Session 105 Notes - Alaska Chiropractic Society

Transcription

Natural Methods to address the “Mayo Clinic Top Ten Health Threats”
Western Mediterranean Cruise 2011
October 22‐29
Liberty of the Seas (RC)
www.continuingeducation.net
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Mayo Clinic Health Threat #1 for Men and Women: Heart Disease
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•As of 2007, it is the leading cause of death in the United States, England, Canada and Wales, killing one person every 34 seconds in the United States alone. •Heart disease is responsible for 40 percent of all the deaths in the United States, more than all forms of cancer combined.
# 1 Division of Vital Statistics; Arialdi M. Miniño, M.P.H., Melonie P. Heron, Ph.D., Sherry L. Murphy, B.S., Kenneth D. Kochanek, M.A. (2007‐08‐21). "Deaths: Final data for 2004" (PDF). National Vital Statistics Reports (United States: Center for Disease Control) 55 (19): 7. http://www.cdc.gov/nchs/data/nvsr/nvsr55/nvsr55_19.pdf. Retrieved 2007‐12‐30. # 2 White House News. "American Heart Month, 2007". http://georgewbush‐
whitehouse.archives.gov/news/releases/2007/02/20070201‐2.html. Retrieved 2007‐07‐16. # 3 National Statistics Press Release 25 May 2006
# 4 Hitti, Miranda (2004‐12‐07). "Heart Disease Kills Every 34 Seconds in U.S.". Fox News – WebMD. http://www.foxnews.com/story/0,2933,142436,00.html. Retrieved 2007‐12‐30.
Heart disease symptoms caused by abnormal heartbeats (heart arrhythmias)
* A fluttering in the chest
* A racing heartbeat (tachycardia)
* A slow heartbeat (bradycardia)
* Chest pain
* Shortness of breath
* Lightheadedness
* Dizziness
* Fainting (syncope) or near fainting
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Heart disease symptoms caused by heart defects
Serious congenital heart defects usually become evident during the first few hours, days, weeks and months of life. Heart defect symptoms could include:
* Pale gray or blue skin color (cyanosis)
* Swelling in the legs, abdomen or areas around the eyes
* Shortness of breath during feedings, leading to poor weight gain
Less‐serious congenital heart defects are often not diagnosed until later in childhood, or even adulthood. Signs and symptoms of congenital heart defects that usually aren't immediately life‐
threatening include:
* Easily becoming short of breath during exercise or activity
* Easily tiring during exercise or activity
* Built‐up fluid in the heart or lungs
* Swelling in the hands, ankles or feet
Heart disease symptoms caused by thick heart muscle (cardiomyopathy)
In early stages of cardiomyopathy, there may be no symptoms. As the condition worsens, cardiomyopathy symptoms include:
* Breathlessness with exertion or even at rest
* Swelling of the legs, ankles and feet
* Bloating (distention) of the abdomen with fluid
* Fatigue
* Irregular heartbeats that feel rapid, pounding or fluttering
* Dizziness, lightheadedness and fainting
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Heart disease symptoms caused by heart infections
There are three types of heart infections: pericarditis, which affects the tissue surrounding the heart (pericardium); myocarditis, which affects the muscular middle layer of the walls of the heart (myocardium); and endocarditis, which affects the inner membrane that separates the chambers and valves of your heart (endocardium). Varying slightly with each type of infection, heart infection symptoms can include:
* Fever
* Weakness or fatigue
* Swelling in your legs or abdomen
* Changes in your heart rhythm
* Dry or persistent cough
* Skin rashes or unusual spots
Heart disease symptoms caused by valvular heart disease
The four valves — the aortic, mitral, pulmonary and tricuspid valves — may be damaged by a variety of conditions leading to narrowing (stenosis), leaking (regurgitation or insufficiency) or improper closing (prolapse). Depending on which valve isn't working properly, valvular
heart disease symptoms generally include:
* Fatigue
* Irregular heartbeat or heart murmur
* Swollen feet or ankles
* Chest pain
* Fainting (syncope)
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Heart disease risk factors include: •Your age. Simply getting older increases your risk!
•Your sex. Men are generally at greater risk of heart disease. However, the risk for a woman increases after menopause. •Family history. A family history of heart disease increases your risk of coronary artery disease.
•Smoking. Nicotine constricts your blood vessels, and carbon monoxide can damage their inner lining, making them more susceptible to atherosclerosis.
•Poor diet. We can debate the individual factors but not the overall effect of bad diet!
•High blood pressure. Uncontrolled high blood pressure can result in endothelial damage.
•Aberrant lipid profile. Please read “Good Calories, Bad Calories” by Gary Taubes!!!
•Diabetes. Diabetes increases your risk of heart disease. Both conditions share similar •Obesity. Excess weight typically worsens other risk factors. •Physical inactivity. Lack of exercise also is associated with many forms of heart disease and some of its other risk factors, as well. •High stress. Unrelieved stress in your life may damage your arteries as well as worsen other risk factors for heart disease. •Poor hygiene. Not regularly washing your hands and other habits that can help prevent viral or bacterial infections can put you at risk of heart infections, especially if you already have an underlying heart condition. Researchers also believe poor dental health may contribute to heart disease. Tests and diagnosis
•Blood tests
•Chest X‐ray
•Electrocardiogram •Holter monitoring. A Holter monitor is a portable device that you wear to record a continuous ECG, usually for 24 to 72 hours. Holter monitoring is used to detect occasional heart rhythm irregularities that aren't found during a regular ECG exam.
•Echocardiogram
•Cardiac catheterization
•Heart biopsy
•Cardiac computerized tomography (CT) scan. This test is often used to check for heart failure or heart arrhythmias
•Cardiac magnetic resonance imaging (MRI).
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NUTRITION
• Antioxidants: vitamin C (1,000 mg tid), vitamin E (400 IU/day),
selenium (200 mcg/day)
• Coenzyme Q10: (30 to 50 mg tid) antioxidant, increases oxygenation of
tissue, including heart muscle (Better: Ubiquinone)
• Essential fatty acids: (1,500 mg bid) anti-inflammatory
• Garlic, ginger and onions all have a beneficial effect on platelet
aggregation. Increase fiber (especially water-soluble), fruits,
vegetables, and vegetarian sources of protein. Increase potassium and
decrease sodium in the diet.
• Homocysteine metabolism: Folic acid (800 mcg/day), B6 (50 mg/day),
B12 (400 mg/day), betaine (200 to 1,000 mg/day)
• Magnesium: (500 mg) mild vasodilation, decreases vascular resistance
• Taurine: (500 mg bid) enhances cardiac efficiency, mild diuretic
• Carnitine: (750 to 1,500 mg bid) important in fatty acid metabolism,
increases efficiency of cardiac function
Protocol: Discuss DIET and EXERCISE, of course!
Catalyn: 6
Cardio-Plus: 6- 9
Vitanox: 2-4
Hawthorn: 3
Folic Acid-B12: 2
B6-Niacinamide: 1
---------consider the following on a case basis:
Biost: 3
Cataplex B: 6
Betacol: 3
Renafood: 3
Organically Bound Minerals: 6
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Mayo Clinic Health Threat #2 for Men and Women: Cancer
•Cancer may affect people at all ages, even fetuses, but the risk for most varieties increases with age. •Cancer causes about 13% of all human deaths. According to the American Cancer Society, 7.6 million people died from cancer in the world during 2007. •Cancers can affect all animals.
•Nearly all cancers are caused by abnormalities in the genetic material of the transformed cells. These abnormalities may be due to the effects of carcinogens, such as tobacco smoke, radiation, chemicals, or infectious agents. •Other cancer‐promoting genetic abnormalities may be randomly acquired through errors in DNA replication, or are inherited, and thus present in all cells from birth. •The heritability of cancers is usually affected by complex interactions between carcinogens and the host's genome. •New aspects of the genetics of cancer pathogenesis, such as DNA methylation, and microRNAs are increasingly recognized as important.
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Genetic abnormalities found in cancer typically affect two general classes of genes. •Cancer‐promoting oncogenes are typically activated in cancer cells, giving those cells new properties, such as hyperactive growth and division, protection against apoptosis (programmed cell death), loss of respect for normal tissue boundaries, and the ability to become established in diverse tissue environments. •Tumor suppressor genes are then inactivated in cancer cells, resulting in the loss of normal functions in those cells, such as accurate DNA replication, control over the cell cycle, orientation and adhesion within tissues, and interaction with protective cells of the immune system.
PDF version at www.ompress.com
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Seven Characteristics of Cancer and Seven Strategies (Boik)
1. Induction of genetic instability. Each cancer cell carries within itself genetic instability, and this instability increases the chances the cell will be able to mutate as needed to adapt to its environment.
2. Abnormal expression of genes. In essence, the function of genes is to make proteins—a process called gene expression. When they are expressed, some genes produce proteins that inhibit cancer progression, and others produce proteins that facilitate it. In cancer cells, abnormal expression of genes occurs, resulting in too few proteins that inhibit cancer and too many that facilitate it.
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3. Abnormal signal transduction. Signal transduction is the movement of a signal from outside the cell toward the cell’s nucleus, where it can stimulate proliferation or other activities. •One important source of external signals comes from growth factors. Growth factors are soluble molecules that bind to specific receptors on the cell’s surface and stimulate the cell’s activities. •A second source of external signals comes from cell adhesion molecules (CAMs). Cells interact with their environment through CAMs located on their surface. Cell adhesion molecules are proteins that act like fingers to regulate the degree of contact with other cells and tissues and inform cells of their surroundings. •Other factors are also involved in signal generation and signal transduction. For example, cancer cells can produce their own growth factors, thereby allowing self‐stimulation; they can produce extra receptors for growth factors; and they can produce free radicals, which can make growth factor receptors more responsive to stimulation.
