrient and nutritional status ��norms�� based on ill people,
rather than healthy ones, is neither rational nor logical. And,
most important, it does not allow for decisions on either a personal,
regulatory or population basis, which support optimal health and the
fullest possible expression of the genetic capacity for health and productivity
inherent in optimal nutrition. These cautions pertain to levels
of both macro and micro nutrients. Dr. Price��s important data is supported
by other medical and physical anthropologists, physicians, cultural
and health workers. (See for example,25,26)
Like SF, carbohydrate intake must be evaluated in the context of its quality and the food environment of the patient. Dr. Price found that while seed foods (i.e., grains, legumes
and nuts) were consumed in
native diets among disease free peoples consuming native diets, they
were always prepared with great care in traditional societies by sprouting,
roasting, soaking, fermenting and sour leavening. 27, 28
These processes neutralize substances in whole grains and other seed
foods that block mineral absorption, inhibit protein digestion and irritate
the lining of the digestive tract. Such processes also increase nutrient
content and render seed foods more digestible. In these societies, in
fact, seed foods are not consumed unless they meet these preparation
criteria. In essence, the food value of our carbohydrates and the native
diet ones is as different as the saturated fat from the animals they
eat and that from our animal food sources.
Thus, it is important to view
dietary consumption an impact of carbohydrates and saturated fat on,
for example, blood lipids in the context of a pattern of dietary intake
because healthy native peoples routinely eat as much saturated fat as
they can get but do so in the context of a dietary environment in which
food is not degraded in nutrient density and carbohydrates are, in fact,
enhanced in nutritional value.
Since the dietary matrix of
modern populations is far inferior to that of the societies Dr. Price
studied, it is important to correct intake to those levels to help move
populations back toward healthy intakes and healthy outcomes.
Hunger and under-nutrition
are devastating realities for the vast majority of the world.
WHO estimates that 30% of the world��s population is malnourished29.
If standards of nourishment are modified to rest on the nourishment
of truly healthy people, such as those studied by Dr. Price in his extensive
research, the result would be to include most of the world��s population
in the undernourished category. Current definitions of homeostatic values
would no longer obtain since these are the homeostatic maladaptations
of challenged and compromised individuals who either have, or are in
the process of developing, preventable chronic degenerative diseases
of under-nutrition.
This expansion of the under-nourished,
is medically and scientifically-based although politically problematic,
would, in fact, be a positive advance since until malnutrition is recognized,
public health policy designed to correct it cannot be created and implemented.
Thus, the important distinction between normal (i.e., well nourished
with an end point of optimal nutrition) and normative (ill-nourished
with an end point of diagnosable dietary deficiency diseases which may
not yet clinically apparent) is a crucial one. Using the second
definition, what is, and what is not, a dietary deficiency disease is
determined by the state of nutritional medicine��s knowledge.
As diseases are added to the category of dietary deficit disorders,
more of the world is categorized as malnourished.
With this perspective in mind
it becomes clear that the current definitions of biological homeostasis
are both incorrect and misleading.
On the other hand, using optimal
nutrition as a public health goal leads to the development of an appreciation
for, and an awareness of, the importance of supporting, real physical
and physiological well-being based in the achievable goal of population-wide
optimal nourishment.
Although the problem is of
massive proportion, unlike many other complex issues it is manageable
and relatively inexpensive to solve. In 2001 preventable chronic
disease accounted for more than 60% of all global deaths (nearly 34
million deaths) and approximately 46% of the global disease burden.30
All estimates suggest a sharp increase in the problem since that time.
In fact, nutritional treatment
and prevention has a major contribution to make in the developing world
because of the unique susceptibility of poorly fed and culturally disrupted
populations. These populations are increasingly open to chronic
preventable diseases and highly susceptible to infectious diseases because
of long-term absence of optimal nutrition which predisposes them to
enhanced vulnerability.
Although HIV/AIDS, malaria,
tuberculosis and other infectious diseases are predominant cause of
death in Sub Saharan Africa (and will continue to be for some time),
of those deaths attributable to chronic disease, 79% occur in the developing
countries.31
WHO projections predict that chronic degenerative diseases, although misnamed ��diseases of affluence�� are, in fact, burdens of the developing world as well so that by 2020 preventable chronic diseases will account for nearly 75% of world deaths and that, of those, non-optimally nourished people of the developing world will account for
Diabetes will increase among
the non-optimally nourished in the developing world from its 1995 rate
of 84 million cases to 228 million in 2025.32
The WHO and FAO notes that
��countries that have actively intervened in the diet and nutritional
behavior of their populations �� have seen decreases in their risk
factors and falling rates of chronic disease.��33
Adoption of a national policy of optimal nutrition could have a tremendous
impact on the economic status of a country while enhancing the well-being
of her people in an unprecedented manner.
The US provides a sad but illustrative
example of a country spending enormous sums on everything except the
powerful combination of preventive nutrition and natural medicine focused
on optimal health. Her efforts are toward slamming the high tech
barn door after
the nutritional horse is well
away. The declining health of Americans testifies to the fact
that this is an alluring, but incorrect strategy toward wide spread
health facilitation. Estimates of cost reduction per year looking
only at hospital costs if preventive nutrition were instituted
in the US are illustrative of the vast amount of money spent on preventable
diseases which could be better spent on increasing health and well-being
by sparing the distress and loss of productivity and life which disease
brings. Savings which could be expected if adequate nutritional
prevention impacted the US population are listed below:
Disease
Reduction in Hospitalization Cost/year
Cardiovascular Disease $ 22 Billion US
Cancer $ 1 Billion US
Low Birth Weight $500 Billion US
Neural Tube Birth Defects $ 70 Billion US
Cataract $ 2 Billion US34
Although the percentage of the US Gross National Product which the United States spends on health care is enormous (15%, twice that of any other nation) 35
and decidedly unproductive in terms of the health of her people compared to other countries with a more natural approach to health care (unnecessary medical procedures and drugs cause nearly 800,000 preventable deaths and hundreds of thousands of severe drug reactions per year36
in the US)37
, the point here pertains to
any economy. Preventing disease through economical and remarkably
safe, non-toxic nutritional strategies offers substantial savings over
allopathic medicine and substantial increase in health and well being.
As drug side effects are eliminated and toxic loads on the body are
reduced to the virtual null point obtaining and maintaining optimal
health becomes easier.
In fact, the side effects and
toxicity of pharmaceuticals are without parallel in the nutrition world.
No class of medicaments in the pharmacological realm offers the safety
of nutrients. The difference is orders of magnitude apart in favor
of nutrients.
Nutritional status and immune
competence are the cornerstones upon which the house of health rests.
Assertions are frequently made that a good diet will supply all needed
nutrients. If this unproven assertion were true, those people eating
such a diet should not develop the preventable diseases of under-nutrition
and should not respond to the introduction of nutrients with resolution
of those diseases. In fact, clinical nutrition confirms what biochemistry
and immunology explain: optimal nutrition is difficult or impossible
to achieve through diet alone given
When the nutritional support available to the individual falls below the combined requirements of metabolic and environmental challenges, the result is either immediate or delayed sub-optimal health resulting in
Given the difference between the quality of food available to us and the food quality that we need to flourish, supplements make sense and add health promoting options to large number of people. It makes sense then, that dietary supplements of micronutrients are beneficial in the prevention and/or treatment of disease as part of the maintenance of optimal health and in helping to end world hunger.39
Dr. Arline McDonald of The
Feinberg School of Medicine of Northwestern University��s points out
��Nutrients are the raw materials that support physiologic and metabolic
functions needed for maintenance of normal cellular activity.
Malfunctioning of cellular activities due to an inadequate level of
support from available nutrients is initially expressed in biochemical
changes that will eventually develop into clinical symptoms characteristic
of the particular roles of the nutrients involved. Nutrient deficiencies
may develop as a result of inadequate intake, impaired absorption, increased
demand, or increased excretion. Excessive intakes of some nutrients
may promote deficiencies of others through impaired absorption, increased
demand, or increased excretion.
Chronic disease can be considered
the result of cellular change resulting from nutrient insufficiencies
since they are, in fact, an expression of cumulative cellular damage
due to environmental assaults for which the threshold of exposure at
which damage is incurred is defined by genetics. An imbalance
in dietary patterns is among the environmental factors that contribute
to the development of chronic diseases. Diet may either be
directly involved in the pathogenesis
of the disease or it may exacerbate pathological changes due to other
environmental factors.�� 40
High Dose Supplementation (HSD)
with available and inexpensive nutrients like folic acid, the B Complex,
(especially vitamins B3, 6 and 12) magnesium, essential fatty acids,
methionine, reduced glutathione, alpha ketoglutarate, dietary fiber,
and vitamin C offer the body the opportunity to repair nutritional and
toxic cellular damage and support the pathways of detoxification overwhelmed
by an imbalance of the required nutritional load (low) and the toxic
load (high). Nutrients have both nourishing (metabolic) and supportive/corrective
functions in the body. Physiological doses of nutrients are required
for metabolic support while HSD is required for correction of tissue,
organ, cellular and sub-cellular pathology and for detoxification support.
Metabolic functions include
supporting growth and maintenance, immune surveillance, maintaining
homeostasis and maintaining adequate reserves for efficient function.
Intake imbalances at the metabolic level result in the classic nutrient
deficiency symptoms and diseases.
Supportive/Corrective nutrient
functions are evoked when HSD offers the body a larger amount of the
nutrient(s) than commonly found in food. The resultant easily
available nutrients drive reaction toward repair and re-equilibration
within the physiological capacity of the organism, often resulting in
the cellular and sub-cellular restoration of balance and health.
Nutrients have a remarkably low toxicity profile so that very large
doses may be offered with great safety. Thus, HSD nutrition stimulates
biochemical and tissue restoration of health or maintains those processes
when such restoration is not possible.
Supplementation of metabolic levels of nutrients supports
HSD of nutrients supports
Offering nutrients at either the metabolic or HSD dosage levels should:
Inadequate nutrient intake
can be detected by clinical symptoms if the deficiencies are severe
or prolonged. Use of clinically-defined signs of deficiency to determine
whether nutrient intakes are adequate has significant limitations that
underscore the need for dietary assessment as a critical component of
clinical evaluation. One is that many nutrients, particularly
trace elements and some vitamins do not have well-defined signs or symptoms
that are targeted to a specific nutrient. Consequently, metabolic
abnormalities may develop that could cause cellular injury or compromise
defenses. In the early stages of iron deficiency, for example,
cellular energy production is compromised even though hemoglobin levels
may still be in a clinically normal range. Another example of
the same process is in folic acid deficiency. Megaloblastic cellular
changes due to folic acid
deficiency occur in the late
stages of progression of the deficiency long after metabolic abnormalities
were established.
Nutrient status is seriously
compromised in the face of environmental or dietary imbalances.
The resulting compensatory mechanisms stress the organs, the glands
and the nutrient base creating a cycle of deepening deficiency which
is ultimately expressed as signs or symptoms of chronic disease, often
after serious or irreversible tissue damage has occurred. ��If
these responses are sustained by prolonged imbalances in intakes of
these nutrients, then adaptive changes to counter these responses may
contribute to cellular injury and pathology. Compensatory responses
and/or adaptive changes are among the risk factors identified for chronic
diseases that can be managed by modifications in dietary habits.��41
The urgency of not ignoring early stages of nutrient deficiencies because of the absence of clearly defined clinical deficiency symptoms is illustrated by vitamin B12. Development of a Vitamin B12 deficiency that is unrelated to lack of intrinsic factor (pernicious anemia) is not uncommon among adults over age 65, but the nonspecific pattern of symptoms associated with a deficiency of this vitamin (e.g., depression, dementia, lassitude, memory loss, unsteady gait, numbness and tingling in the extremities, etc.) are difficult to separate from other possible causes in this age group. Consequently, abnormalities in vitamin B12-dependent cellular activities may go uncorrected resulting in irreversible damage to nervous tissue (e.g., demyelineation).42
The functional capacity of
a cell depends on its genetics, nourishment, exposure to environmental
toxins like smoking, personal hygiene, exercise, stress levels, environmental
pollutants like pesticides and UV exposure, and habitual nutrient intake.
The absorption of ingested
nutrients depends upon absorptive efficiency; the rate at which they
are consumed is determined by metabolic demand; excretory rate excreted
depends on excretion efficiency.