4. Abnormal cell‐to‐cell communication. By decreasing their contact with normal cells, cancer cells are freed to act independently. As mentioned previously, cell‐to‐cell communication occurs via portals between adjacent cells (gap junctions) and through cell adhesion molecules. Normal cell‐to‐cell communication through gap junctions maintains homeostasis and discourages cancerlike behavior. Normal CAM activity keeps cells in place and prevents signal transduction that may be initiated by abnormal CAM activity.
5. Induction of angiogenesis. Angiogenesis is the growth of new blood vessels toward and within tumors (or other tissues). Solid tumors require angiogenesis in order to grow. Tumors need blood vessels to supply oxygen and nutrients, and the blood vessels created by angiogenesis provide the channel by which tumor cells metastasize to distant locations.
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6. Invasion and metastasis. Tumors can spread both locally, via invasion of adjacent tissues, and distantly, via metastasis through the blood and lymph circulation. The spread of cancer, along with uncontrolled proliferation, is a central hallmark of malignancy.
7. Immune evasion. Cancer cells shield themselves from immune attack, thereby evading destruction; they can hide from immune cells by employing various camouflaging techniques or can produce immunosuppressive compounds that impair the ability of immune cells to function.
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Seven Strategies to “reverse” the Seven Characteristics:
1. Reduce genetic instability. Genetic instability is aggravated by oxidative stress (stress caused by free radicals). Cancer cells exist in an oxidative environment, and although such an environment kills some cells, many continue to survive. As oxidative stress increases, the declining population of surviving cells exhibits greater instability and higher mutation rates, in theory eventually producing more aggressive and successful cancers. Thus one way of reducing genetic instability is by reducing oxidative stress. “RedOx”
• The term redox comes from the two concepts of reduction and oxidation. It can be explained in simple terms:
– Oxidation describes the loss of electrons / hydrogen or gain of oxygen / increase in oxidation state by a molecule, atom or ion
– Reduction describes the gain of electrons / hydrogen or a loss of oxygen / decrease in oxidation state by a molecule, atom or ion
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What’s a “free radical”?
•In chemistry, radicals (often referred to as free
radicals) are atoms, molecules, or ions with
unpaired electrons on an otherwise open shell
configuration.
•These unpaired electrons are usually highly
reactive, so radicals are likely to take part in
chemical reactions.
•Radicals play an important role in combustion,
atmospheric chemistry, polymerization, plasma
chemistry, biochemistry, and many other
chemical processes, including human physiology.
•For example, superoxide and nitric oxide regulate
many biological processes, such as controlling
vascular tone.
•The first organic free radical identified was
triphenylmethyl radical, by Moses Gomberg in
1900 at the University of Michigan.
Moses Gomberg, the founder of radical chemistry (1866‐1947)
The electron transport chain in the mitochondrion is the site of oxidative
phosphorylation in eukaryotes. The NADH and succinate generated in the
citric acid cycle is oxidized, providing energy to power ATP synthase.
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The LIVER produces large quantities of free radicals in the very process of detox!!! The Oxidant Defense System
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Seven Strategies to “reverse” the Seven Characteristics:
2. Inhibit abnormal expression of genes. One way that gene expression can be normalized is through modifying the activity of transcription factors. Transcription factors are proteins that act as switches in the nucleus to turn on gene expression. Genes that inhibit cancer progression are commonly underexpressed in cancer cells, and genes that facilitate cancer are commonly overexpressed. Therefore, cancer can be inhibited by normalizing the activity of those transcription factors that control the expression of these genes. 3. Inhibit abnormal signal transduction. The movement of a signal from outside the cell toward the nucleus relies on several proteins (including kinase enzymes and ras proteins, discussed later), and so signal transduction can be inhibited by blocking the actions of these proteins; using natural compounds. Signal transduction is a normal process needed by healthy cells, but in cancer cells the volume of signal transduction is excessive, and the signals that flow favor proliferation and spread. Thus the intent is not to eliminate signal transduction but to bring it down to normal levels.
4. Encourage normal cell‐to‐cell communication. Normal cell‐
to‐cell communication can be fostered by improving gap junction communication and by normalizing CAM activity. 18
5. Inhibit tumor angiogenesis. Like signal transduction, angiogenesis is a normal process; it is needed during wound healing and in other situations. Angiogenesis in tumors, however, unlike that in normal conditions, is uncontrolled and ongoing. Our intent then is not to eliminate angiogenesis but to normalize its occurrence by normalizing the factors that control it. Angiogenesis is most successful if certain chemicals called angiogenic factors are present, as well as certain environmental conditions, such as hypoxic (low‐oxygen) ones. Cancer can be inhibited by blocking the release or action of angiogenic factors or by otherwise altering the local environment to inhibit tumor angiogenesis. 6. Inhibit invasion and metastasis. Invasion requires enzymatic digestion of the healthy tissue surrounding the tumor. It also requires the migration of tumor cells. Invasion can be reduced by inhibiting enzymes that digest local tissues, by protecting normal tissues from the enzymes, and by reducing the ability of tumor cells to migrate. Metastasis requires that cells detach from the primary tumor, enzymatically digest blood vessel walls to gain access to and exit from the blood circulation, and evade the immune system while in the circulation. Thus metastasis can be checked by inhibiting any one of these processes. 7. Increase the immune response. The immune response against cancer cells can be increased by stimulating the immune system and by reducing the ability of cancer cells to evade immune attack. Both actions are best taken in tandem, since without prevention of immune evasion, immune stimulation will have little benefit; healthy, vital immune cells can destroy cancer cells, but only if the cancer cells can be recognized as foreign to the body.
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PMG’s
• PMG Theory: “Protomorphology: The
Principles of Cell Auto-Regulation”
(1947)
y Products released in the early 1950’s
y 23 individual and 3 combination
products
y Virtually every tissue type is supported!
Dr. Lee’s PMG Theory was derived from
(and verified by) the work of many others.
•Allelocatalyst - T.B. Robertson
•Cytost - F.. Turck
•Archusia/Ergusia - M.T. Burrows
•Mycrozyma - Antoine Bechamp
•Proteinogen - J.H. Northrup
•Protogene - G.W. Beadle
•X-Substance - Mast and Pace
•Biophores - M.R. Drennan
•Heat stable growth inhibitor - Alexis Carrel
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The “Mysteries” of Growth
Lee’s Protomorphogen Theories
Theory #2
PMG's released
PMG+
Antigen/antibody
complex
"NTA"
Theory
#1
+
Mast
Cell
Histamine release
Exogenous
PMG’s
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Biost®
Cardiotrophin PMG®
Dermatrophin PMG®
Drenatrophin PMG®
Hepatrophin PMG®
Hypothalamus PMG®
Mammary PMG®
Myotrophin PMG®
Neurotrophin PMG®
Oculotrophin PMG®
Orchic PMG®
Ostrophin PMG®
Ovatrophin PMG®
Pancreatrophin PMG®
Paraplex®
Parotid PMG®
Pituitrophin PMG®
Pneumotrophin PMG®
Prostate PMG®
Renatrophin PMG®
Spleen PMG®
Symplex F®
Symplex M®
Thymus PMG®
Thytrophin PMG®
Utrophin PMG®
A Synopsis of PMG Links with Cancer
1. Cancer seems to be associated with extraordinary concentrations of
PMG’s in the local tissue fluids.
2. The Phospholipid “wrapper” tends to prevent this local accumulation
from becoming carcinogenic
3. Irritation assists in the local accumulation of PMG and thus may
lead to cancer.
4. X-Rays and carcinogenic hydrocarbons have been shown to dissolve
the “wrapper”, thus leading to cancer.
5. A strong immune system is essential to remove the high local
[PMG] via Natural Tissue Antibody activity.
6. Cancer cells possess a strong depolymerizing effect that dedifferentiates cells to the point of embryonic competence and which
prevents the subsequently produced PMG from acting as an
antigen.
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A Synopsis of PMG Links with Cancer
7. Cancer cell PMG’s seem to have “mutated”, thus giving rise to
aberrant tissue.
8. A virus is undoubtedly involved and either causes the PMG mutation
or it IS the mutated PMG!
9. The intense local accumulation of PMG in cancerous tissue does
NOT inhibit mitosis (as it does in normal cells) because:
a. PMG regulation mechanisms are altered.
b. There are factors which depolymerize intracellular PMG,
thus preventing the normal feedback between intra and
extracellular concentrations of PMG.
c. Cancer cell PMG is heterologous to normal PMG, thus
cancer cells are not inhibited by it.
Lee’s “Clinical Considerations in the Handling of
Cancer Patients”
According to the book ”Protomorphology” there is in cancer
a lack of cell blueprints or protomorphogens. As a result the cell
division goes on without the proper control. There is an
imbalance between the protomorphogens of specific tissue
(which promote repair and normal growth) on the one hand and
natural tissue antibodies (which regulates this protomorphogen
function) on the other. If the patient has an excess number of
natural antibodies to any specific tissue there will then be a
regression or atrophy of that tissue. The growth that would
predominate in that particular tissue then would be of an
uncontrolled variety.
The following factors would have some bearing upon the
promotion of protomorphogen function. They would also have
an inhibiting action upon excess amounts of natural antibodies.