Unless given by a novel route
such as transdermal application or IV, nutrient absorptive efficiency
depends upon a healthy GI tract and kidneys (e.g., no diarrhea, loss
of electrolytes, vomiting or fat malabsorption which would limit absorption
of Vitamins A, D, E, K). Bio-availability of Iron, Calcium and
Zinc depend on pH, and the absence or presence of factors and anti-factors
such as phytic acid.
Ratios of nutrients are crucial
for absorption and utilization. For example, Calcium and Iron
must be in a proper balance with each other as must Iron and Zinc.
Zinc must also be in an appropriate ratio to Copper and these balances
must be maintained over extended periods whether the dose of nutrients
is low, intermediate or in the HSD range with the proviso that there
are absolute limits on safe intake some nutrients like copper if absorption
is normal although persons with impaired absorptive capacity.
The concept of optimum nutrition, with its inherent recognition of biochemical
individuality, allows for
personal deviation from the
statistical norm since normal values are statistically, not biologically,
derived.
Absorptive deficiencies (often
based in absolute or relative nutrient imbalances) can prevent proper
absorption of other nutrients. For example, if Vitamin B12 is
low, folate deficiency will result, if Vitamin D is low, calcium will
be deficient and if Magnesium is low, Calcium absorption will be impaired.
Thus, not only absolute amounts of nutrients must be considered, the
unique biochemical makeup of that person at that particular time needs
to be factored in for efficient and effective nutritional therapy so
that it either enhances long-term well-being or addresses the current
situation on a responsive, as well as a preventive, level.
Health, disease, balance/imbalance
in nutrients, medications and sequestrants all change the excretion
pattern of nutrients. Happily, because the toxic profile is so
low, there is a huge safety margin for nutrients. Because of this,
it is easy to have a beneficial impact using nutrients but very hard
to do harm using them, unlike drugs where the opposite is true.
During apparent health (before
deep cellular changes make themselves apparent in symptoms or disease
entities) metabolic requirements for nutrients go up rapidly under many
circumstances.
Growth, for example, increases
the need for Iron, Zinc and Folate, Pyridoxine, Vitamins A and D and
Calcium while stress (including alcohol intake) not only causes mineral
wasting and, over a long period, accelerates bone loss, but also causes
Vitamin C to be rapidly depleted. Magnesium, Vitamin K, Zinc,
Magnesium, Chromium, Pyridoxine and all antioxidants are depleted rapidly
as a consequence of dietary excesses.
On the other hand, once disease
(accumulated profound cellular damage) develops and symptoms and dysfunctions
are apparent, other shortfalls develop rapidly. During infection,
for example, Iron, Zinc, Pyridoxine and Vitamin C are in short supply.
All of the functions they carry out and modulate are now either halted
or challenged to keep up with the metabolic demands which are usually
increased in illness. Alcoholism depletes Magnesium, Zinc, Magnesium
and Thiamin while medications routinely deplete CO Q 10, Vitamin D,
Folate and Pyridoxine plus many other nutrients. It is important
to remember that just as the requirements for a nutrient are individual
points along a cpntinuum of requirement and that point may change with
age, nutritional status, stress, toxicity, etc., so, too, the absorptive
pathways and particulars of nutritional requirements vary widely within
and between people.
For those people who neither absorb nor metabolize vitamins well, an activated form of, for example, B1 (Thiamin Pyrophosphate or TPP), B6 (Pyridine 5 Phosphate or P5P) or B12 (dibencozide) is required to provide optimal nutritional status.43
The reality, then, is
that the individual status of a patient determines his/her nutrient
requirements and that appropriate treatment takes this into account
and capitalizes on it.
Few people live in the pristine
environments many of our ancestors did 250 years ago. We are,
regrettably, no longer free of pesticides, human and veterinary drug
residues, xenobiotics, flame retardants, petrochemicals, formaldehyde
and heavy metal residues in
our bodies and our surroundings.
Fewer people still partake of an unadulterated food chain grown in fully
mineralized soil, diets which provide them with perfect ratios of omega
3, 6 and 9 fats, zero hydrogenated and other dangerous fats, adequate
unprocessed and well prepared food which has made its way swiftly from
a nearly farm to their daily feast.
Assuming that these pristine
eaters (and breathers) never come into contact with any of the toxins
of an industrial food supply and the industrial world, they may find
themselves in the tiny minority of people who might be able safely to
avoid judicious consideration of nutritional supplement at one or more
points of their lives. Vitamins and minerals are essential for
both cellular processes and cellular detoxification. The greater
the body burden of toxins, the greater the requirement for nutrients
and, in the uniquely toxic modern world, the greater level and diversity
of nutrients required to support not just a standard of minimal health
(which can be described as the absence of overt deficiency diseases),
but optimal and robust health. This sought-after and achievable
goal requires nutritional support at a level far greater than the amount
of these nutrients reasonably consumed from food.
Personal nutritional optimization
though supplementation in addition to the best available diet is an
effective strategy which, when properly individualized, offers a country
the opportunity to increase the well being of its citizens while reducing
the fiancial and social cost of medical care to the society substantially
compared to a national strategy of allowing cellular damage/chronic
degenerative diseases to develop and suppressing their symptoms with
toxico-pharmacology.
Put simply, prevention of
the staggering personal, social and economic
burden of nutritional diseases can be accomplished through nutritional
supplementation, but cannot be accomplished without it.
The paradigmatic opposite of preventive health is reactive medicine,
in which a condition presents itself with already apparent pathology
and that pathology, not the underlying cause of it, is addressed, usually
with pharmaceuticals that inhibit or poison enzyme pathways to produce
specific desired (and undesired) changes. Reactive medicine is
effective and important in acute and traumatic situations while preventive
medicine is significantly more effective at reducing the personal and
social burden of degenerative disease. Preventive medicine is
significantly less expensive than reactive medicine since it is low
tech and uses substances whose costs are low; the bulk of the nutrient
materials cannot be patented since they are found in nature.
Properly designed, an economical
and effective health system which makes an active and meaningful contribution
to ending preventable ill health and disease combines the strengths
of conventional reactive, allopathic medicine and those of natural,
preventive medicine and public health. Reactive medicine��s strength
in acute/trauma care and diagnosis can be effectively used to guide
preventive and natural medicine. Natural medicine excels at prevention
and at repairing underlying cellular damage while prevention of disease
represents one of conventional allopathic medicine��s weakest areas.
Nutritional strategies are employed at various levels of organization from the cellular to the organismic in order to achieve several goals which conventional medicine is rarely able to achieve:
Elevated blood pressure (Hypertension) is a compensatory response which often (but not always) results from hypervolemia required to maintain plasma osmolality/osmolarity and volume when Sodium intake exceeds renal excretory capacity44
. Increased Potassium
in conjunction with decreased Sodium, Calcium supplementation, Garlic,
L-tryptophan, Vitamins A, B 3, B6, C, E, Co Q 10, Zinc, Omega
3 Fatty Acids and Flax Seed meal, Magnesium, Taurine and Arginine all help to correct this underlying maladaptive response.
Nutritional strategies for prevention, mitigation, treatment and cure are exceptionally powerful modalities in any disease condition or degenerative trend which occurs because of:
A comprehensive discussion
of the prevention, mitigation, treatment and cure of all preventable
diseases and treatment strategies for acute conditions is beyond the
scope of this discussion so a few representative diseases and conditions
have been chosen to demonstrate the power, depth and profundity of nutritional
strategies to the nutritional treatment of serious, potentially life
threatening disease. The outlines of the nutritional therapy picture
will be sketched here to be filled in later. Nutritional strategies
are not only promising in their prevention and treatment but in many
cases, have already been proven and effective.
Several framing assumptions
are important here.
A. Natural Health and Western Medicine. There is no intent to undermine or displace conventional Western Medicine its areas of strength
1. Technical diagnosis (including radiological and other visualization techniques and laboratory studies of all types)
2. Acute care for emergencies
and trauma. No other type of medicine offers as much power in
acute and traumatic situations as allopathic medicine.
B. Natural Health and Botanicals. This paper focused on nutritional strategies for
No discussion is offered of
the many important herbal and non-nutritional strategies which form
a vital core in the natural and non-toxic prevention and treatment of
disease. Exercise, smoking cessation, safe or absent alcohol use,
lack of illicit drug use, sanitation, education and other vital areas
of public health have likewise not been addressed.
The current threat to consumer
(and health professional) choice is to nutrients for which unwarranted
and dangerous restrictions are being urged by various international
organizations. It would be foolhardy to attempt to deliver wise
and effective natural health care without botanicals and other non-nutrients
or without considering the other aspects of a healthy – or an ill
-- population.
C. Natural Health across the Life Span and Diversity of Chronic Degenerative Diseases. The field of Natural Health encompasses the immense areas of
Although this field is vast,
it is crucial to this dialogue that the power and depth of Natural Health
options based in nutrition be clear. The representative conditions
which are presented here were selected because they present important
public health problems and are paradigmatic for the remainder of the
universe of chronic degenerative illnesses and are suitable for treatment
at a reduced monetary cost to the health care system compared to conventional
Western Medicine at a significant savings in the human dimension. in
efficacy and population well-being.
Nutrients as Foods
Nnutrients are essential ingredients necessary to feed, supply, activate, regulate and indeed, create our cell structures, interstitial materials, bones, hormones and, importantly, our enzymes. ��The physiology of organisms is based on the existence and speed of chemical [enzyme] reactions46
: the optimal function of
our enzymes depends on optimal nutrient availability when and where
those nutrients are needed. Optimum enzyme function is intimately
associated with a supra-abundance of nutrients since excesses are either
excreted from the body or stored in fat for future use.
Optimal health is possible
only in the sustained presence of sufficient nutrients in the form,
amount and type required at that moment. Optimal health is one
of the common goals of people everywhere. People know instinctively,
from countless eons of human memory, that food and health are intimately
linked. They may or may not know biochemistry and nutritional
science, but they understand that health and food are deeply connected.
Biochemistry has illuminated many of the mechanisms by which this common human truth is expressed. At any given moment, about 35,000 enzymes in each cell are actively carrying out all of the processes of life. They are, in fact, the very stuff of life. In his presentation speech of the 1965 Nobel Prize in Medicine, Professor Sven Gard, a member of the Nobel Committee, stated, ��one of the principal functions of genes must be to determine the nature and number of enzymes within the cell, the chemical apparatus which controls all the reactions by which the cellular material is formed and the energy necessary for various life processes is released. There is thus a particular gene for each specific enzyme��47
Thus, every aspect of biological
life can be seen as providing what enzymes need so that they can carry
out the functions which, in total, comprise a human being. Nutrition
is provided to the cells so that their enzymes have the means to carry
out their functions and, in the process, life emerges. But illness
emerges, too, if poor choices, limited availability, degraded foods
from degrades soils and chemical contamination a variety of sources
force a distortion on the sequence of events, numbers, status or health
of those enzymes.
Common sense and the life sciences converge at the perception that nutrients are foods:
Our current norms for biological
normality and health have been derived from information gathered from
a population which has the poorest health of any society in the history
of mankind-- ours. We have more cardiovascular disease, cancer,
diabetes, autism and other neurological disorders, macular degeneration,
arthritis, osteoporosis, MS and a host of other diseases than any population
known to history. Human remains of the past hundreds of thousands
of years make it clear that our ancestors were better fed and therefore
better nourished than we. Numerous observers of pre-technological
peoples and of the archeological record conclude atherosclerosis, cardiovascular
disease, cancer diabetes, osteoporosis, rickets and other common western
diseases were absent when humans were eating much more nutrient dense
food and became common as the nutrient density in our food declined.
Weston Price, DDS, studied
both the food supply and the health status of pre-technological peoples
all over the world and found them to be superior to the peoples of the
industrialized world in their physique, dentition, and health.
He documented that rather than being short and ill, these peoples were
tall and healthy. Moreover, they were free of cardiovascular disease,
cancer, osteoporosis, diabetes and other diseases of the developed and
developing world. These tribes of the world ate a diet that was
many fold richer in nutrients than our modern diet and which a prudent
modern diet with nutritional supplementation could approach.
The populations Dr. Price studied consumer food that contained at least:
The human experience and the
life sciences tell us that nutrients are food and that their toxic profile
is virtually inconsequential with the possible exception of nutrients
derived from genetically modified sources. But the options available
to us in the conventional Western medical tradition when our nutrient
status fails us, when we develop the preventable diseases of under nutrition,
are not substances and procedures with a low toxicity profile.
In fact, in the conventional allopathic model, when nutrition fails
and disease develops, pharmaceuticals are routinely employed.
Pharmaceuticals are, however, dangerous and highly toxic. Drugs work by a common mechanism: they poison enzyme systems. If the outcome is acceptable, it is labeled a ��therapeutic effect��. If not, it is a ��side effect��. Side effects pile on top of one another until the body can no longer compensate or tolerate the poisoning and, if the drug is not discontinued, the iatrogenic (doctor caused) problem either results in another drug being introduced to counter the first or death. In fact, in the United States alone, properly used prescription drugs are the 4th leading cause of death (a minimum of 106,000 people per year)48
while total drug-related deaths
reach at least 200,000 per year.49
It is important to remember that in the conventional Western medical model, nutrition is neglected until disease manifests and then toxic, expensive and, if the goal is restoring underlying health, ineffective treatment is instituted. In short, devastatingly toxic drugs are the conventional option for treatment if nutrient status is not adequate to prevent the development of disease. Dietary adjustments may not only influence present health, but may determine whether or not an individual will develop such diseases. Some statistical analyses will make the point clear through Ronald Law, MD��s simple and illustrative figures.
Risk of Hospital Care, Drug
Treatment, Traffic Accidents, Foods and Dietary Supplements
In the prevention, treatment
and mitigation of the preventable chronic diseases of under nutrition,
Natural Medicine has treamendous safety issues illustrated here in several
different ways.
Risk of Iatrogenic Injury (Australia)
Much of the risk of being a
patient in a hospital is due to the risk of medication reaction or death.
In a study of patients leaving the hospital, out-patient adverse events from drugs occurred in at least 66% of patient50
Nutrients are orders
of magnitude away from that disastrous level of risk.
Relative Risk of Death from
Natural vs. Western Medical Compared to the Risk of Dying in a Boeing
747 Crash
Statistical Risk of Death from
Various Causes, Australia, 2004
Risk of Dying in Canada Relative
to Being Killed on a Boeing 747
Do Ultra Safe Options Need
Regulation?
Accompanying his graphs, Ron Law, MD, includes this relevant information which is quoted in full:
Properly researched, regulated, prescribed and properly used drugs are the fourth most common cause of death – but they are never reported. (Source, Journal of the American Medical Association - Range 90,000 to 160,000 deaths per year.) That��s a Boeing 747 crashing every day! 46 people die every day from Aspirin alone in the USA.
Avoidable medical misadventure is the sixth most common cause of death. (Source, CDC - range 40,000 to 90,000) In Australia 9,000 people die from avoidable medical misadventure every year. (Source, Australian Medical Journal). In Australia 50,000 people are maimed by medical misadventure every year. (AMJ)
The figures used in this chart are at the lower end of the range (we wouldn��t want to be accused of exaggerating!)
Food poisoning/adverse
reactions cause between 5,000 to 9,000 deaths per year. (Source, CDC.)
Dietary supplements have averaged less than 5 confirmed deaths per year over the past 25 years in the USA. Most of those relate to a single batch of genetically engineered tryptophan introduced in the late 1980��s. (Source, CDC/FDA) There have been no proven deaths to dietary supplements in NZ.
A wide range of dietary supplements are consumed by over 50% of the population in both the USA and New Zealand (Source, NIH/MOH)
You are less likely to die from taking a supplement than dying from bee stings, sports injuries, lightening, animal bites, horse riding, radon gas, etc, etc.
Dietary supplements are incredibly safe.
Dietary supplements have the potential to reduce deaths from cancers and heart disease by over 50%. (Optimists would go as high as 75%)
Greater than 26,000 times more people die from preventable medical misadventure and properly regulated properly prescribed and properly used drugs than from dietary supplements.
You can have every confidence in assuring the safety of dietary supplements.
There have been two deaths reported as being linked to dietary supplements in NZ – both were in people with malignant cancer who consumed the herbal mixture K4. Neither were proven to be due to K4. The coroner in one case said there was no evidence to link K4 to one of the deaths – he had terminal cancer of the liver, took K4 and died of liver failure. Officials tried to blame his death on K4. Despite the evidence to the contrary, K4 was banned.
There was a recent media
report linking Ginkgo Biloba to the death of a heart patient due to
cerebral haemorrhage. The patient had been taking Ginko for some time.
He was taking blood thinning drugs which are notorious for causing cerebral
haemorrhage. Contrary to media reports, papers obtained by the NNFA
under the official information act revealed that the MARC did not find
Ginkgo to be the cause of death.51
In ratifying the Vitamin and Mineral Guideline (VMG) on July 4, 2005, the Codex Alimentarius Commission made several serious errors which will, if enancted by Codex member countries, have disastrous impact on the health of their peoples. Codex adopted a standard which allows for the assessment of risk without the possibility of any consideration of benefits. Thus, if a nutrient could be said to be toxic at any level it can be considered a dangerous substance. Clearly, this is not a game being played on a level playing field: any substance, including oxygen and water, are toxic at some dose.
Worse yet, the definition of
an adverse event accepted is the scientifically untenable position that
any substance which changes a bio marker so that it is no longer in
homeostasis should have an Upper Limit (UL) created for it by Codex��s
modified risk assessment protcedures.
Codex toxicology is far an
appropriate methodology for determining upper limits for Vitamins and
Minerals if they were needed. Toxins and dangerous industrial chemicals
should have safe ULs.
We have seen how far from toxic or dangerous nutrients are in Dr. Law��s
figures.
The VMG specifies that ��upper
safe levels of vitamins and mineral established by scientific risk assessment
based on generally accepted scientific data�� should be used to determine
these values. Since there is no ��scientific risk assessment
based on generally accepted scientific data�� which exists for the
evaluation of a substance essential to life and beneficial over a wide
dosage range, this is not a meaningful requirement. The inappropriate
application of the tool will inevitably lead to incorrect answers to
incorrect questions. In fact, Codex nutrient risk managers are
urged to create ULs out of incomplete and inaccurate data which does
not pertain to the populations under regulatory control by making corrections
on imaginary corrections on top of corrections based on poor quality
or absent data. The net result for those countries which adopt this
system of thought will be mandated under-nutrition and a predictable
rise in the death and suffering resulting from preventable diseases.
Risk assessment is a discipline
of toxicology which is designed for, and has been peer reviewed and
evaluated within the context of, the evaluation of the highest dose
of a toxin which can be tolerated by a human being before there is a
discernable change in that human being��s state. It is appropriately
used for poisons, dangerous industrial chemicals, agricultural chemicals
and the like.
Codex has accepted the use
of Risk Assessment procedures for nutrients without scientific justification
either in the focus of the risk assessment analysis, (i.e., ultra low
toxicity components of food) or the methodology used to make the determinations
of dangerousness in order to set ULs on nutrients.
Codex acted unwisely in ratifying the Vitamin and Mineral Standard which focuses only on risk of nutrients with no consideration of benefits. Risk Assessment is a methodology relevant only to toxicology and both irrelevant and antithetical to Nutritional Science and Biochemistry. The Risk Assessment methodology employed by CODEX has been arbitrarily modified without scientific validation or professional consensus to restrict permissible dosages of nutrients essential to life to levels which can, by intent, have no meaningful impact on any human being, no matter how sensitive. This misapplication, distortion and misconstruction of Risk Assessment is in clear contradiction to the principles of toxicology and scientific Risk Assessment procedures which have been developed to determine the highest dosages of dangerous industrial and natural toxins to which humans can be exposed to without discernable effect. For this reason, instead of evaluating vitamin and mineral upper limits using inappropriately modified and unscientific Risk Analysis, the Natural Solutions Foundation is urging the US to change its policy on this and related issues. We urge the use of Nutritional Science rather than toxicology to support the liberal access to nutrients enjoyed under legislative protection in the US. Under the Dietary Supplements Health and Education Act, passed by unanimous Congressional consent in 1994, while a nutrient may be dealt with by the FDA if it is shown to pose a significant risk to health and safety, barring that, nutrients are treated as foods and, as such, may have no upper limits set upon their use.\
The inappropriate classification of nutrients as dangerous substances from which the public needs protection lacks a scientific basis. None the less, this is precisely what Codex articulated in its October 2004 document on Risk Assessment52
. In that document, the preface states:
The need for an internationally
relevant or ��harmonized approach for nutrient risk assessment is well
recognized. The increased consumption of fortified foods, formulated
so-called ��functional foods�� and dietary/food supplements has made
nutrients risk assessment highly relevant to protecting public health
and to the practice of setting science-based international standards
for food��53
when, in fact, the premise
of public danger is not supported by data or experience. Nutreints
are not toxins or dangerous industrial chemicals.
The document then goes on to make it clear that the form of risk assessment used is not science-based because the application of risk assessment to substances vital for life is a newly created mis-application of the process:
��Certain nutrients and related substances, like other ingested substances (e.g., food additives, contaminants) can produce adverse effects if intake exceeds a certain amount. This potential for harm is described by the process of risk assessment, which is a science-based evaluation of available data followed b y a series of decision points. Risk assessment is well established for non-nutrient chemicals in foods. However, nutrients and related substances are unlike non-nutrients in that, within a range of intake, they provide benefit. For this reason, new paradigms have had to be considered that build upon the principles established for assessing the risk from non-nutrients, but also go beyond to incorporate additional or different principles that take into account the special characteristics of nutrients and related substances.��54
[Emphasis added]
The bold face phrases make
clear the problematic and illogical process at work here.
The October 2004 document states
It should be noted that the
document goes on to state that it is the intent to apply this procedure
to all nutrients in all categories since the ��overarching interest
is dietary substances that provide benefit but may cause harm
at a different level of intake
[and] ��should have applicability to other nutrients and related substances.��56
When the FOA/WHO released the results of the workshop (anticipated by the October, 2004 documents announcing it], the demonstrated bias was evident in that report57
. Despite its dire health consequences, this system has not been tested in the real world and, since it is explicitly not based on real data, can be expected to create confusion and inaccuracy.58
In the table of contents to the 357 page FAO/WHO document, there is no mention of benefits from nutrients. The report does mention that while attention was paid to the hazards of high nutrient intake (a fictitious risk), no attention was paid to the impact of low nutrient intake (a very real risk).59
This flight of imagination
continues as the report goes on to state that the risk assessment process
has been modified in novel ways and that the fact that risk assessment
is being used to deal with non toxic substances ��influences approaches
used to estimate an upper level of intake and also necessitates that
the homeostatic mechanisms specific to essential nutrients be taken
into account��60
This means that an entirely different standard of scientific relevance has been introduced to create a new standard of nutrient impact without any scientific justification: ��biochemical changes outside the homeostatic range can be relevant surrogates for adverse health effects associated with nutrient substances.��61
[Emphasis added]
The dangerous illogic of this methodology is apparent: homeostatic measurements derived from an unhealthy population are now the yardstick for toxicity: any nutrient which brings about a change (or is likely to lead to an enhanced stated of health) will be declared a hazardous substance at that dose. ��Hazard�� is defined in this document as ��the inherent property of a nutrient or related substance to cause adverse health effects depending on level of intake.��62
By this standard, all
substances are hazardous, nutrients among them. Since adverse
events are defined as biochemical responses, including desirable ones,
and since there was no participation in this workshop of nutritionists,
clinicians or other persons knowledgeable in the clinical uses of nutrients,
the toxic slant given to all nutrients may make some sort of sense politically.
But the imposition of this skewed system on trade and health makes no
sense and is a very dangerous policy.
The report makes it clear that anything other than a definition of nutrients as hazardous was outside of the interest of the group, ����other aspects of evidence-based systematic review, notably the kinds of questions it seeks to address were generally not viewed as appropriately suited to nutrient risk assessment.��63
This is further confirmation
that clinical and population health concerns were ��not appropriately
suited�� to the task at hand.
Of course, if every nutrient
is toxic under this definition no possible significant deviation based
on consumer preference or individual biochemistry will be possible.
Although this system was created de novo and does has not been validated
or tested, the world's health can be expected to be seriously impacted
by it.
The report states that ��issues related to the physiological severity of adverse health effect are considered separately rather than as a component of selecting the critical adverse health effect.��64
The impact of this curious
standard is that even the tiniest "adverse effect" is enough
to ban a nutrient at a dose which is greater than the dose at which
the effect was noted: for example, the flush felt with niacin at, for
sensitive people, 10 mg, would make that an adverse reaction.
The fact that the physiological severity is to taken into account means
that Niacin could be regarded (incorrectly) as a toxin at that level.
Applying a safety margin of 100, as risk assessment procedure demands,
the permitted dose would then be 100 ug, a meaningless dose designed
to have no discernable impact on the human body.