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PROTOMORPHOGENS3rotomorphogens of any specific
type of tissue, that can be taken by mouth, will normalize
excessive amounts of natural tissue antibodies of that same
tissue. This would reestablish proper growth and repair with
control.
THE LIVER Kasper Blond, M.D., in his book, THE LIVER
AND CANCER says the patient does not die of cancer but
from liver failure. Max Gerson, M.D., in his book, “A
CANCER THERAPY”, discusses liver regeneration and aims
a large part of his therapy at that key organ. Many doctors
claim the human body cannot develop cancer unless the blood
stream is toxic from partial liver failure. With these
statements in mind the doctor can recognize the important
role that the use of Hepatrophin will play in the regeneration
of that organ.
Garlic, Onions And Prostate Health 11/09/02
Eating lots of onions, garlic, scallions and shallots may not do much for a
man's popularity, but it could help him avoid prostate cancer. A study
published in the Journal of the National Cancer Institute finds that a diet
rich in foods from the allium group may cut the risk of prostate cancer in
half. The study looked at the dietary habits of men in Shanghai,
China. The location was chosen because China has the lowest prostate
cancer rate in the world, The Associated Press reports. Researchers from
the National Cancer Institute interviewed 238 men who had prostate
cancer and 471 men who did not and asked how often the men ate 122
food items. Men who reported eating more than one-third of an ounce
per day of garlic, onions, shallots or scallions were about half as likely to
have prostate cancer than men who ate less of those foods. This was true
regardless of the men's body size, how many calories they took in, and
what other foods they ate. Scallions appeared to offer the most
protection; men who ate one-tenth of an ounce or more per day had a 70
percent lower risk of prostate cancer. The researchers note that the
amount of allium vegetables needed for prostate cancer protection was
very small -- as little as one clove of garlic per day. They say their
findings need to be replicated in another study before allium vegetables
should be recommended to lower a man's risk of prostate cancer, the AP
says.
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Herbal Protocol for Enhanced
Hepatic Detoxification
♦
♦
♦
♦
♦
♦
♦
Cynara scolymus
A,C
core herbs
Silybum marianum
A,B,C
Schizandra chinensis
B,D
Taraxacum officinale
A,B
Rosmarinus officinalis D
select from
Curcuma longa
A,D
Allium sativum
D
A= choleretic B = hepatoprotective
C = hepatic trophorestorative D = Phase I/II or Phase
II
[Super-EFF] This will supply the phospholipid wrapper
material that protects the protomorphogen and in fact, the
whole cell chromosome. Its use is essential in all degenerative
conditions. This material is supplied to the body in natural fats
but it is destroyed by hydrogenation. Aluminum has a great
affinity for phosphorus and will break down this phospholipid
complex, exposing cell chromosomes to attack and
destruction. Aluminum gets into the body through the use of
aluminum utensils, aluminum in some baking powders and
aluminum in some deodorants.
IODINE This will activate the thyroid gland and hence the
production of Thyroxine. Thyroxine is known as a
protomorphogen releasing factor. When the protomorphogens
are released for action this immediately causes cell division,
growth and repair. …..
[Prolamine Iodine, Trace Minerals-B12]
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PAROTID PROTOMORPHOGEN Since the Parotid has a
definite place in the Thyroxine-Protomorphogen cycle, its
indicated purpose is to aid in the combining of a released
protomorphogen (by Thyroxine) with new protein from the
food to form specific repair cells; that is, the replacing of
abnormal tissue with normal tissue.
POTASSIUM AND SODIUM These salts are vitally important
to the cancer patient. Their apparent function is to maintain a
normal mineral balance of the body. This mineral balance is
absolutely essential in order to keep the protomorphogens in
solution and active in the body fluids. Potassium salts are found
in green leafy vegetables and in vegetable juices. It is also
available in high concentration in [Organically Bound
Minerals]. Sodium salts are available in Organic Sea Salt.
BODY FLUID pH The pH of the body tissues is also an
important item in maintaining proper protomorphogen
presence in body fluids. The majority of cancer patients are
alkaline (or acid) and must balance their proper body
chemistry with the proper mineral. The pH can be checked
in urine and saliva by using Hydrion Papers ranging from
4.0 to 9.0 and 7.0 to 8.0 respectively. Most doctors consider
the urine pH to be best at 6.3 to 6.8 and the saliva at 7.0 to
7.5. If the urine becomes too alkaline, kidney stones may
form. If it is too acid, uric acid crystals will form.
VITAMIN C COMPLEX Our Cataplex C has factors high in
Tyrosinase. Tyrosinase is organic copper and it is essential to
support the adrenals under this time of stress. [Note: Use
Drenamin]
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LIPOTROPIC B FACTORS These are important since they
help the liver metabolize fats and cholesterol and promote
the liver activity of blood detoxification. They have the
multiple purpose of improving circulation, relaxing nerves,
improving the healing rate and metabolizing the fats in the
liver. They are available in Cataplex G and [Betacol].
ALKALOSIS AND ACIDOSIS If the body is too alkaline
after the pH test is made it can be swung to the acid side by
using Cal-Amo. Vinegar made from apples can also be used.
If it is too acid more alkaline foods can be eaten and selected
from the Acid-Alkaline Food Chart. [Organically Bound
Minerals] will also aid in making the body fluids more
alkaline.
ADRENAL FUNCTION Some doctors put their cancer patients
on a salt-free diet as a part of the therapy. To arrive at a balance
between sodium and potassium by starving the patient for sodium
chloride is obviously the wrong way to go about this problem.
Sodium is necessary to support the adrenal glands. Sufficient
adrenal function is essential for normal healing and repair. A
better approach is to let the patient have all the salt they crave and
balance it up with the proper amount of high potassium foods and
concentrates.(Organically Bound Minerals)
BILE STASIS If the gall bladder does not function effectively the
elimination of toxic materials by the bile route is reduced. Bile is
also needed to aid in the assimilation of the fatty acid vitamins
and fats in the diet. The use of A-F Betafood will promote fluidity
of bile. Betafood is much more effective here than betaine alone.
This well illustrates clinically the importance of natural
concentrates with their natural synergists.
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TADPOLE EXPERIMENT Iodine is needed by the thyroid
gland to produce thyroxine. An experiment that emphasizes the
ability of thyroxine to release protomorphogens can be
accomplished by adding thyroxine to water that contains
tadpoles. When this is done the tadpoles in any stage of growth
will immediately develop into frogs regardless of size, showing
that thyroxine releases the cell blueprint or protomorphogens
which in turn activate the maturity, growth, and development of
the organism. This is also true of the repair and regeneration of
glands in the human body, when ample protomorphogen
stimulation release is accomplished. The importance of iodine
in the treatment of cancer has been recognized and tabulated
from scientific and clinical data by F. E. Chidester in his book,
“NUTRITION AND GLANDS IN RELATION TO
CANCER”. Many references to the merits of iodine can be
found in this volume.
PMG Cycles
“Wrapped” in
phospholipid coating
PMG’s
Released by cells
Gonads
Connective Tissue
1. PMG’s stimulate production of CT
2. PMG’s adsorbed on CT (storage)
Elimination Cycle
(Urine-Bile-Lungs)
PMG Released by Elutogenic Factors
1. Estrogen/Testosterone
2. Epithelial Fibrinolysin
3. Thyroid Hormones
4. Blood Trypsin
Local Growth
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Nutritional Support for Cancer
Catalyn – 6
Cataplex D -- 2
Super EFF -- 2
Albaplex -- 3
Betacol – 3
Silymarin Tablets -- 3
Drenamin -- 3
Prolamine Iodine – 1+ (see Iodine discussion!)
Parotid PMG -- 1
Specific PMG –3
Epimune Complex -- 2
Cat’s Claw Forte– 3
Gotu Kola Complex -- 3
Burdock Complex – 3
Ganoderma-Shiitake Mushroom--3
Vitanox– 3-6
Mayo Clinic Health Threat #3 for Men #6 for Women: Injuries
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Phases of Tissue Healing
The healing process is divided into three overlapping
phases:
Inflammatory phase
Proliferative phase
Remodelling or maturational phase
Porth CM. Pathophysiology 7th Ed. Lippincott Williams and Wilkins, Philadelphia, 2005
Inflammatory Phase
Begins at the time of injury
Results in a vascular response leading to fluid
exudate → edema
This facilitates a cellular response characterized by
the infiltration of phagocytic WBCs that digest and
remove invading organisms, fibrin, and extra-cellular
debris
After several days, recruited cells produce a range of
growth factors and cytokines that promote the next
phase
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Proliferation Phase
Begins several days after injury
Primarily involves the generation of repair material
and, for the majority of musculoskeletal injuries,
involves the production of scar tissue
Involves the generation of repair cells,
the most important of which are the
fibroblasts
Fibroblasts are connective tissue cells
that synthesize and secrete collagen
Proliferation Phase
Fibroblasts also produce glycosamino-glycans and
proteoglycans needed for the “ground substance”
They also produce a range of growth factors that
induce angiogenesis and endothelial cell
proliferation and migration
Fibroblastic production of new collagen is oxygen
dependent and low tissue oxygen will limit the
efficacy of the process
Watson T. SportEX Med 2006; 28: 8-12
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Proliferation Phase
Angiogenesis is essential in the
production of collagen as it ↑ local
blood flow and thus ↑ oxygen
availability → enabling the
fibroblasts1
Myofibroblasts derived from fibroblasts are
responsible for wound contraction and early
strength of the repair2
1
2
Li WW et al. Adv Skin Wound Care 2005; 18(9): 501-502
Watson T. SportEX Med 2006; 28: 8-12
Remodelling Phase
Begins approximately 3 weeks after injury and can
continue for 6 months or longer
There is continued remodelling of
scar tissue by the simultaneous
synthesis of collagen and lysis
by collagenase enzymes
Resulting in changes in the
architecture of the repair to ↑ tensile strength
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Factors That Inhibit Healing
Malnutrition
Vit C deficiency results in improper
amino acid sequencing and collagen
synthesis by products are not
removed from cells
Zn deficiency results in poor cellular
proliferation
Protein deficiency prolongs the inflammatory
process and impairs the proliferation phase by
impairing fibroblast proliferation, collagen synthesis
and angiogenesis
MacKay D, Miller AL. Altern Med Rev 2003; 8(4): 359-376
Factors That Inhibit Healing
Poor Blood Flow
For healing to occur, wounds and
injuries must have adequate blood
flow to supply the necessary
nutrients and to remove waste
such as debris, toxins and bacteria
Arterial disease and venous pathology are well
known causes of impaired wound healing
As mentioned fibroblastic production of new
collagen is oxygen dependent and the blood carries
the oxygen
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Key Herbs
There is good evidence for several herbs that can
assist in all the phases of tissue healing
These include:
• Gotu Kola
• Standardized extract of Ginkgo
• Grape Seed
Gotu Kola
The actions associated with Gotu Kola are:
Vulnerary
Anti-inflammatory
Depurative
Adaptogenic
Nervine tonic
Bone K. A Clinical Guide to Blending Liquid Herbs. Churchill Livingstone, USA, 2003,
pp. 254-260.