For a science-based document, the workshop report is surprising. For example, the document makes clear that there are few circumstances in which data exists for the substance being controlled but that, ���� adjustments for uncertainly must make use of uncertainly. Factors��.In any case, the these uncertainty considerations must be checked against the level of recommended intake relative to biological essentiality or the levels of intake associated with the demonstrated impact on health. ��After uncertainties are taken into account, the resulting value is the UL for the specified sub-population. When data are insufficient for setting a UL for one or more sub-populations (as is often the case) the risk assessor fills the gap by adjusting a UL that has been established for another sub-population. It is desirable [but not necessary – author] to make these adjustments based on understandings of physiological differences between the groups. Lacking such information, however, an alternative is the use of scaling based on body weight. This type of scaling adjusts the UL on the basis of energy requirements.��65
Most nutrients have little or no impact on energy requirements so setting
intake criteria on this basis is more than a little surprising.
Biochemistry and biochemical individuality is nowhere to be found.
The weaknesses of the system are prominent in the report. Consider, for example, ��If available intake data obtained from individuals is the most useful type of data. The group recognized, however, that such data are rare in most regions of the world. Thus, the report outlines approaches that allow the use of aggregated data. The derivation of an intake distribution may be accomplished even with limited aggregated data by using special statistical methods to estimate and refine a distribution curve for the (sub) population of interest. Special considerations were given to considerations for strategies for combining data from different sources in order to estimate intake.��66
[Emphasis added]
The clinical, medical and scientific
weakness of this method, which is central to the entire nutrient risk
assessment process, is clear. Imagined data will be combined with
other imagined data to create ULs on nutrients which will have no adverse
effect even if that is a statistical concept, not a clinical one.
This pro-illness system does not even require data for its globe-spanning
determinations.
According to the Workshop Report, the process of risk assessment is designed primarily to meet the ��risk manager��s special needs��67
. Those needs are referred
to many times in the document but they are never specified.
It is clear that rigorous data
have only a facultative part to play in this process since ��risk managers��
are told that they may ��make additional corrections��, the nature
of which is
not specified. Managers are told, ��Because a nutrient risk manager typically needs a UL even in the face of limited data, efforts should be made to establish ULs if at all possible. Of course, the nutrient risk assessor clarifies the degree of uncertainty surrounding the value of the UL which in turn enables the nutrient risk manager to take this factor into account in his or her decision making.��68
Even more surprising is the following statement which follows immediately after the previous one:, ��The absence of evidence of an adverse heath effect is not equivalent to evidence of the absence of an adverse health effect. That means that it is inappropriate to make conclusions about the risk or lack of risk associated with nutrient substances based solely on studies designed for purpsoses other than studying risks��69
which says quite plainly that
all nutrients are guilty until proven innocent but that there will be
only kangaroo trials for nutrients for some time to come!
The Report struggles with how
to deal with substances for which no known risk is known and decides
that the upper limit will be the highest observed dose despite any
evidence of toxicity. The report does not state the rationale
for this odd position nor does it give a reason for stating that it
does not consider people who are ill or in poor nutritional status to
need separate guidelines although should data come to light, perhaps
other limits could be set.70
Nutrient Risk Managers, who
are unelected bureaucrats, are given the authority to remove nutrients
from the food supply through regulation or other means. Given
the poor quality data which is allowed, this is a very ominous empowerment.
In short, the application of
risk assessment to nutrients is unwarranted, unscientific and admittedly
based on poor quality data. Since there is no health problem,
fixing�� it with a restriction of nutrients is a highly irrational
act.
Clinical Examples of Nutrition
in Prevention and Treatment
Nutrition, Wounds and Trauma
Nutritional status is strongly predictive of disease or trauma outcome.71
Maintenance of optimal
nutritional status has been shown to reduce the incidence of complications
such as infection/sepsis, respiratory distress, acute renal failure,
hepatic encephalopathy, congestive heart failure, and multiple organ
system failure.
Recovery from disease or trauma is more likely to occur over a shorter duration and with fewer complications in well-nourished individuals. Optimal nutritional status also allows more aggressive treatment to be tried with minimal risk of adverse events. The ability to restore optimal nutritional status to a poorly nourished individual with a serious illness or injury is limited not only by the accompanying metabolic, physiological, and hormonal perturbations associated with the conditions, but also by the patient��s lack of interest or ability to consume the additional amounts of nutrients required.72
Malnutrition causes a decreased rate of fibroblastic proliferation and neo-vascularization and impairs both cellular and humeral immunity. A high rate of metabolic activity is present at the wound site, especially within new granulation tissue. If nutrients necessary for those activities are not provided, the health of the tissue is tenuous. Proteins and their amino acid building blocks, such as Methionine, Proline, Glycine, and Lysine, are essential for normal cell function and the repair of cutaneous wounds. Linolenic and linoleic acid must be supplied in the diet, which is why they are termed essential fatty acids.73
Because they are critical constituents
of the cell membrane and are the source of prostaglandins that mediate
inflammation, deficiency of essential fatty acids causes impaired wound
healing. Deficiency of vitamins C or K leads to scurvy and coagulopathy,
respectively. Minerals, including calcium, iron, copper, zinc, and manganese,
must be delivered to the wound milieu to act as cofactors for vital
reactions in the synthesis of proteins needed in the healing process.
If the diagnosis is impaired
wound healing resulting from malnutrition, ensure that the patient receives adequate protein and energy (caloric) intake. Specific vitamin and mineral supplements [often at high doses] may be required for rapid recovery of the necessary nutrients.74
Cellular injury occurs in trauma and disease and requires abundant and diverse nutrient availability to provide the factors and co-factors necessary to support and provide:
Tissue-specific requirements
for nutrients depend upon the nature of the disease (renal, hepatic,
pulmonary, cardiovascular) or type of injury (burns, fractures, head
injury, multiple trauma, major surgery) while person-specific requirements
for dosage vary greatly dependant upon underlying nutritional, genetic,
toxicologic, health status and other factors unique to each individual.
Careful clinical assessment of the clinical complex consisting of the
patient and his/her disease or condition rather than assessment of the
disease or condition isolated from the underlying host realities of
nutrition, genetic and biochemical individuality. This is true whether
the issue is wound healing or any other disease or condition requiring
healing.
The hyper metabolic
states which frequently follow trauma alter cellular metabolism and create special nutritional requirements. In additio
n to increased energy, there is a
corresponding
increased
demand for vitamins, minerals and cofactors which support energy metabolism
under these conditions. The demand for increased metabolic and cellular support
is superimposed
upon the
spot
where
t
he
patient
rests
up
on the nutritional continuum
which ranges from highly deficient through marginal on towards
adequate
and finally reaching
optima
.
The nutrients required in abundance specifically for wound healing
include:
Coenzymes for their role in the reactions of oxidative metabolism
Loss of Lean Body Mass (LBM),
a common sequel of trauma, reduces the size of the metabolically active
compartment responsible for repairing the underlying cellular injury
and fighting infection. A weight loss of 20% of total body weight is
associated with impaired wound healing and host immune defense with
potentially cataclysmic results. All tissues except brain lose
LBM proportionately to the total weight loss. Critical tissues
such as cardiac and respiratory muscle are not spared. Increased
hydration and fatty infiltration of muscle and liver may actually underestimate
actual weight loss of metabolically active tissue. When appropriate
nutrition is provided, immune system and plasma proteins recover cell
mass most rapidly, but skeletal muscle may take months or even years
to fully recover.104
Glucose and protein metabolism are severely altered in traumatic hyper metabolism and wound healing. In addition to macronutrients and energy, specific amino acids are required for wound healing:
Delayed wound healing represents
a massive burden on the personal and social productivity as well as
the costs of care and is predictably delayed or complicated by under
nutrition, specific and general shortfalls in nutritional status and
failure to treat the wounded with appropriate nutritional support based
not on the nature of the wound, but the reality of the spot they occupy
at that moment on the nutritional continuum.
Easy access to a wide variety
of high quality nutrients along with easily available information on
the nutritional support of wound healing is a very good bargain for
any country and for its people.
Nutrition, Blood Lipids
and Blood Pressure
Cardiovascular disease (CVD)
presents a major world health problem which can be positively influenced
by nutritional approaches both in prevention and treatment. Prevention
is obvious, but often ignored by those who develop CVD until they can
see for themselves that their lives are threatened by the impact of
their behavioral choices, that is, when they realize that they now have
CVD. Since the medical impact of risk factor-enhancing behavior
(e.g., smoking, unbalanced diet, lack of exercise, etc.) is delayed,
sometimes for decades, behavioral change is often initiated long after
cellular damage has occurred. In spite of this, the cardiovascular
system is remarkably responsive even to late-stage nutritional strategies
which therefore thus have a tremendous role to play in the prevention,
mitigation and remediation of CVD.
WHO notes in the Global Strategy on Diet, Physical Activity and Health136
:
While nutritional deficiencies and imbalances are believed to pose another set of significant risk factors.137
These nutritional deficiencies and imbalances include Vitamin C and other vitally important nutrients which are either low or undetectable in many CVD patients. It should be remembered that a biological marker which is low may actually be severely depleted since the norms for biological markers and nutrient levels were developed in a population which was ill nourished and ill.138
WHO notes further that of that 16.7 million global CVD deaths per year, an estimated 16.7 million (29.2%) result from the various forms of cardiovascular disease (CVD) which are preventable by positive action on the major primary risk factors: unhealthy diet, physical inactivity, and smoking. More than 50% of the deaths and disability from heart disease and strokes, which together kill more than 12 million people each year, can be cut by a combination of simple, cost-effective national efforts and individual actions to reduce major risk factors such as high blood pressure, high cholesterol, obesity and smoking. And, once CVD is diagnosed, nutritional strategies can often reverse or cure many types of CVD.
CVD is no longer only a disease issue of the developed world: according to the WHO, some 80% of all CVD deaths worldwide took place in developing, low and middle-income countries, while these countries also accounted for 86% of the global CVD disease burden while WHO estimates that by 2010, CVD will be the leading cause of death in developing countries.139
In fact, WHO identifies CVD as ��the major contributor to the burden of disease among the non communicable diseases��.In the next two decades, the increasing burden of CVD will be borne mostly by developing countries��140
CVD is subdivided into the following clinical pictures:
According to WHO, of the 16.7 million deaths from CVDs yearly:
In addition, at least 20 million people world-wide survive heart attacks and strokes every year. A significant proportion of these CVD patients require ongoing and costly clinical care, which puts a major burden on long-term care resources. This burden is costly in man power, money, lost productivity and other resources. CVD makes itself apparent through clinical manifestations primarily in the otherwise economically and socially productive mid-life years, undermining socioeconomic development, not only of affected individuals, but families, communities and nations. Members of lower socioeconomic groups generally have a greater prevalence of risk factors, diseases and mortality in developed countries and a similar pattern is emerging as the CVD epidemic matures in developing countries.142
Thus, preventing and controlling the maturing non-communicable CVD epidemic is especially beneficial to nations whose resources must be devoted to their emergence into healthy, stable and powerful economies with a healthy and socially productive work force and community structure.
Primary Risk Factors:
WHO notes that while CVD is influenced by a host of risk factors,143
the five strongest influences, representing the majority of the risk144
, are those which can be positively modified by dietary strategies:
Items in boldface are currently
believed to have the greatest impact on CVD morbidity and mortality,
especially in combination.
WHO further states ��In developing
countries, the effect of the nutrition transition [to nutrient poor
and processed food] and the concomitant rise in the prevalence of cardiovascular
disease will be to widen the mismatch between healthcare needs and resources,
and already scarce resources will be stretched even more thinly.
Because
unbalanced diets, obesity and
physical inactivity all contribute to heart disease, addressing these,
along with tobacco use, can help stem the epidemic.149
Although they are independent
risk factors, obesity and diabetes mellitus are usually associated with
elevated blood lipids and blood pressure thus compounding their dangers.
While successful weight loss and blood glucose control alone reduce
CVD risk, to achieve the most meaningful results, blood lipids and blood
pressure and nutritional status must be controlled along with them.
Blood Lipids:
Risk Factors for Morbidity and Mortality
Serum Markers for
Risk Factors Predictive of CVD
|
Dietary modifications that reduce total and LDL-cholest
erol must not also decrease HDL
cholesterol or contribute to elevated triglyceride levels.
Oxidation of LDL-cholesterol is a key step in the formation of fatty streaks, the initial lesions of at
herosclerosis. LDL can be protected from oxidative stress by reduction of sources of free radicals that come into contact with it
and by nutritional enhancement of free radical scavengers. Absolute reduction of
LDL levels also reduces the potential amoun
t of oxidized LDL that may be formed regardless of the level of oxidative
stress.
Compensatory Markers of the
Chronic Degenerative Changes Associated with CVD:
Blood Pressure: Hypertension increases risk of both coronary
heart disease and stroke. Elevations in either systolic or diastolic
pressure are associated with increased CVD risk. The age-related
increase in blood pressure typically observed may be minimized or delayed
by dietary modifications earlier in life that normalize and sustain
normal blood pressure and by nutritional interventions later in life
either before or after hypertension has become clinically established.
Diabetes Mellitus:
Diabetes mellitus increases risk of CVD independent of weight, blood
lipids and blood pressure. Both Type I diabetics (5-10% of total
prevalence) and Type II diabetics (90-95% of total prevalence) experience
increased risk of cardiovascular complications. Type II diabetes
is often accompanied by obesity (especially metabolic fat), hyperlipidemia
and hypertension. Cellular insulin resistance is the common link
between each of these risk factors. The relationship between insulin
and increased CVD risk is probably related to its vasoactive and proliferative
effects. Nevertheless, two prospective studies have recently confirmed
that poor blood glucose
control can contribute to vascular complications of diabetes with or without accompanying hyperinsulinemia.
150
,
151
Obesity: Although obesity is not as strongly associated
with risk of CVD as hyperlipidemia or hypertension, it may have a greater
impact on morbidity and mortality because the prevalence is higher.
Obesity among children is increasing at a much greater rate than among
adults. Obesity is linked to consumption of high fat foods/high
energy ��food�� in the face of reduced energy output including abandoning
free play by children in favor of passive activities like television
and computer games. Inappropriate intake of sweetened, nutrient empty
drinks and food substitutes like candy and pastries with their low nutrient
density and high energy input is contributory to the growing epidemic
of overweight and obesity.
The relationship is so common between obesity and
diabetes
that some health experts have begun to refer to the constellation as
��
dia
besity
©
��
152
,
153
, 154
, 155
Nutritional Status:
Suboptimal serum Vitamin C levels, although the subject of intense
controversy has a long-established history of association with CVD beginning
with the
lectures and teaching of Nobel Laureate Linus Pauling.156
. Dr Pauling, his associates and followers postulate that CVD cannot develop in the presence of optimal levels of Vitamin C and state that amount of Vitamin C manufactured in stress free primates of our size would be between 8 and 10 grams per day157
. Stress of all types
(including nutritional
insufficiency) is well known to increase the need for one of the most potent antioxidants known: Vitamin C. For examples:
arterial disease by 14 times.180
This well-documented fact alone could reduce the burden of CVD significantly. Vitamin C is a safe, non-toxic and highly useful nutrient public health at little expense if adequate doses of Vitamin C are achieved population-wide.
Unstable arterial plaque is associated with more than a half-million sudden-death heart attacks that occur annually, mostly in males with normal or low circulating cholesterol levels.182
This strongly suggests that sudden normo-cholesterol heat attack risk can be sharply reduced with this simple, and remarkably inexpensive, dietary strategy.
Arterial disease is initiated by activation of the peroxisome proliferators-activated receptors (PPARs). Sub-optimal Vitamin C "severely compromises collagen deposition and induces a type of plaque morphology that is potentially vulnerable to rupture."183
The mechanism by which
Vitamin C controls and eliminates this genetic initiation of intimal
inflammation is identical to the mechanism of the statins. Vitamin
C is as effective as the
statins at controlling this inflammatory reaction: ��[this research] provides incontrovertible evidence to support the view that both statins and vitamin C have identical effects on the expression of genes coding for PPARs" at levels "well within the permissible dose of this vitamin."184
The question, of course, is
what is an adequate or optimal supply of this particular (or any) nutrient
and what would be classified as ��within the permissible dose�� of
a substance with many-fold variation in requirements for optimal dosing
and without a meaningful toxic profile? Appropriate doses must
be determined on a clinical, not an administrative or epidemiological,
basis.
In addition to Vitamin C, briefly
considered here for the purposes of illustration are a host of vitally
important nutrients which must be repleted in order to stop the progression,
or even reverse CVD. Since the amounts of food which would
provide high dose nutrients is impractical and unhealthy for consumers
to eat in a day, the only practical alternative is to use nutrient supplementation
both under the guidance of professionals and by free consumer choice.
Secondary Risk Factors
A number of less familiar risk
factors for CVD may also be amenable to control by dietary means.
Of these, the strongest evidence supports a role for elevated plasma
homocysteine levels and alterations in levels of blood coagulation factors
through nutritional strategies.
Homocysteine:
Hyperhomocysteinemia (elevated blood
homocysteine) is recognized as
an independent risk factor for coronary heart disease, cerebrovascular disease
, and peripheral vascular disease. At moderate elevations of only 12% above the upper limits of normal, homocysteine has been prospectively associated with a three-fold risk in acute myocardial infarction in men.
Elevated homocysteine predisposes to arte
riosclerosis and stroke. In fact, in 47% of patients with arterial occlusion, a moderate elevation of homocystein
e
was found.
185
Homocysteine is an intermediate on the pathway to methionine. If it is not methylated in the presence of adequate Folate, using either the B6 or the Folate and B12 dependant pathways, (and B2 in those with a genetic mutation in the MTHFR gene), it is instead oxidized to homocysteic or cysteic acids. It is believed that the dangerous impact of homocysteine is, in fact, the result of the oxidative pathway of homocysteine to homecysteic acid which occurs when insufficient Folate and B12 are available.186
Homocysteine metabolism is accomplished
via
one of two known pathways
in humans
: one is dependent upon the presence of adequate B6
and the other upon adequate levels of
Vitamin
B12
and F
olate.
Insufficient effective levels of
B 6,
B12 and F
olate (which may be the result of dietary, genetic an
d
/or
patholo
gic
al
conditions) lead to the accumulation of
homocysteine
in the blood
with toxic
impact upon brain, bone and vascular systems
.
Blocks in either of these pathways due to inadequate amounts of these or other vitamins can produce hyperhomocysteinemia. Other causes of this condition include inherited disorder of metabolism and impaired
renal function.
At elevated levels, homocysteine
stimulates proliferation of
smooth muscle cells and inhibits proliferation of endothelial cells
by a mechanism that is not well understood.
Blood coagulation factors:
Atherosclerosis promotes endot
helial injury which initiates platelet adhesion, aggregation and formation of a thrombus. Hemodynamic alterations associated with turbulent blood flow or hypertension may be involved in thrombogenesis associated with endothelial injury. Dietary factors a
re involved at several points in the coagulation cascade as cofactors for prothrombin and thrombin formation. High fat intakes resulting in
dangerous
postprandial lipemia may enhance thrombogenic activity through association with increased levels of Facto
r VII. Dietary fat composition may influence platelet
aggregation
through synthesis of prostanoids
either favoring blood clot production or retarding it
. Dietary fiber may have an antithrombogenic effect as levels of intake have been inversely associated
with levels of plasminogen activator inhibitor-type, possibly mediated by effects of fiber on insulin
.
Dietary enzymes may reduce the predisposition toward thrombogenesis and are an important preventive strategy as well as a treatment option should a clot form in, or migrate to, the brain. Enzymes like nattokinase and lumbrokinase have profound impact upon clot formation and, with sustained regular use, safely digest extra fibrin, lessening clot formation and promoting good circulation while reducing clot formation.
187
,
188
, 189
, 190
, 191
, 192
Diet and the Impact of Diet on Blood Lipid Levels: Control of blood lipid levels by dietary modifications is the first step in prevention and treatment of hyperlipidemia in both adults and children. It is crucial to the immediate and long term health of a population to improve the lipid profile by natural, effective, non-toxic and inexpensive methods which will allow low-to-absent side effect levels, provide workable long term solutions for prevention and attractive options to patients with already established disease. Medications for these elevations and ratio distortions are toxic, expensive and have a serious side effect profile which nutritional interventions lack.193
According to the National Guidelines Clearinghouse of the US government, findings of the Institute of Medicine support the use of nutritional treatment for the reduction of blood lipids and state in their Guideline on CVD and nutrition, ��Benefits of Nutrition Management to Patients��,
Benefits of Nutrition Management to Health Services Providers
The same source notes that
only downside to the use of nutrients as a treatment for CVD is that
the frail elderly must be monitored carefully against loss of weight.195
Serum Cholesterol:
Saturated fat (SF) intake is generally considered to be a strong predictor
of elevated LDL-cholesterol. However, as we have seen, this relationship
only obtains when relevant nutrients are in short supply and carbohydrates
have not been prepared in a wholesome fashion.
Cholesterol Molecule
Consideration of the hazards and necessary precautions which must be taken when SF is consumed are, it should be remembered, not applicable when the SF is from healthy and uncontaminated sources. While eating SF from healthy, free range animals untreated with chemicals, veterinary drugs or contaminated feed, is a not a risk factor, it is true that SF from sick, toxic and stressed animals (unhealthy saturated fat or ��USatFat��) in the context of a poor nutritional environment raises LDL-cholesterol by decreasing expression and functional activity of hepatic LDL receptors. Polyunsaturated fat (PUFA) lowers LDL-cholesterol, but at twice the level of intake that it takes for USatFat to raise it by the same increment. When consumed in high amounts (>12% of total energy), PUFAs will lower also lower HDL-cholesterol however if
-6 fatty acids (linoleic and arachidonic acids) are the predominant PUFAs consumed, suppression of immune function may occur. It is very important for cardiovascular, immune and brain function that the PUFAs consumed have a beneficial ratio of
-3, 6 and 9 moieties. Monounsaturated
fat (MUFA) lowers total and LDL cholesterol as effectively as PUFAs,
but in contrast to PUFAs, will not unfavorably alter HDL-cholesterol
levels. Thus substitution of a proportion of the unsaturated fat
component of total fat with MUFA (10% of total energy) will promote
an optimal ratio of total to HDL-cholesterol.
Total fat intake may also contribute
to increased LDL-cholesterol levels when large amounts are consumed
(> 30% of total energy). At high levels of total fat intake,
it is more difficult to keep healthy at optimal levels (< 8 - 10%
of energy) or to maintain an energy intake compatible with weight control.
High intake of dietary cholesterol and total fat also result in elevated
chylomicrons which are produced in order to facilitate absorption.
When triglycerides are released from these chylomicron particles, the
cholesterol-rich remnants have atherogenic effects similar to LDL-cholesterol
itself. The life span and composition, as well as the size of chylomicrons
vary with the composition and nature of ingested fats with the most
favorable profile being derived from coconut oil and medium chain triglyceride
diets. Thus, dietary fat type and amount have a profound impact
on the dynamic metabolism of lipids in the blood and the composition
of those lipids.196
Not only is the composition
of the fats consumed significant for cardiovascular and immune health,
the ratio of PUFAs to USatFat is also of great importance to heart health.
LDL-cholesterol levels may be raised by dietary cholesterol but only
if the ratio of PUFAs to USatFats is low (< 1). Adequate intake
of PUFAs relative to USatFats can lower LDL-cholesterol while inadequate
levels promote the oxidation of cholesterol to form LDL-cholesterol.
At intakes higher than 400
mg, dietary cholesterol inhibits hepatic cholesterol synthesis by negative
feedback control. However when large amounts of USatFats are consumed
with significant amounts of cholesterol (< 400 mg), this feedback
control is overwhelmed and cannot by itself effectively reduce plasma
cholesterol levels. The effect, however, is more complex: several
theories have been proposed to explain the synergy between saturated
fat and dietary cholesterol which elevates LDL-cholesterol levels by
more than can be explained by an additive effect. These theories
focus on mechanisms involving down regulation of hepatic cholesterol
receptors and/or increased activity of cholesterol ester transfer protein.
In addition to dietary fat,
total energy, simple carbohydrates [prepared in familiar Western ways,
rather than those which promote healthy carbohydrate utilization], fructose,
and alcohol intake may also affect blood lipid levels. Elevated
LDL-cholesterol levels have been found in individuals consuming low
fat diets when the fat component has been replaced by carbohydrates
consisting mostly of simple sugars from low fiber sources. If
these individuals also have elevated triglycerides in response to this
dietary pattern, they are characterized as ��carbohydrate-sensitive��.