35
Gotu Kola
This is the most extensively studied herb in the
clinical management of the healing process
The key constituents are the
triterpenoids such as asiaticoside
The science is supported by the
use of the aerial parts of Centella
asiatica in both TCM and Ayurvedic
medicine to promote tissue healing
Bone K. A Clinical Guide to Blending Liquid Herbs. Churchill Livingstone, USA 2003, pp.
254-260.
Gotu Kola and Collagen
Synthesis
Several pharmacological studies indicate the
mechanism of action behind the tissue healing
activity of Gotu Kola
Oral administration of either Gotu Kola extract or
the triterpenes of Gotu Kola have demonstrated an
↑ rate of collagen synthesis
and maturation of collagen →
improved strength of scar
tissue in dermal wounds
Vogel HG et al. Acta Therapeut 1990; 16: 285
Suguna L et al. Indian J Exp Biol 1996; 34(12): 1208-1211
36
Gotu Kola: The Healer
Early European Research
Research in the 1980s showed
benefit in healing gastric and
duodenal ulcers1
Early French and Italian clinical
research (1960s and 1970s) demonstrated good
healing rates in refractory cases of:
• skin and leg ulcers2
• episiotomies3
1
2
3
Rhee JC, Choi KW. Korean J Gastroenterol 1981; 13(3): 5-40
Huriez CL. Lille Med 1972; 3(Supp 17): 574-579
Castellani L et al. Bull Fed Soc Gynecol Obstet Lang Fr 1966; 18(2): 184-186
Early European Research
• corneal wounds1
• surgical wounds2
Beneficial effects were also
noted in 20 children with
scleroderma in Spanish research3 and also in
adults4,5
1
2
3
4
5
Marcone GJ, Esposito RJ, Dias CA. Arch Oftalmol B Aires 1962; 37: 233-239
Cioffi L. Minerva Urol 1964; 16: 165-170
Frati Munari AC et al. Bol Med Hosp Infant Mex 1979; 36(2): 201-214
Sasaki S et al. Acta Derm Venereol 1972; 52(2): 141-150
Guseva NG, Starovoitova MN, Mach ES. Ter Arkh 1998; 70(5): 58-61
37
Early Indian and Egyptian Research
Indian research demonstrated good healing rates in
leprosy1,2
Egyptian research has shown
benefits in:
• liver fibrosis3
• cataract surgery4
1
2
3
4
Chakrabarty T, Deshmukh S. Sci Culture 1976; 42(11): 573
Nebout M. Bull Soc Pathol Exot 1974; 67(5): 471-478
El-Zawahry MD et al. Bull Societe Int Chirurgie 1975; 6: 573-577
Abou Shousha ES, Khalil HA. Bull Ophthalmol Soc Egypt 1967; 60(64): 451-470
Gotu Kola and Keloid
Scarring
Oral administration of the triterpenes of Gotu Kola
(TGK) for elevated scars and keloids, including post
burn keloids was investigated
Of the 139 patients, dose
60-90 mg/day, 82% benefited
from TGK after 2-18 months,
either by relief of symptoms or
disappearance of inflammation
Bosse JP et al. Ann Plast Surg 1979; 3(2): 13-21
38
Gotu Kola: Other Clinical
Studies
Beneficial for patients with leg ulcers
60 mg/day, with rapid stimulation of healing in
some cases
A placebo controlled trial demonstrated a reduced
tendency to sclerosis in cellulitic tissue
Morgan M, Andrews C. Nutritional Perspective 2007; 26: 1-3
Gotu Kola and Vein Health
According to a recent review TGK has the following
actions:
Acts on fibroblasts in the vein wall; improves the
synthesis of collagen and stimulates collagen
remodelling
May decrease endothelial cell damage
Improves microcirculation and ↓ edema and
improves lymphatic drainage
Incandela L et al. Angiology, 2001; 52(Suppl 2): S9-S13
39
Gotu Kola and Vein Health
Results from further studies indicate that TGK:
• Improves microcirculation
• Protects blood vessel
connective tissue
• ↓ edema
• ↓ capillary filtration rate
• By controlling collagen synthesis, modulates
scarring of soft plaques
Arpaia MR et al. Int J Clin Pharmacol Res 1990; 10(4): 229-33
Montecchio GP et al. Haematolgica 1991; 76(3): 256-259
TGK and Chronic Venous
Insufficiency (CVI)
A 4-week, dose-finding study compared normal
volunteers (180 mg/day) and patients with CVI
(doses 0, 90 and 180 mg/day) for changes in
capillary flow and ankle edema
A dose-response effect was observed,
with no change in the placebo group
and normal volunteers
These improvements were correlated
with symptom changes
De Sanctis MT et al. Angiology 2001; 52(Suppl 2): S55-S59
40
TGK and CVI
Average score obtained by considering four major
symptoms*
Groups
Before
After Treatment
A
7.7 ± 1.5
4.6 ± 1.1†
B
7.8 ± 6.2
6.2 ± 1.7†
C
7.7 ± 1.2
7.6 ± 1.3 ns
A = 180 mg/day, B = 90 mg/day, C = placebo
* (1) swelling sensation, (2) restless lower extremities, (3) pain and cramps, and
(4) tiredness. The analogue scale line ranged from 1 to 10
† p<0.05
ns: not significant
De Sanctis, MT et al. Angiology 2001; 52(Suppl 2): S55-S59
TGK and Diabetic Neuropathy
Gotu Kola improves venoarteriolar parameters
consistent with preventing and treating diabetic
neuropathy
Placebo-controlled randomized trial:
• Patients with severe diabetic neuropathy
• TGK 60 mg twice daily for 12 months
Outcome:
• Significant ↓ in resting blood flow
• Significant ↑ in venoarteriolar
response
• Significant ↓ in ankle swelling
Incandela L et al. Angiology 2001; 52(2): S27-31
41
Gotu Kola and the Brain
Both Gotu Kola and Bacopa are called brahmi
Recent Thai clinical research demonstrated that
Gotu Kola improved memory and accuracy in both
short-term and long-term studies
In addition, long-term use also
lifted reaction times and recognition
skills
Gotu Kola also boosted calmness
and mood in this study
Wattanathorn J et al. J Ethnopharmacol 2008; 116(2): 325-332
Ginkgo
The actions associated with Ginkgo are:
• Antioxidant
• Antiplatelet activating factor
• Tissue perfusion enhancing
• Circulatory stimulant
• Cognition enhancing
• Neuroprotective
Bone K. A Clinical Guide to Blending Liquid Herbs. Churchill Livingstone, USA, 2003,
pp. 232-239.
42
Ginkgo
The standardized extract of Ginkgo biloba contains
at least 26 phyto-chemicals and is standardized to
contain:
• 24% flavonoid glycosides termed ginkgo flavone
glycosides
• 6% terpenoids comprising the ginkgolides and
bilobalide
The use of standardized extracts allows for the
consistent dosing of active constituents
Mills S, Bone K. Principles and Practice of Phytotherapy: Modern Herbal Medicine. Churchill
Livingstone, Edinburgh, 2000, pp. 404-417.
Ginkgo: Role in Tissue
Healing
The activities associated with Ginkgo that support its
use in tissue healing are:
Anti-PAF, as platelet activating factor (PAF) is
associated with inflammation
Improves circulation in arteries, veins and
capillaries, especially the microcirculation
Antioxidant in order to address the oxidative stress
associated with damaged tissues
Smith JV, Luo Y. Appl Microbiol Biotechnol 2004; 64(4): 465-472
43
Ginkgo and Peripheral
Circulation
A single dose of standardized Ginkgo extract
(112.5 mg) resulted in a significant increase in
blood flow in nail capillaries in healthy volunteers1
Another study demonstrated increased blood flow
to the forearms of volunteers2
This confirms the ability of Ginkgo to enhance
peripheral circulation, an important factor in the
healing process
1
2
Jung F et al. Arzneimittelforschung 1990; 40(5): 589-593
Mehlsen J et al. Clin Physiol Funct Imaging 2002; 22(6): 375-378
Ginkgo and Diabetic
Complications
In other clinical trials standardized Ginkgo extract at a
dosage of 120 mg/day:
Improved blood supply and peripheral nerve
functions in patients with type 2 diabetes and
diabetic neuropathies
Increased blood flow to the eye
of healthy volunteers
Mills S, Bone K. Principles and Practice of Phytotherapy: Modern Herbal Medicine. Churchill
Livingstone, Edinburgh, 2000, pp. 404-417.