Carbohydrate sensitivity is seen almost exclusively with high intakes
of fructose or sucrose (fructose + glucose), especially when consumed
in liquid form. The mechanism for this effect is unknown but may
relate to metabolism of fructose to glyceraldehyde-3-phosphate which
is involved in endogenous triglyceride synthesis. However, de
novo lipogenesis accounts for only a small amount of hepatic VLDL production
and the increase in VLDL synthesis is not accompanied by decreased LDL
in carbohydrate sensitive individuals. The greatest
sources for many people for
their intake of fructose are soft drinks, candy, and desserts secondary
to increased industrial usage of high fructose corn syrup as a sweetening
agent.
It is interesting to note that fructose was forbidden as a sweetener in these items because of its deleterious impact until the soft drink industry forced the US FDA to change their
regulation to allow it since it was permitted under the relevant Codex standard.
197
In contrast to total and LDL-cholesterol,
HDL-cholesterol is less responsive to dietary modifications. Physical
activity and alcohol have a substantial impact on raising HDL-cholesterol.
Alcohol may also increase triglyceride levels which are generally inversely
related to HDL. Thus consumption of large amounts of alcohol would
not be an effective means for raising HDL in individuals with low HDL
levels accompanied by elevated triglyceride levels. In fact, the neurotoxic,
hetpatotoxic, nutrient depleting and caloric impact of alcohol makes
it clear that it is not a cardio vascular health promoting agent.
Consumption of garlic extracts
and allium vegetables (onions, garlic, leeks, etc,) has been shown to
lower LDL-cholesterol effectively while raising HDL, probably due not
only to factors intrinsic in these vegetables but also to their high
content of manganese, Vitamin C, Iron, Folate and Vitamin B6.198
Cranberries contain polyphenols which inhibit the oxidation of LDL cholesterol. According to a recent study, 100 grams (100,000 mg) of cranberries are equivalent to 1000 mg of vitamin C or 3700 milligrams of vitamin E in countering LDL cholesterol oxidation.199
Fresh cranberries typically
provide 0.3% polyphenols, while cranberry extracts typically provide
7.0% polyphenols. A new type of concentrated cranberry extract
(CRAN-X) yields 30 percent polyphenols, making it at least as good at
inhibiting LDL cholesterol oxidation as an equal amount of vitamin C.
In addition, cranberries have potent anti-adhesion factors that help
prevent bacteria and cholesterol from sticking to artery walls.200
Serum Triglycerides: Alcohol and simple sugars consumed from low fiber sources can elevate serum triglycerides. Conversely, this cardiovascular risk factor is highly responsive to dietary strategies which include supplementation with
Seasonal Cholesterol Variation: Seasonal fluctuations observed in blood cholesterol levels have been attributed to changes in vitamin C intake. The controlling enzyme of bile acid synthesis (cholesterol-
-hydroxylase) is dependent
on vitamin C to provide antioxidant protection for the iron moiety at
its catalytic site.
Postprandial Hyperlipemia:
The period following ingestion of a meal containing fat is a time of
active lipid and lipoprotein metabolism. In general, plasma triglycerides
peak 3 hours following a meal and return to fasting within 9-12 hours.
Although postprandial
lipemia typically extends over
a 9-12 hour period, its duration can be modified by the total amount
of fat and dietary fiber consumed. The major effect of postprandial
lipemia on fasting lipids is observed in the concentration and composition
of the lipoprotein fractions. The duration of postprandial lipemia
is believed to be associated with eventual development of fasting hyperlipemia
and insulin resistance. Hyperinsulinemia may result from sustained
high levels of fatty acids in the portal circulations which decrease
hepatic insulin clearance.
Effects of Diet on Regulation of Hypertension: Blood pressure is a function of cardiac output and total peripheral resistance. Control of blood pressure is achieved over the
short term by sympathetic nervous system activity and over the long term by renal
mechanisms involving control of urinary sodium excretion. Dietary factors can influence
blood pressure through either
direct effect on plasma volume and vasoactivity or by interfering with
sympathetic and renal control of these parameters. Dietary contributions
to the control of blood pressure include:
Effects on Plasma volume:
Increased plasma volume may result when renal capacity for sodium excretion
is decreased. Urinary sodium excretion imposes an osmotic workload
on the kidney that can exceed functional capacity if sodium intakes
are repeatedly high. When this point is reached, the obligatory
amount of fluid is retained with sodium in the extra cellular (interstitial
and plasma) compartment. The level of sodium intake at which decreased
efficiency of sodium excretion is observed will vary with age, ethnicity,
and family history of hypertension. Moderate reductions in sodium
intake can improve the efficiency of renal sodium excretion and thus
enhance the therapeutic index of diuretics and minimize side effects
associated with their use.
The efficiency with which sodium
is excreted can also be modified by dietary factors other than the amount
of sodium consumed. These factors include calcium and potassium
which promote sodium excretion, and long-term consumption of high protein
and high glycemic index diets which may decrease it. Modifications
in intakes of these dietary factors can influence tolerance to any level
of sodium intake. High potassium and calcium intakes will enhance
urinary sodium excretion, thus enabling higher sodium intakes to be
consumed when renal excretory capacity is reduced without an increase
in plasma volume. High intakes of protein have been proposed to
reduce renal functional
capacity over time as a consequence of glomerular capillary damage from the repeated high perfusion pressures required to excrete excess nitrogenous waste. High glycemic index diets may contribute to the eventual development of hyperinsulinemia which may decrease the efficiency of sodium excretion through stimulation of sympathetic activity. Insulin also inhibits sodium efflux from cells through effects on membrane ion transporter activity and thus hyperinsulinemia would favor renal sodium retention.279
Effects on Vasoactivity:
Changes in vascular tissue reactivity are observed in response to changes in efficiency of sodium excretion in order to maintain consistency of blood flow through the peripheral vasculature with fluctuations in plasma volume. Whe
n sodium is retained as a result of decreased renal excretion, plasma volume is increased and thus the peripheral vasculature must compensate by decreasing vessel diameter to maintain a constant blood flow through the capillary bed. Increased stimulation
of sympathetic nervous system activity also increases vasoconstriction
of the peripheral vasculature.
Dietary patterns that favor elevated fasting insulin levels can contribute to increased vascular resistance by insulin-mediated effects on sympathetic a
ctivity and renal sodium retention. In contrast, calcium, potassium, and polyunsaturated fatty acids enhance sodium excretion and thus would favor relaxation of the peripheral vasculature. Increased availability of magnesium directly affects capillary ve
ssel resistance by inducing dilation through relaxation of vascular smooth muscle. As precursors for synthesis of the prostacyclin and thromboxane, the balance of intakes between
-6 and
-3 PUFA will determine whether vasodilation or vasoconstriction act
ivities will dominate.
280
Other Effects: Excess alcohol consumption adversely affects blood pressure by mechanisms that have not been clearly defined. Among the possibilities proposed are induction of sodium retention by stimulation of vasopressin and increased sympathetic nervous system activity. 281
Injury to vascular endothelial tissue can interfere with ability of the peripheral vasculature to normalize blood pressure with changes in plasma volume. Vitamin C and vitamin E protect the vascular endothelium from oxidative injury.
Heart Healthy Nutrients:
L-carnitine is synthesized in a reaction which is catalyzed by five enzymes which require
Because L-Carnitine is so important
in energy production and management, an early sign of vitamin C deficiency
is fatigue, related to decreased synthesis of L-carnitine.287
L-Carnitine provides myocardial
support and increases the efficiency of cardiac contraction when taken
on an on-going basis. Used in the immediate post-myocardial period,
the same substance has both immediate impact on survival and long term
effect on the regaining of cardiac function.
In coronary artery disease,
the accumulation of atherosclerotic plaque in the coronary arteries
may prevent parts of the heart muscle from receiving adequate circulation,
ultimately resulting in damage and impaired pumping ability. In
MI, heart tissue may be
damaged resulting in compromised pumping ability and clinical heart failure. Damage to the heart results in degraded exercise tolerance and decreased left ventricular ejection fraction (LVEF), indicative of heart failure when less than 40%.290
The addition of L-carnitine to standard medical therapy for heart failure has been evaluated in several clinical trials.
Nutrition and Glucose Control
Both absolute glucose values
and fluctuations in those values are of extreme importance in the short
and long term outcome of diabetics. Digestible carbohydrates make a
major contribution to post-pirandial glucose levels. In addition
to the macro nutrient impact that carbohydrates have on blood glucose,
minerals and other nutrients which are part of the diet or taken as
supplemental nutrition have a significant and crucial role to play in
mediating the body��s ability to restore or maintain post-pirandial
blood glucose levels to fasting levels over time. When properly
mediated, this cycle allows proper absorption and utilization of glucose
from the GI tract. Minerals and other nutrients have a secondary
impact on hormones and mediators which in turn impact the secretion
of insulin, clearance and cellular response to it.
Numerous diseases, life style choices and conditions, as well as pharmaceuticals impair or impact glucose control. In each condition or drug reaction they are mediated not only with the often recommended physical exercise and diet, but are also strongly impacted by nutritional correction and control of blood glucose. Disease conditions impacting glucose include: metabolic syndrome
Hyperinsulinemia, (with or
without hyperglycemia), is the most commonly observed abnormality in
blood glucose regulation. Large amounts of rapidly absorbed simple sugars
which lead to an insulin ��overshoot�� (a sharp rise in insulin greater
than that required to accommodate the total glucose load). This
is rapidly followed by a rapid decline to below-fasting levels of glucose.
This hyperglycemia is rapidly followed by hypoglycemia within 60 to
120 minutes following the carbohydrate intake. As a consequence
of this recurring cycle over time, widespread consequences result including
metabolic obesity and serious renal, retinal, cardiovascular, neurological,
endocrine and reproductive abnormalities and diseases.
Habitual dietary abuses create pathological metabolic changes and aberrations at the cell receptor level which are difficult to mediate without adequate dietary and supplemental nutrients. In fact, long term glucose patterns have a greater impact than short-term intakes because tissue response to insulin is a receptor-mediated phenomenon with more or fewer receptors induced by characteristic dietary intake296
Sucrose intake should be restricted. Both laboratory animals297
and healthy humans298
caused glucose tolerance to be impaired and rendered the tissues less sensitive to glucose.
Since fructose is a disaccharide composed of glucose and a sucrose moiety, the glycemic response in diabetics is determined largely by the glucose fraction.301
Fructose, however, is superior to sucrose and may be similar to starch in terms of glycemic control.302
However, it is the fructose moiety of the sucrose molecule which appears to be responsible for the adverse effects of sucrose on serum lipids 303
so the addition of fructose
may increase insulin resistance.
Because fructose leads to increase
copper excretion, inclusion in the diet of diabetics can lead to a copper
deficiency which can, in turn, impair glucose tolerance.
Changing not only the amount, but also the timing of meals and snacks has a beneficial impact if the change is to small frequent meals with no increase in caloric intake over the desired range. Improvement in both serum insulin and 24 hour urinary C peptide levels decreased significantly in type I and type II diabetics. Blood glucose was reduced in diabetic subjects but not in normals. Non diabetic normals showed the same sharp improvement in their values which, in their case, took them from normal to near-optimal.304
Among Australian aboriginal
peoples diabetes was totally unknown as long as a hunter-gatherer lifestyle
was followed. In the 1970s missionaries introduce flour and sugar to
their converts. By the 1980��s diabetes was rampant, diagnosed
in more than 20% of urban aboriginals. Prior to urbanization,
they lived on what they could kill or collect and ate meat from wild
animals so their diet was high in protein and dietary fiber but low
in fat.
During the 7 week study,
their activity level increased and food intake was reduced to 1200 calories
per day. Although 64% of their diet (which they caught) was protein
and only 13% was fat all subjects lost weight steadily Blood pressure
and triglyceride levels fell. Glucose tolerance improved greatly
from an average fasting glucose of 200 mg/dl to 120 mg/dl indicating
major improvement in post-pirandial clearance.305
Juvenile intake of coffee,
tea,306 nitrates307 and nitrosamines308
potentiate the development of insulin dependent diabetes. Many
foods are diabetogenic including wheat, soy309 and cow��s milk310
especially in children and infants. Other factors may potentiate insulin
resistance but, regardless of cause, the final common expressions of
hyperinsulinemia and hyper/hypoglycemia are responsive to dietary strategies
for regulation of glucose and prevention or amelioration of glucose
related degenerative pathologies.
Non-diet-related insulin resistance
is frequently precipitated by pregnancy, stress or sepsis. Post-receptor
defect in signal transduction involving glucose transporter synthesis
and activity is a frequent complication of injury or sepsis which is
potentiated by stress-mediated elevations in epinephrine, glucagon,
and cortisol. Although diet is not involved in the development
of insulin resistance in conditions associated with metabolic stress,
dietary adjustments and nutritional strategies can prevent the worsening
of hyperinsulinemia and hyperglycemia frequently observed in pregnant,
injured or septic patients.311
Protein restriction may delay
or prevent the development of nephropathy. Twenty two insulin
dependant diabetics randomly received either an unrestricted protein
diet or a moderately protein-restricted diet for 6 months. Patents
on the unrestricted diet showed progressive decline in glomerular filtration
rate with no change in protinuria. Protein-restricted patents
showed a marked decrease in protinuria and a stabilization of glomerular
filtration rate independently of changes in blood pressure or glycemic
control.312
In patients whose insulin secretion
is insufficient to carry out the tasks of glucose regulation, a wide
variety of metabolic burdens are imposed on every cell and tissue in
the body. Correction and protection of the widespread damage caused
by this metabolic deviation requires vigorous nutritional supplementation.
Commonly used pharmaceuticals exacerbate the nutritional requirements
and their use makes the employment of nutritional strategies particularly
important in order to reduce the complications of diabetes and assist
in good control of the patient��s glucose.313
Availability of dietary glucose
from food sources is the primary contributor to post-prandial hyperinsulinemia
since maximal levels of circulating insulin are attained immediately
following ingestion of a carbohydrate source. However, total energy
intake and its distribution throughout the day, type and amount of fat,
type and amount of protein, and intakes of specific micronutrients may
each modify the insulin response to a particular glucose load and/or
protect against or modify the enzymatic, cellular, organ, tissue and
systemic impact of poor glucose control. Nutrients which show
an important impact on insulin and glucose utilization and correction,
amelioration or protection of hyperinsulinemia and diabetes-related
damage include:
.
The following summary is used,
with permission, from the excellent Preventive Medicine lectures of
Dr. Arline McDonald, who teaches this subject at the Feinberg School
of Medicine of Northwest University, Chicago, IL.442
Consequences of diet-induced
insulin resistance: The role
of diet-induced hyperinsulinemia and insulin resistance in the etiology
of noninsulin-dependent diabetes mellitus (NIDDM) has not been clearly
defined. Hyperinsulinemia and hyperglycemia may precede development
of diabetes characterized by insulin resistance by a 5 to10-year period.
Both of these abnormalities can have adverse cellular and systemic effects.
Adverse effects associated with hyperglycemia are a consequence of cellular
injury in noninsulin-dependent tissues that occurs with increased intracellular
concentration of glucose. These include vascular, renal, ocular, and
infectious complications which are frequently observed in poorly controlled
diabetes. In the absence of diabetes, hyperglycemia is not usually
observed in association with hyperinsulinemia because normalization
of blood glucose is achieved at the expense of higher insulin levels.
Adverse effects of sustained hyperinsulinemia include increased sympathetic nervous system activity, alteration in calcium transport by smooth muscle cells, and increased proximal and distal tubular reabsorption of sodium. Each of these effects may contribute to increased peripheral vascular resistance and elevated blood pressure. Insulin also has mitogenic activity that promotes proliferation of vascular smooth muscle cells resulting in thickening of capillary and blood vessel walls and narrowing the arterial lumen. These structural changes contribute to increased peripheral resistance and formation of atherosclerotic plaques. Fibrinolytic activity may also be increased with hyperinsulinemia since levels of plasminogen activator inhibitor are increased by insulin. Insulin resistance is frequently observed in both hypertension and coronary heart disease. Insulin resistance induced by dietary factors (e.g., obesity) differs from that which characterizes noninsulin-dependent diabetes mellitus (NIDDM) in severity and associated metabolic derangements. Diet-induced insulin resistance also tends to be peripheral (e.g., skeletal muscle) rather than hepatic and appears to affect nonoxidative glucose disposal (e.g., glycogenesis) more than oxidative pathways. In NIDDM, insulin is ineffective in suppressing hepatic glucose output and insulin resistance interferes with adipocyte lipogenesis and oxidative glucose metabolism by skeletal muscle.
443
The glycemic index:
The glycemic index is a physiological measure that is used to predict
the effects of a source of digestible carbohydrate on blood glucose.
The glycemic index is calculated as the AUC of the blood glucose response
over a 2-hour period to the amount of carbohydrate ingested in a 100
g serving of a food expressed as a percentage of the response to a standard
(white bread or glucose solution) providing an equivalent amount of
carbohydrate. For example, the AUC for whole wheat bread is 811
compared to the AUC for an isocarbohydrate serving of white bread which
is 866. The glycemic index of whole wheat bread would then be
calculated as 0.94 (811/866) or 94%. A glycemic index of 94 means
that whole wheat bread will elicit a blood glucose response that is
94% of the response that would be observed with white bread over the
same time period. Glycemic response to a mixed meal can also be
estimated using the glycemic indices of the individual foods.
Each food is then weighted by the proportion of total carbohydrate it
contributes to the meal to obtain an estimate for the meal. The
percent difference among meal glycemic indices has been shown to accurately
predict the mean
incremental glycemic response areas for different mixed meals consumed by groups of subjects.
Specific effects of dietary
components on blood glucose control.
Carbohydrate:
Digestible carbohydrate contributes directly to glycemic load which
is the primary determinant of insulin response. Foods that provide
the largest glycemic loads are sources of carbohydrate that are readily
digested to soluble sugars, and then rapidly and completely absorbed.
The glycemic effects of simple sugars (disaccharides and monosaccharides)
can be predicted from differences in solubility in aqueous solutions.
Soluble sugars consumed in liquid form, e.g., beverages, will empty
from the stomach faster than the identical sugars consumed in solid
form and will thus reach the surface mucosal digestive enzymes sooner.
Simple sugars in solid form will solubilize more rapidly when consumed
from highly refined (processed) sources, e.g., candy, beverages, pastries,
processed cereals, jelly, and will be absorbed more rapidly than the
same simple sugars consumed in fruits and whole grain cereals where
solubility is reduced by the presence of dietary fiber. Sucrose
is the most soluble simple sugar while lactose (milk sugar) is the least
soluble. Fructose is relatively insoluble and contributes less
to an increase in plasma glucose than the equivalent amount of carbohydrate
consumed as sucrose. The presence of sodium will accelerate the
absorption of simple sugars in both liquid and solid form.
The glycemic effects of starches
or polysaccharides can be predicted primarily from differences in digestibility
which will determine how quickly the oligosaccharide and disaccharide
fragments are released from amylase activity and solubilized in intestinal
fluids. Starches are consumed from cereal grains (e.g., wheat,
corn, rice, barley, rye, oats), legumes (e.g., lentils, navy beans,
chickpeas), and vegetables (e.g., potato). Undigested starches
are less soluble than simple sugars, but if starch is consumed from
a refined source, it may be more quickly digested and thus solubilized
and absorbed faster than simple sugars consumed from a source rich in
dietary fiber. Not all processed starches are rapidly digested
and absorbed due to differences in molecular structure which can substantially
influence digestibility. Methods of processing that include extrusion
(pasta and cereal shapes), as well as exposure to high temperature followed
by cooling, promote a rearrangement of starch crystals such that the
glycosidic bonds become resistant to digestive enzymes (alpha-amylases).
A high content of amylopectin (branching) relative to amylose (straight
chain) will also facilitate digestion because the branch points of amylopectin
provide more available sites for amylase to act upon. Starches
from unprocessed or less processed sources are digested more slowly
than refined starches (e.g., whole wheat bread vs. white bread), and
thus more slowly absorbed, because of the higher amount of dietary fiber
present.
The glycemic effects of carbohydrate
sources that also contain dietary fiber are differentiated by the viscosity
of the fiber. Viscous dietary fibers are classified as soluble
fiber and include gums, pectins, mucilages, glucans, and hemicelluloses.
Soluble fiber has the greatest effect on slowing the rate of digestive
and absorptive processes. This type of dietary fiber forms a viscous
gel when mixed with the aqueous solutions that comprise gastric and
pancreatic fluids. Viscosity creates a barrier that reduces access
of the digestive enzymes to the food matrices. Soluble fiber also
increases the viscosity of the unstirred water layer adjacent to the
mucosal absorptive surface, thus slowing the rate of diffusion of disaccharides
and monosaccharides to the mucosal membranes where
digestive enzymes and membrane
transport systems are located. Soluble fiber is found in oats,
barley, citrus fruit, legumes, and psyllium.
Fat: Dietary
fat can reduce the glycemic load available from ingestion of digestible
carbohydrate by slowing gastric motility through stimulation of enterogastrone
secretion in the duodenum. A decrease in gastric motility will
delay gastric emptying, thus slowing the release of sugars available
to undergo digestion and absorption. These short-term effects
of fat may be offset by the long-term adverse effects of habitual high
fat intakes on insulin sensitivity. When consumed in large amounts,
dietary fat reduces insulin sensitivity by increasing fat stores.
Body fat as measured by body mass index has been significantly correlated
with dietary fat intake in both lean and obese adults. Insulin
sensitivity has also been related inversely to fat intake. High
fat diets apparently predispose to weight gain to a greater extent than
other energy sources at equivalent energy intakes when total energy
intake is moderate. This observation has been explained by differences
in fuel storage regulation between fat and carbohydrate. The rate
of carbohydrate oxidation increases as intake increases once glycogen
stores have been maximized because the capacity to store carbohydrate
as glycogen is limited. In contrast, fat oxidation does not have
to increase as intake increases to regulate the total body pool because
fat storage capacity is virtually unlimited.
Dietary fat can also affect
tissue sensitivity to insulin without weight gain or an increase in
body fat. A possible explanation is that high fat intakes proportionately
reduce the amount of carbohydrate consumed, and thus may reduce the
number of glucose transporters in the intracellular pool and down-regulate
insulin receptors. The composition of fat consumed may also influence
tissue insulin sensitivity. Because circulating fatty acids are
deposited in membrane phospholipids, membrane fatty acid composition
will reflect dietary fat composition. A high saturated fat content
in cell membranes will decrease membrane fluidity and adversely affect
recruitment of glucose transporters to the plasma membrane from the
intracellular pool. The number of glucose transporters measured
in rat adipocytes was higher in animals fed polyunsaturated fat than
in those fed saturated fat. Intakes of both monounsaturated fatty
acids and medium chain saturated fatty acids (coconut oil) can promote
insulin secretion. This effect of these fatty acids may be helpful
for controlling blood glucose among ��carbohydrate-sensitive�� individuals.
A significant proportion of diabetics are unable to decrease total fat
intake by proportionately increasing carbohydrate without an increase
in serum triglycerides and cholesterol. For these people, increasing
the proportion of monounsaturated fat ingested will allow a higher total
fat to be consumed without compromising insulin sensitivity.
Protein.
Insulin responsiveness to dietary protein is a function of its amino
acid composition. The ratio of insulin to glucagon determines
whether metabolism will favor increased (low ratio) or decreased blood
glucose (high ratio). The insulin to glucagon ratio also
controls accretion of lean body mass by favoring either protein synthesis
(high ratio) or catabolism (low ratio). It also influences cholesterol
metabolism by either stimulating (high ratio) or inhibiting (low ratio)
the activity of HMG-CoA reductase, the rate-limiting step of cholesterol
synthesis. Lysine has been shown to be particularly effective
in raising the ratio of insulin to glucagon in both animals and humans
while arginine appears to diminish the effect of lysine. Plant
protein sources tend to be lower in lysine and higher in arginine than
animal protein sources such as casein (cow��s milk).
Micronutrients.
Insufficient intakes of vitamins and minerals that support insulin function
and carbohydrate metabolism may also contribute to impaired glucose
tolerance. These micronutrients include chromium, potassium, magnesium,
and vitamin E. Chromium is required for normal glucose tolerance,
but the mechanism of its effect has not been identified. Tissue
chromium levels appear to decrease with age coincident with increased
glucose intolerance and risk of NIDDM. The requirement for chromium
is increased by high intakes of refined carbohydrate. Since the
primary dietary source of chromium is whole grains, replacement of whole
grain products with refined grain products will reduce chromium intake
while increasing requirements for the mineral.
Potassium and magnesium are
more involved with glucose metabolism than with direct effects on insulin
function. Potassium is a cofactor for phosphofructokinase, a rate-limiting
enzyme for glycolysis. Magnesium is required for oxidative metabolism
of glucose. It is unclear whether supplementation with these minerals
will improve glucose tolerance above the response to correction of the
deficiencies. Abnormal blood levels of copper, zinc, and magnesium
are frequently observed in individuals with diabetic complications,
but it is unknown whether these abnormalities are a cause or an effect
of the associated pathology. Low blood levels of chromium, magnesium,
potassium, and pyridoxine have been reported in pregnant women with
gestational diabetes. This condition is characterized by insulin
activity that is insufficient to balance the glucose-elevating effects
of the placental, pituitary, and adrenal hormones.