44
Ginkgo and Diabetes
A Ginkgo extract demonstrated either:
A “resuscitation” of previously exhausted pancreatic
beta cell function
An effect of increasing the activity of the functional
beta cells in type 2 diabetic patients as measured
by C-peptide response
Kudolo B. J Clin Pharmacol 2001; 41(6): 600-611
Ginkgo and Diabetic
Neuropathy
Studies demonstrate that standardized extracts of
Ginkgo reduce the abnormal blood parameters seen
in diabetic retinopathy (DR):
↓ lipid peroxidation1,2
↓ clotting factors and ↓ RBC deformity
Improved blood viscosity and elasticity resulting in
improved retinal capillary blood flow rate2
1
2
Kudolo GB et al. Diabetes Res Clin Pract 2005; 68(1): 29-38
Huang SY et al. Clin Nutr 2004; 23(4): 615-621
45
Ginkgo and Diabetic
Neuropathy
Ginkgo has produced the following changes in
vision for patients with DR:
• Improvement in visual acuity and field of vision1
• Improvement in near and far vision, color
recognition and field of vision1
Ginkgo also improves the functioning of higher
brain centers associated with vision2
1
2
Mills S, Bone K. Principles and Practice of Modern Phytotherapy. Churchill Livingstone,
Edinburgh, 2000, pp. 413-414.
Page JW et al. J Gerontol A Biol Sci Med Sci 2005; 60(10): 1246-51
Grape Seed
The actions associated with Grape Seed are:
Antioxidant
Collagen stabilizing
Vasoprotective
Venotonic
Astringent
Bone K. The Ultimate Herbal Compendium, Phytotherapy Press, Warwick, 2007, pp. 39.
46
Grape Seed
Grape Seed extract is obtained from the seeds of
red or white grapes
Contains a range of polyphenols, mostly oligomeric
procyanidins (OPCs)
OPCs have a number of key actions related to tissue
healing
Gabetta B et al. Fitoterapia 2000; 71(2): 162-175
Grape Seed and Collagen
In vitro and in vivo studies demonstrate that Grape
Seed extract:
Supports connective tissue, by protecting collagen
and elastin within the microvessel wall1
Stabilizes connective tissue by facilitating the
formation of collagen microfibrils and collagen
crosslinking2
Protects vascular endothelium during ischemia2
1
2
Robert AM et al. Biomed Pharmacother 2006; 60(3): 113-120
47
Grape Seed and Capillaries
Numerous clinical trials using doses of between 100
and 150 mg/day of OPCs have demonstrated a
beneficial effect on capillary resistance and capillary
permeability
For example, 100 mg/day of OPCs was
administered to elderly patients with capillary
fragility
Very good results were achieved in
67%, good in 17% and moderate in
13%
Grape Seed and Venous
Insufficiency
Various clinical trials on patients with venous
insufficiency and/or oxidative stress have
demonstrated that Grape Seed extract (100 to
150 mg/day):
• ↓ edema
repairs capillary damage
increases peripheral circulation
48
Grape Seed and Venous
Insufficiency
80% of patients with chronic venous insufficiency
had a significant ↓ in lower limb swelling after 10
days of OPC treatment (100 mg/day)1
In comparison to placebo and diosmin (a
flavonoid), 150 mg/day of OPCs ↓ the functional
problems associated with impaired venous back
flow2
Treatment with 150 mg/day of OPCs stabilized
retinopathic lesions in 80% of patients2
1
2
Costantini A et al. Minerva Cardioangiol 1999; 47(1-2): 39-46
Protocol for Tissue Injuries:
Ligaplex® II – 6‐9
Cataplex® ACP: 6‐9
Gotu Kola Complex: 4
Glucosamine Synergy: 3
Boswellia Complex: 3
Consider: calcium and other minerals in diet.
‐‐Calcium Lactate or Calcifood
‐‐Organically Bound Minerals
49
Mayo Clinic Health Threat #4 for Men #3 for Women: Stroke
Stroke
50
In Western countries, stroke is the third most common cause
of death and the second most common cause of neurologic
disability after Alzheimer's disease. Its incidence has
decreased in recent decades, but the decrease appears now
to have leveled off, and cerebrovascular disease remains the
leading cause of institutional placement for loss of
independence among adults.
Most vascular injury to the brain is secondary to
atherosclerosis or hypertension. The major types of
cerebrovascular disease are cerebral insufficiency due to
transient disturbances of blood flow or, rarely, hypertensive
encephalopathy; infarction due to embolism or thrombosis of
intracranial or extracranial arteries; hemorrhage, including
hypertensive parenchymal hemorrhage and subarachnoid
hemorrhage due to congenital aneurysm; and arteriovenous
malformation, which can cause symptoms of a mass lesion,
infarction, or hemorrhage.
Symptoms and signs in cerebrovascular disease reflect the damaged
area of brain and not necessarily the affected artery. For example,
occlusion of either the middle cerebral or internal carotid artery can
produce a similar clinical neurologic abnormality. Nevertheless,
cerebrovascular injuries generally conform to fairly specific patterns of
arterial supply; knowledge of these patterns helps distinguish stroke
from other brain lesions that occasionally produce acute symptoms
Differential Diagnosis for Stroke:
•Brain tumor
•Cerebral hypoxia
•Cranial or peripheral nerve palsy
•Functional disorder
•Hypoglycemia
•Migraine
•Multiple Sclerosis
•Peripheral Vascular disease
•Seizure
•Subdural hematoma
•Syncope or near syncope
51
An accurate history, including onset and duration of symptoms and identification
of stroke risk factors, is key to diagnosing cerebrovascular lesions.
Hemorrhagic stroke has a more catastrophically acute onset than ischemic
stroke, although both tend to develop abruptly. A brain CT or MRI scan can
distinguish between ischemic and hemorrhagic strokes, thus assisting in urgent
treatment decisions.
Stroke Risk Factors
Various standardized tests are used to assess the severity of stroke. For
example, the National Institutes of Health Stroke Scale assesses
consciousness, vision, extraocular movements, facial palsy, limb strength,
ataxia, sensation, speech, and language using 15 items scored from 0 to 2 or 3.
Higher scores reflect increased severity of the deficit; the highest possible total
score is 42.
Protocol:
Cataplex ACP: 6-12 for 1st week then 6
Protefood: 3
Neuroplex: 3
Cataplex G: 3
Ginkgo tablets: 3
Bacopa Complex: 3
52
Mayo Clinic Health Threat #5 for Men #4 for Women: COPD
•Chronic obstructive pulmonary disease (COPD) refers to a clinical syndrome of chronic dyspnea as a result of expiratory airflow obstruction due to chronic bronchitis or emphysema (often both).
•Chronic bronchitis is defined clinically and is associated with chronic cough, resulting from excessive tracheobronchial mucus production and impaired mucus elimination, lasting for at least three months of the year for more than two consecutive years. •Emphysema is defined anatomically and is characterized by enlarged air spaces distal to the terminal bronchioles with destruction of the alveolar walls; there is also a loss of elastic recoil in the lung. •In the United States, COPD affects an estimated 15 million people and is the fifth leading cause of death.
53
Etiology:
•Smoking is the number one cause of COPD. Obstruction of airflow in the small airways has been shown to be the earliest detrimental effect of smoking. •Exposure to environmental air pollutants •Alpha1‐antitrypsin deficiency, the only known inherited form of the disease Risk Factors:
•History of smoking or passive smoke exposure •History of working with high levels of airborne particulates (e.g., dusts), gases, and fumes (such as coal and gold miners; farmers; and cement, cadmium, and cotton workers) •Low socioeconomic status •Male gender •Allergy and airway hyper‐responsiveness (e.g., asthma) •Women in undeveloped countries exposed to open fires for cooking and heating •Living in heavily industrialized urban areas •Recurrent respiratory illnesses •Family history of chronic bronchitis and emphysema (e.g., alpha1‐
antitrypsin deficiency) •Emotional stress and repressed emotions have also been shown to contribute 54
Signs and Symptoms:
Patients with emphysema present with a long history of dyspnea on exertion. Patients with chronic bronchitis present with chronic cough productive of sputum.
•Cough •Cyanosis •Weight gain •Dyspnea on exertion (and eventually at rest) •Excessive sputum production •Wheezing •Recurrent bronchial infections •Weight loss in late stages •Peripheral edema secondary to cor pulmonale
Differential:
•Asthma •Bronchiolitis obliterans
•Pneumonia •Lung cancer •Cystic fibrosis •Congestive heart failure •Interstitial lung disease •Primary pulmonary hypertension •Acute viral infection
55
Physical presentation:
•There is considerable variability in the clinical presentation of COPD, which can range from simple chronic bronchitis (cough without airway obstruction) to severe respiratory disability and fatal respiratory failure.
•The classic patient with emphysema is often very thin and barrel chested and shows obvious difficulty breathing, manifesting tachypnea
(rapid respirations) with prolonged expiration through pursed lips.
•Patients often assume a "tripod" position, leaning forward while sitting, bracing with the arms. Cyanosis is not present so the patient is considered a "pink puffer." •The classic patient with bronchitis is often overweight, even obese, and appears cyanotic. The respiratory rate is normal, and there is no obvious distress. These patients are called "blue bloaters." •In reality most patients with COPD have a combination of chronic bronchitis and emphysema
Pharmacologic therapies:
•Alpha1‐antitrypsin replacement therapy •Supplemental oxygen (1 to 3 liters/min)—dosage should be appropriate to relieve hypoxemia (i.e., to maintain a PaO2 of 55 to 60 mm Hg) •Bronchodilators—to increase airflow and reduce dyspnea
•Anticholinergic agents (e.g., ipratropium, 0.18 mg, 2 puffs qid) •Beta2‐adrenergic agonists (e.g., metaproterenol, terbutaline, or albuterol, 2 to 6 puffs every three to six hours) •Theophylline (200 to 400 mg bid)—requires frequent blood monitoring for toxicity •Corticosteroids (e.g., prednisone, 40 mg/day for two weeks then reduce to 0 to 10 mg every day or on alternate days) •Broad‐spectrum antibiotics (e.g., ampicillin or amoxicillin, 2 g/day; erythromycin, 2 g/day; or trimethoprim‐sulfamethoxazole, 1 double‐strength capsule/day)—for treatment of exacerbations •N‐acetylcysteine—for mucolytic therapy; however, it may cause bronchospasm •Magnesium can also be markedly helpful as an IV infusion of 5 to 10 g of elemental magnesium over 6 to 10 hours
56
Generic Nutritional support:
•Dairy products and bananas increase mucus buildup and should be avoided. Garlic, onions, and horseradish may actually decrease mucus production. IgG ELISA food allergy testing can determine other foods that can cause inflammation in the lungs. •Some essential fatty acids are anti‐inflammatory, dose is 1,000 to 2,000 IU, mixed omega‐3 and omega‐6 oils (flaxseed, fish, borage, and/or evening primrose oil; avoid vegetable oils and saturated fats) •Coenzyme Q10 prevents fatty acid oxidation and increases exercise tolerance as a cardio‐protective antioxidant. Dose is 10 to 50 mg tid. •Other important supplements: selenium (200 mcg/day), vitamin E (400 IU/day), vitamin C (1,000 mg tid), L‐carnitine (750 mg bid). Note that beta‐
carotene increases the risk of lung cancer in smokers. •Bromelain is a mucolytic, 250 to 500 mg tid away from meals. People with pineapple allergy may be sensitive to this product. Bromelain may also aggravate gastritis. •N‐acetylcysteine is a mucolytic, 400 mg tid. •Magnesium promotes muscle relaxation in bronchial smooth muscle and blood vessels (100 to 500 mg bid). Magnesium may cause diarrhea in some sensitive individuals. Boswellia serrata
57
Boswellia
Phytochemistry
The resin contains:
• Triterpenoids known
as boswellic acids
• Essential oil, resin
components
MediHerb Professional Review No. 69
pp 1-5, Jun 1999
Boswellia
Pharmacology
• Boswellia and boswellic acids inhibit the enzyme
5-lipoxygenase and reduce the formation of
leukotrienes (are non-redox inhibitors)
• Anti-inflammatory activity has been confirmed in
various experimental models
• Boswellic acids also exhibit anticancer activity
MediHerb Professional Review No. 69, pp 1-5, Jun 1999
58
Boswellia
Therapeutic indications
• Disorders in which leukotriene-generated
inflammation plays a significant role, such as IBD
and asthma
• Adjuvant therapy in arthritis
Dosage
•300 mg of standardized extract (60%
boswellic acids) 3 times a day for arthritis, 2
to 3 times a day for asthma and IBD
MediHerb Professional Review No. 69, pp 1-5, Jun 1999
Boswellia and Asthma
A double-blind placebo-controlled study of 80
patients over 6 weeks:
• Improvement in FEV1 (p=0.0001)
• Improvement in PEFR (p=0.0001)
• Reduced frequency of attacks (p=0.0001)
• Improvements in ESR, eosinophil count (p<0.05)
Gupta I et al. Effects of Boswellia serrata gum resin in patients with
bronchial asthma: results of a double-blind, placebo-controlled, 6-week
clinical study. Eur J Med Res 1998; 3(11): 511-514
59
Turmeric
• Contains essential oil and curcuminoids, mainly
curcumin
• Oral doses of curcumin have displayed
significant anti-inflammatory activity in both
acute and chronic experimental models1
• Curcumin is a dual inhibitor of arachidonic acid
metabolism, inhibiting both the enzymes 5lipoxygenase and cyclooxygenase in vitro1
1 Mills S, Bone K. Principles and Practice of Phytotherapy: Modern Herbal
Medicine. Churchill Livingstone, Edinburgh, 2000, pp 569-580 .
Turmeric
• Turmeric and curcumin have considerable
antioxidant activity1
• Curcumin has demonstrated antiasthmatic
activity in an experimental model2
Mills S, Bone K. Principles and Practice of Phytotherapy: Modern
Herbal Medicine. Churchill Livingstone, Edinburgh, 2000, pp 569-580.
2
Ram et al. Biol Pharm Bull 2003; 26(&): 1021-1024
1
60
Adhatoda
Phytochemistry
• Alkaloids including vasicine,
vasicinone and vasicinol
•
Bone K. Clinical Applications of Ayurvedic and
Chinese Herbs. Phytotherapy Press, Warwick,
1996, p 91.
Adhatoda
Pharmacology
• Bronchodilating and respiratory stimulant effects
from vasicine1
• The drug bromhexine with expectorant effects
was developed from vasicine1
• Studies on the whole herb extract have shown
antiasthmatic, expectorant, antiallergic,
antitussive and bronchodilating effects1,2
1
Bone K. Clinical Applications of Ayurvedic and Chinese Herbs.
Phytotherapy Press, Warwick, 1996, pp 91-93.
2
Dhuley JN. J Ethnopharmacol 1999; 67: 361-365
61
Adhatoda
Clinical Studies
• No clinical studies of note, but a strong
traditional use for asthma and other respiratory
disorders1
• Contraindicated in pregnancy
1 Claeson UP. J Ethnopharmacol 2000; 72: 1-20
Albizia
Phytochemistry
• The bark contains saponins, tannins and flavonoids
Pharmacology
Indicates multiple effects in allergic processes:
• Stabilizes mast cells: in vitro-degranulation was inhibited
by 62%
• Levels of allergy-inducing antibodies decreased
• T-lymphocyte activity significantly decreased
• Protects against anaphylaxis
62
Albizia
Clinical Studies
• An uncontrolled study on 60 patients with asthma excellent response if recent onset (< 2 years)
• Promising results from a preliminary study of
allergic rhinitis
Therapeutic Indications
• Atopic allergy - hayfever, asthma, eczema
Address the Sustaining Factors
• Control inflammatory mediators e.g. Boswellia
Complex, Turmeric and Ginkgo (PulmaCo)
• Dilate the airways e.g. Grindelia, Adhatoda
(PulmaCo)
• Clear the airways e.g. Grindelia, Adhatoda
(PulmaCo)
• Allay debilitating cough e.g. Marshmallow and
PulmaCo
• Dampen the factors driving the allergic
response e.g. Albizia, Baical Skullcap (Albizia
Complex)
63
Protocol:
Emphaplex®: 6‐9
Betacol®: 3
Pulmaco: 3‐4
Boswellia Complex: 3
Albizia Complex: 3 (for allergic component if present)
Mayo Clinic Health Threat #6 for Men #7 for Women: Diabetes
64
•Diabetes mellitus results from the body's failure to regulate blood glucose levels
adequately.
•It is a common endocrine disease, with more than 600,000 new cases diagnosed in
the United States each year.
•It affects men and women of all ages, races, and income levels.
•Among those over 40, it affects 1:15 Caucasians and 1:10 to 1:8 AfricanAmericans and Hispanics.
•Among those over 65, 1 of every 5 persons has diabetes and up to 50% of patients
are undiagnosed.
•There is a strong familial susceptibility to the condition.
•Two major forms are seen:
•Type I (insulin-dependent diabetes mellitus [IDDM]): usually occurs before
age 30, most likely between ages 11 and 13; accounts for about 10% of cases.
•Type II (non-insulin-dependent diabetes mellitus [NIDDM]): usually occurs
in those over age 40; accounts for about 90% of cases; 30% to 40% need
insulin.
•Gestational diabetes (GDM) can occur in pregnant women.
•Diabetes can be secondary to pancreatic disease, the use of chemicals or drugs,
various genetic syndromes (Turner's syndrome, myotonic dystrophy, or PraderWilli syndrome), rare abnormalities in the cellular receptor for insulin, or an
autosomal dominant inherited disorder.
65
Etiology
Unknown, but most likely a combination of genetic predisposition, viral infection,
lifestyle, nutrition and diet, obesity, autoimmune disorders, and exposure to toxic
agents.
• Type I probably results when pancreatic beta cells are attacked and destroyed by
an autoimmune process triggered by a viral infection in a genetically susceptible
individual.
• Type II develops in older, overweight individuals whose insulin production is
insufficient to meet body needs or whose response to insulin is diminished by a
loss of insulin receptors on the surface membranes of target cells.