Vitamin E may improve glucose
tolerance by inhibiting membrane lipid peroxidation and thus preserving
membrane integrity. Optimal insulin tissue activity is observed
when cell membranes are enriched with polyunsaturated fatty acids.
The high degree of unsaturation in membrane lipids increases their fluidity
and also their vulnerability to oxidative damage. Plasma peroxides
have been measured at higher concentrations in diabetics than in controls.
A recent study reported significantly lower fasting and two-hour plasma
insulin, and a significant increase in nonoxidative glucose metabolism,
among postmenopausal women taking vitamin E supplements at doses of
900 IU/day.
Energy Intake and Distribution.
Excess energy intake can contribute to insulin resistance by increasing
the concentrations of glucose and fatty acids in circulation and by
contributing to increased body fat stores. Obesity has been associated
with both receptor and post-receptor defects in insulin function.
Abdominal obesity is more strongly related to insulin resistance than
gluteal or peripheral obesity. Hyperinsulinemia is more likely
to develop with abdominal obesity because hepatic insulin clearance
is inhibited by high concentrations of free fatty acids in the portal
circulation. The mobilization of free fatty acids from abdominal
fat depots also stimulates hepatic glucose production, which initiates
the metabolic cascade that begins with hyperglycemia and is followed
by establishment of hyperinsulinemia and down-regulation of insulin
receptors. Abdominal adipocytes also require significantly higher
levels of insulin to promote glucose uptake than peripheral adipocytes.
The increase in body fat associated
with aging occurs at the expense of skeletal muscle and is primarily
the result of decreased physical activity. Muscle mass enhances
insulin sensitivity because skeletal muscle accounts for the majority
of insulin-facilitated glucose uptake. Exercise also protects
against accumulation of fat stores by increasing energy expenditure.
Exercise enhances insulin sensitivity directly by lowering the km of
skeletal muscle glucose transporters both during activity and after
activity to replenish muscle
glycogen stores. Exercise
also enhances the mobilization of free fatty acids from adipocytes for
uptake by working (skeletal) muscle and favors fatty acids mobilization
from abdominal adipocytes. Thus abdominal fat is more responsive
to exercise resulting in a rapid improvement in insulin sensitivity
as a result of a decline in portal free fatty acid levels that inhibit
hepatic insulin clearance.
The pattern in which energy
is distributed throughout the day may also influence insulin sensitivity.
A high frequency of eating occasions (e.g., ��grazing��) is often
recommended to prevent the wide excursions in insulin levels between
fasting and postprandial periods. Since the post-prandial state
typically lasts 3-4 hours following ingestion of a meal, timing of eating
occasions at 3-4 hour intervals should stabilize delivery of glucose
during the day, provided that the total energy requirement is evenly
distributed and not exceeded, and the composition of the meal provides
a moderate to low glycemic load. Since post-prandial hyperinsulinemia
must be chronic to elicit glucose intolerance by down-regulating receptors,
frequent consumption of high glycemic loads could offset the benefits
of dividing total energy intake into frequent small evenly divided meals.
Author��S NOTE:
I have practiced Natural Health for approximately 35 years since I was graduated from the Albert Einstein College of Medicine444
, in 1970. Practicing Natural
and drug-free Psychiatry and drug free Primary Care Medicine during
that time I have come to expect ��near-miracles�� on a daily basis
as reliably diagnosed ��irreversible��, ��terminal�� and ��hopeless��
patients made their way to my office from around the world. Using
simple, but physiologically and biochemically profound, treatment options,
it has been my privilege and honor to preside over the change in status
from ��hopeless�� to ��radiantly well�� of thousands of patients.
I have been fortunate to have the tools in my hand to offer many other
patients (and, inevitably, friends and family members as well) the opportunity
to defy the customary expectations for health and longevity derived
from the statistics of an ailing and ill population. The results
have been gratifying in the extreme as people confronting illness and
death, or the sad decay which we mistakenly identify as ��normal ageing��
have chosen options for themselves of continuing robust and healthy
life in keeping with the genetic potential given to us all but foreshortened
for so many through poor nutrition and industrial toxicity.
It is possible for many, perhaps
most, people to enjoy robust good health in the midst of continuing
and escalating challenges to the detoxification and immune systems which
an increasingly industrial society and food supply present to us all
if inexpensive, simple, science-based and logical prevention and treatment
strategies are available to us.
If my experience were unique,
however, it would be of little concern. In fact, every doctor
and health care professional who has chosen to practice their profession
using
natural means to treat the
underlying causes of disease (as conventional Western Medicine cannot
do) has a similar clinical experience to which they can testify.
It is for that reason that the Revised Vitamin and Mineral Guideline has been endorsed by several eminent associations and organizations including
Biochemistry, Nutritional Science,
Integrative and Nutritional Medicine��s clinical practice and wisdom
all offer important guiding information in developing a framework in
which optimal nutrition can be supported in a population reducing the
joint burdens of the personal, social and economic cost of preventable
disease.
Consumers and their health
providers have the right, the need and the wisdom to make choices about
nutrients without governmental restraint or regulation provided only
that the nutrient is clean, unadulterated, and poses no unreasonable
threat. Within that framework, it is the right and the responsibility
of consumers and care givers to use that freedom wisely. If they
do not, however, the inherent lack of toxicity in nutrients protects
those who might be immoderate. No such protection rests in pharmaceuticals
which are usually toxic and, with appropriate or excessive use, often
cause disease and death. Nutrients are inexpensive and allow public
health systems to use the same amount of money spent on non-acute, non-emergency
care for the few and instead provide outstanding care for the many at
the same or smaller cost.
Rima E. Laibow, MD
Medical Director
Natural Solutions Foundation
1 http://www.fao.org/documents/show_cdr.asp?url_file=/DOCREP/005/AC911E/AC911E00.HTM
),
2 http://www.who.int/hpr/NPH/docs/who_fao_expert_report.pdf
, p12
3 Ibid
4 Price, W, DDS, Price, Nutrition and Physical Degeneration, 1945, Price-Pottenger Nutrition Foundation, San Diego, CA, (619) 574-7763
5 Ibid
6 http://www.westonaprice.org/traditional_diets/nasty_brutish_short.html
7 Watkins, B A, et al, "Importance of Vitamin E in Bone Formation and in Chrondocyte Function" Purdue University, Lafayette, IN, AOCS Proceedings, 1996
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20 Cohen, L A, et al, J Natl Cancer Inst ,1986, 77:43
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23 Sally Fallon, "Vitamin A Vagary," PPNF Health Journal, Price-Pottenger Nutrition Foundation, Summer 1995, 19 l
24 Evidence, B A, et al, Arterioscler Thromb, Vasc Biol, 1997, 17:1657-1661:(2):1-3 (619) 574-7763
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29 http://www.who.int/hpr/NPH/docs/who_fao_expert_report.pdf
, p. 18
30 Ibid
31 http://www.who.int/hpr/NPH/docs/who_fao_expert_report.pdf
, p. 14
32 http://www.who.int/hpr/NPH/docs/who_fao_expert_report.pdf
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33 http://www.scielosp.org/pdf/rpsp/v13n5/a15v13n5.pdf
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35 http://www.burtonreport.com/InfHealthCare/ManagedHlthCare.htm
36 http://www.lef.org/magazine/mag2004/mar2004_awsi_death_02.htm
37 http://www.huppi.com/kangaroo/L-healthcare.htm
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39 Leibovitz, B, Nutrition at the Cross Roads, JON 2(4), 1993
40 McDonald, A, Relationship of Nutrition to Prevention of Diseases, http://www.feinberg.northwestern.edu/nutrition/tools-resources/sbm.html
41 Ibid
42 Ibid
43 Erasmus, U., Fats that Heal Fats that Kill, Revised, Alive Books, Burnaby BC, 1993, p. 78
44 It should be noted that there are people in whom hypertension results when renal excretory capacity is excessive. The compensatory mechanism in these people is an increase in aldosterone and resultant hypertension which is responsive to an increase in sodium.
45 http://www.natap.org/2003/DDW/day10.htm
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49 Ibid
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53 Ibid, preface.
54 Ibid. p. 2
55 Ibid. p. 5
56 Ibid.
57 130106 FAO WHO risk assessment full_report.pdf
58 Ibid. p. 18
59 Ibid. p. 12
60 Ibid. p. 13
61 Ibid. p. 15
62 Ibid. p. 14
63 Ibid. p. 17
64 Ibid. p. 17
65 Ibid. p. 18
66 Ibid. p.18
67 Ibid. p. 19
68 Ibid.
69 Ibid.
70 Ibid. p. 20
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94 Barbul A, Lazarou SA, Efron DT, et al. Arginine enhances wound healing and lymphocyte immune responses in humans.
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95 De Bandt JP, Coudray-Lucas C, Lioret N, et al. A randomized controlled trial of the influence of the mode of enteral ornithine alpha-ketoglutarate administration in burn patients.
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96 Cynober L. Ornithine alpha-ketoglutarate in nutritional support.
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99
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103
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104 Ibid
105 Ibid
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107 Alvarez OM, Gilbreath RL. Effect of dietary thiamine on intermolecular collagen cross-linking during wound repair: a mechanical and biochemical assessment
.
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114 Ringsdorf WM Jr, Cheraskin E. Vitamin C and human wound healing.
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115 Bartolomucci E. Action of vitamin E on healing of experimental wounds on parenchymatous organs.
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126 Barbul A, Lazarou SA, Efron DT, et al. Arginine enhances wound healing and lymphocyte immune responses in humans.
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127 Barbul A, Rettura G, Levenson SM, et al. Wound healing and thymotropic effects of arginine: a pituitary mechanism of action.
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128 Kirk SJ, Hurson M, Regan MC, et al. Arginine stimulates wound healing and immune function in elderly human beings.
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136 http://www.who.int/dietphysicalactivity/publications/facts/cvd/en/
137 http://www.thecureforheartdisease.com/owen/HeartCure.htm
138
See pp. 2-5 of this document for a discussion of this important issue.
139
http://www.who.int/dietphysicalactivity/publications/facts/cvd/en/
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p. 81
141 Ibid
142 Ibid
143 Grundy et al. Assessment of Cardiovascular Risk, J Am Coll Cardiol 1999;34:1348--59
144 Lowe, L, Greenland, P, Ruth, K, Dyer, A, Stamler, R Stamler, J, Impact of Major Cardiovascular Disease Risk Factors, Particularly in Combination, on 22-Year Mortality in Women and Men , Arch Intern Med. 1998;158:2007-2014.
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146 http://www.internetwks.com/owen/Synopsis.pdf
147 http://www.nutraingredients.com/news/news-ng.asp?n=56749-high-dose-vitamin
148 http://www.thecureforheartdisease.com/owen/suppress.htm
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150Diabetes Control and Complications Trial, 1995 http://diabetes.niddk.nih.gov/dm/pubs/control/#what%20is
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152 http://www.eurodiabesity.org/
153 http://www.shapeup.org/diabesity.html
154 http://www.annecollins.com/obesity/diabetes-diabesity.htm
155 http://www.medicineau.net.au/clinical/diabetes/diabete2262.html
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160 Lehr, Hans-Anton, et al. Protection from oxidized LDL-induced leukocyte adhesion to microvascular and macrovascular endothelium in vivo by vitamin C but not by vitamin E. Circulation, Vol. 91, No. 5, March 1, 1995, pp. 1525-32
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174 Weber, Christian, et al. Op. Cit.
175 Lehr, Hans-Anton, et al. Protection from oxidized LDL-induced leukocyte adhesion to microvascular and macrovascular endothelium in vivo by vitamin C but not by vitamin E. Circulation, Vol. 91, No. 5, March 1, 1995, pp. 1525-32
176 Gale, Catherine R., et al. Vitamin C and risk of death from stroke and coronary heart disease in cohort of elderly people. British Medical Journal, Vol. 310, June 17, 1995, pp. 1563-66
177 Woodhouse, P.R. and Khaw, Kay-Tee. Seasonal variations in vitamin C status, infection, fibrinogen and cardiovascular disease - Are they linked? Age and Ageing, Vol. 23, Supplement No. 2, 1994, p. P5
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