Risk Factors
Type I:
• Family history of diabetes, thyroid disease, or other endocrinopathies
• Family history of autoimmune diseases such as Hashimoto's thyroiditis, Graves'
disease, myasthenia gravis, or pernicious anemia
• Cow's milk consumption in infancy
Type II:
• Obesity and age over 40 years
• Family history of diabetes, thyroid disease, or other endocrinopathies
• Sedentary lifestyle with diet high in fats and calories
• African-American, Hispanic, American Indian, or Asian or Pacific IslandAmerican
66
Signs and symptoms:
•Polyuria, polydipsia, rapid weight loss, and hyperglycemia
•Glycosuria
•Increased susceptibility to infection
•Dehydration
•Polyphagia
•Fatigue or weakness
•Blurred vision
•Stiffness in the shoulder and upper back
•Pruritus, numbness, and tingling in the hands and feet
•Leg cramps
•Hyperlipidemia
•Ketoacidosis
67
Differential Diagnosis:
•Polydipsia—medication side effect, psychogenic factors, diabetes
insipidus (a condition characterized by excretion of large amounts of
severely diluted urine, which cannot be reduced when fluid intake is
reduced. It denotes inability of the kidney to concentrate urine. DI is
caused by a deficiency of antidiuretic hormone (ADH), also known as
vasopressin, due to the destruction of the back or "posterior" part of the
pituitary gland where vasopressin is normally released from, or by an
insensitivity of the kidneys to that hormone. It can also be induced
iatrogenically by various drugs.)
•Polyuria—hypercalcemia, medication side effect, renal wasting,
urologic or prostate conditions
•Blurred vision—myopia, presbyopia
•Fatigue or weakness—thyroid disorder, anemia, adrenal insufficiency,
depression
•Pruritus—allergy, renal failure
•Cushing's disease
•Corticosteroid use
Diagnosis:
Physical Exam:
Patient may present with fatigue, lethargy, poor
concentration, and atypical thirst for liquids.
Laboratory:
•Two or more fasting plasma glucose levels over 140
mg/dL or one level over 200 mg/dL plus other signs
and symptoms.
•Oral glucose tolerance test values 120 to 140 mg/dL
•Glycosylated hemoglobin test showing consistently
elevated values.
•Glycosylated hemoglobin is used to track treatment
efficacy, not to diagnose DM.
68
Pathology/Pathophysiology:
•Elevated blood sugar levels with weight loss,
•decreased blood pressure,
•nonhealing wounds (especially on the extremities),
recurrent cutaneous infections,
•decreased extremity sensation,
• retinal abnormalities or cataract formation,
•carotid bruits,
•abdominal tenderness,
•dry skin,
•and hair loss over lower leg and foot.
Treatment Options:
Strategy:
•Control blood sugar levels; helps reduce complications.
•Requires patients to be self-disciplined, able to
concentrate, able to maintain a positive attitude, and
honest with self and physician.
•Components are diet, exercise, blood glucose selfmonitoring, oral hypoglycemic agents (Type II), and
insulin (Type I).
•Because diabetes affects so many body systems,
treatment planning must include a whole-body
approach.
69
Treatment Options:
Type 1 specific:
•Diet—consistent timing/content (same gram amount of
carbohydrates, protein, and fat at each meal); consult dietitian
for meal planning.
•Exercise—daily; wear proper shoes and protective equipment;
avoid extreme heat or cold; check feet daily and after exercise;
suspend exercise when blood glucose control is poor.
•Self-monitoring—teach the patient to use a home glucose meter
and make needed adjustments in diet, exercise, and/or insulin.
Type II specific:
•Diet—use moderation; lose weight by decreasing calories/carbs
while increasing activity.
•Exercise—as for Type I; do moderate aerobic exercise (50% to
70% of VO2 max) for 20 to 45 minutes at least three days a
week; include low-intensity warm-up and cool-down exercises.
•Self-monitoring—as for Type I, with adjustments in diet,
exercise, and/or oral hypoglycemic agent as needed.
Drug therapies:
•Insulin (used for Type I and occasionally Type II [30% to 40%]).
Taken subcutaneously, with dose and type individualized to the
patient's condition. Possible treatment regimens:
•Three-injections/day, doses adjusted to variations in control
•Long-acting and short-acting preparations taken at meals for
stable background levels
•External insulin pump for tight control
•Single injection/day for those with some pancreatic function
•Sulfonylureas (Type II only). Oral hypoglycemic agents used when
diet and exercise are ineffective or in conjunction with diet and
exercise. Doses individualized to the patient's condition. Side effects
include hypoglycemia, nausea, heartburn, stomach fullness;
intolerance and allergy (<2% of patients). Use with caution in
persons with liver or kidney impairment and those with sulfa
allergy. See list on next slide…………..
70
Drug therapies:
• Acetohexamide (Dymelor)—250 to 1,500 mg; slight diuretic effect
• Chlorpropamide (Diabinese, Glucamide)—100 to 750 mg; very long duration of action,
antidiuretic effect
• Tolazamide (Tolinase)—100 to 1,000 mg; slight diuretic effect
• Tolbutamide (Orinase)—500 to 3,000 mg; usually taken in two to three doses/day
• Glipizide (Glucotrol)—5 to 40 mg; take on empty stomach
• Glipizide-extended release (Glucotrol XL)—20 mg; do not break tablet, take once/day
• Glyburide (Diabeta, Micronase)—1.25 to 30 mg
• Glyburide-micronized (Glynase)—12 mg/day; not equivalent in action to glyburide
• Glimepiride (Amaryl)—8 mg/day
• Metformin (Glucophage)—Used as a supplement to or substitute for sulfonylureas. Side
effects include weight loss, nausea, abdominal discomfort, and diarrhea. Use with caution
in persons with conditions leading to lactic acid buildup (congestive heart failure, severe
vascular disease, kidney or liver disease). Discontinue 24 to 48 hours before surgery or
radiographic dye study. Dose: 1 to 2.5 g/day in two to three doses; available in 500 and 850
mg tablets; take before meals
• Acarbose (Precose)—Slows absorption of carbohydrate into blood, acts locally in the
intestine. Take at the beginning of a meal for immediate action. Major side effect is
increased gas production (up to 75% of users). Dose: 50 to 100 mg depending on results
and side effects
• Troglitazone (Rezulin)—In trials for use with insulin; liver damage reported
• Repaglinide (Prandin)—Meglitinide class; use in Type II disease
Complementary and alternative therapies:
•Treatments stabilize blood sugars. Also, alternative therapies have an
important role in preventing vascular damage and some of the serious
complications that may be involved with DM.
• A combination of herbs and nutrition, along with lifestyle changes, can
be quite helpful.
•Regular exercise is extremely important. Ten minutes/day of exercise
has been shown to have an effect on glucose tolerance, although a
minimum of 30 minutes three times/week is required to see significant
changes. Extended exercise is desired. Short bursts of activity may
actually increase glucose levels.
71
Nutrition:
•Diet: the “classic” diet for DM is high in complex carbohydrates and fiber. Some
people, however, achieve better glucose control with a high-protein diet with very
few carbohydrates. If the classic diet does not stabilize blood sugar, a trial of highprotein diet may be indicated.
•Essential fatty acids: anti-inflammatory, decrease insulin resistance, and prevent
cardiovascular and neurological complications of DM. Evening primrose oil
(2,000 mg bid) or fish oil (1,200 mg bid) rather than flax or borage may be
required, since a greater percentage of diabetics are lacking enzymes required for
utilization of flax and/or borage oil.
•OPCs (oligomeric procyanidins) such as grape seed extracts help to support
vascular health and prevent oxidation side effects associated with diabetes
•B-complex: biotin (300 mcg), B1 (50 to 100 mg), B2 (50 mg), B3 (100 mg), B6
(50 to 100 mg), B12 (100 to 1,000 mcg), folate (400 mcg/day) help prevent
neuropathy, control glucose levels, and prevent nephropathy
•Vitamin C (2 to 3 g/day) may prevent microangiopathy and hypertriglyceridemia
•Vitamin E (400 IU/day) may reduce insulin requirements so should start at 100 IU
and gradually increase the dose; enhances healing of ulcers, and is
cardioprotective.
Nutrition:
•Brewer's yeast: contains chromium, which may improve glucose
tolerance, and glutathione, an antioxidant (9 g or 3 tbsp. brewer's
yeast/day and/or 200 mcg chromium)
•Magnesium: (400 mg/day) low in diabetics, may help prevent the
calcium deposition in arterial walls
•Manganese: (500 to 1,000 mcg) low in diabetics, may help stabilize
glucose levels
•Zinc: (30 mg/day) may decrease fasting glucose levels and help prevent
fatty acid oxidation
•Coenzyme Q10: (50 to 100 mg bid) depleted by oral hypoglycemic
agents, prevents fatty acid oxidation
•Vanadium: (5 to 10 mg/day) to normalize serum cholesterol and
triglycerides
•Some feel that chromium (200 mcg) helps normalize sugar metabolism.
72
Herbs:
•Gymnema: Gymnema sylvestre leaves have been found to cause
hypoglycemia in laboratory animals and have found a use in herbal
medicine to help treat adult onset diabetes mellitus (NIDDM).
•Garlic (Allium sativum) increases fibrolysis, inhibits platelet aggregation,
lowers lipids
•Onion (Allium cepa) lowers lipids and blood pressure, inhibits
thrombocyte aggregation
•Bilberry (Vaccinium myrtillus) is a flavonoid, historic use in DM,
especially to prevent diabetic retinopathy
•Fenugreek (Trigonella foenum-graecum) historically used to stabilize
blood sugar
•Garlic and onions should be consumed liberally in the diet; bilberry and
fenugreek, equal parts, can be used as 1 cup tea tid or 30 to 60 drops
tincture, tid
•Cayenne (Capsicum annum): 0.075% capsaicin cream topically, decreases
pain in peripheral neuropathy after two to four weeks of use
Protocol:
•Catalyn
3-6
•Pituitrophin30*
1-6 Trophic control of endocrine system
•Pancreatrophin PMG®
3-9 Specific cell activator
•Betacol®
1-3
Carbohydrate metabolism of liver cells
•Arginex®
3-9
Kidney support factors
•Cataplex® B
3
Lactic pyruvic acid factor
Muscle Metabolism Factors:
•Cardiotrophin PMG®
1-3 Increases muscle demand for sugar
• Organically Bound Minerals 2
Potassium ions necessary for muscle
contraction
•Inositol
3-6
Phosphorilization factor (ATP production)
•Cataplex® G
3
Cholinesterase precursors (myoneural junction
factor)
Completes blood amino acid pattern, promotes
•Protefood®
1-2
transfer to tissue (muscle)
Consider: Diaplex: 6-9, Vitanox: 2, Gymnema: 3
73
Mayo Clinic Health Threat #7 for Men # 8 for Women: Flu
•Influenza, commonly referred to as the flu, is an infectious disease caused by RNA viruses of the family Orthomyxoviridae (the influenza viruses), that affects birds and mammals. The name influenza comes from the Italian influenza, meaning "influence" (Latin: influentia). •The most common symptoms of the disease are chills, fever, sore throat, muscle pains, severe headache, coughing, weakness and general discomfort. Fever and coughs are the most frequent symptoms.
•In more serious cases, influenza causes pneumonia, which can be fatal, particularly for the young and the elderly. Although it is often confused with other influenza‐like illnesses, especially the common cold, influenza is a much more severe disease than the common cold and is caused by a different type of virus. •Influenza may produce nausea and vomiting, particularly in children,
but these symptoms are more common in the unrelated gastroenteritis, which is sometimes called "stomach flu" or "24‐hour flu".
74
There are three main types of orthomyxoviruses that cause influenza.
•Influenza A: Responsible for near‐annual epidemics of disease with relatively severe symptoms. Mutates by gradual antigenic drift and also by occasional abrupt protein changes (antigenic shift) which can cause pandemics, as occurred most recently in 1918 ("Spanish flu"), 1957 ("Asian flu"), and 1968 ("Hong Kong flu"). •Influenza B: Near‐annual outbreaks, but usually less serious than type A influenza. Mutates by antigenic drift only. •Influenza C: Causes mild illness, or is asymptomatic. Not responsible for epidemics. Antigenically stable
.
Viral replication:
75
Nutritional support (generic):
•Vitamin C (1,000 mg three to six times/day) enhances immune
function (may affect interferon and interleukin); some studies
show that it shortens the duration and ameliorates the symptoms of
the common cold.
•Zinc (23 mg lozenges taken every two hours) may shorten the
duration of a cold, and may also protect against the development
of symptoms. This high a dose is for short-term use only.
•Vitamin A (25,000 IU/day) maintains integrity of mucous
membranes and stimulates antibody response. Use high dose
short-term only.
•Avoid dairy and bananas, foods that increase mucus production.
•Garlic and onions are antivirals that can be included in the diet.
76
Herbal support (generic):
•Coneflower (Echinacea purpurea): immunomodulating,
increases phagocytosis; controversy exists whether to use for
longer than two to six weeks at a time and whether to use in
autoimmune conditions or AIDS.
•Goldenseal (Hydrastis canadensis): antiviral, antibacterial
•Astragalus (Astragalus membranaceus): increases interferon
to shorten duration of colds
•Licorice (Glycyrrhiza glabra): antiviral, soothing to mucous
membranes
•Elderberry (Sambucus nigra): antiviral, increases bronchial
secretions
Protocol:
•Antronex®: 1 - ?
Dr. Lee: “The symptoms of coryza and catarrh may often
be completely controlled within a few hours by the use of
one Antronex every hour the first day.”
•Congaplex®: 6 – 12
•Calcium Lactate: 6 – 18
•Cataplex® F Perles: 3 – 6
Herbal:
•Echinacea Premium Tablets/Liquid: 3 tabs or 1 tsp
•Andrographis Complex: 3 – 6
•Euphrasia Complex: 3 – 6
•Astragalus Complex: 3
77
Mayo Clinic Health Threat #8 for Men: Suicide
Be sensible!! This is probably NOT the time to focus on nutritional support – get help!
Later: Orchex, Inositol, blood‐sugar handling, etc.
Mayo Clinic Health Threat #9 for Men and Women: Kidney
Note: this may simply be kidney infection, more commonly in women. We will assume more serious for this discussion, but the protocol would actually be much the same.
78
Renal Failure:
•Often a complication of diabetes or hypertension!
•Biochemically, it is typically detected by an elevated serum creatinine.
•Renal failure is described as a decrease in the glomerular filtration rate. When the kidneys malfunction, problems frequently encountered are abnormal fluid levels in the body, deranged acid levels, abnormal levels of potassium, calcium, phosphate, hematuria, and (in the longer term) anemia. •Long‐term kidney problems have significant repercussions on other diseases, such as cardiovascular disease
•Symptoms of kidney disease can vary from person to person. Some people with kidney disease may not even feel sick, or they may not notice their symptoms. •If the kidney function fails, the waste products accumulate in the blood and the body, termed azotemia. Very mild levels of azotemia may produce little or no symptoms, but if the kidney failure continues then symptoms will become noticeable. •If the kidney (or renal) failure is of sufficient degree to cause symptoms. Renal failure accompanied with noticeable symptoms is termed uremia
•A build‐up of urea may cause:
Vomiting and/or diarrhea, which may lead to dehydration Nausea Weight loss Nocturnal urination Foamy or bubbly urine More frequent urination, or in greater amounts than usual, with pale urine Less frequent urination, or in smaller amounts than usual, with dark coloured urine Blood in the urine Pressure, or difficulty urinating 79
Causes of acute renal failure
•Acute kidney failure usually occurs as the result of a sudden interruption in the blood supply to the kidney, or as a result of a toxic overload of the kidneys. Some causes of acute failure include accidents, injuries or complications from surgery where the kidneys are deprived of normal blood flow for an extended period of time. Heart‐
bypass surgery is an example of a situation in which the kidneys receive reduced blood flow.
•Drug overdoses, whether accidental or from chemical overloads of drugs such as antibiotics or chemotherapy, may also cause the onset of acute kidney failure. Unlike in chronic kidney disease, however, the kidneys can often recover from acute failure, allowing the patient to resume a normal life. People suffering from acute failure require supportive treatment until their kidneys recover function, and they often remain at an increased risk of developing future kidney failure.
Causes of chronic kidney disease
•There are many causes of CKD. The most common cause is diabetes mellitus. The second most common cause is long‐standing, uncontrolled, hypertension. Polycystic kidney disease is also a well known cause of chronic kidney disease. The majority of people afflicted with polycystic kidney disease have a family history of the disease. Many other genetic illnesses also affect kidney function. •Overuse of some common drugs, such as aspirin, ibuprofen, cocaine and acetaminophen can also cause chronic kidney damage.
Protocol:
Albaplex®: 6‐9
Cataplex® ACP: 6‐9
Cranberry Complex: 3
Urico Phytosynergist: 5ml, 1‐3 times daily
80
Mayo Clinic Health Threat #10 for Men #5 for Women: Alzheimer’s Disease
ALZHEIMER'S DISEASE
A progressive, inexorable loss of cognitive function associated
with an excessive number of senile plaques in the cerebral cortex
and subcortical gray matter, which also contains b-amyloid and
neurofibrillary tangles consisting of tau protein.
Epidemiology
Early-onset forms account for only 2 to 7% of cases and are
usually due to an inherited genetic mutation. The common form
affects persons > 60 yr old, and its incidence increases as age
advances.
Four million Americans have Alzheimer's disease, at an annual
cost of about $90 billion, including medical and nursing home
care, social services, lost productivity, and early death. The
disease is about twice as common in women as in men (perhaps
because women live longer, but female sex may be a risk factor).
It accounts for > 65% of the dementias in the elderly. Vascular
dementia and Alzheimer's disease coexist in about 15% of cases.
81
Etiology
The cause of Alzheimer's disease is not known. The disease runs
in families in about 15 to 20% of cases. The remaining, so-called
sporadic cases have some genetic determinants. At least four
distinct genes, located on chromosomes 1, 14, 19, and 21,
influence initiation and progression. Chromosome 21 generates
the precursor protein for the amyloid protein, which accumulates
in the brain of patients with Alzheimer's disease (as well as with
other conditions). Chromosome 19 generates apolipoprotein (apo)
E alleles 1 to 4 ( 1 to 4). The presence of the 4 allele increases
the risk for Alzheimer's disease in whites; 2 and 4 alleles
increase the risk in blacks. Trisomy 21 produces early Alzheimer's
disease in persons with Down syndrome. These findings support
the epidemiologic observation that the disease has an autosomal
dominant genetic pattern in most early-onset and some late-onset
cases but a variable late-life penetrance. Environmental factors
are the focus of active investigation. Unproven speculations
include low hormone levels and exposure to metals.
Pathogenesis
Neurons are lost within the cerebral cortex, hippocampus, and
subcortical structures (including selective cell loss in the nucleus
basalis of Meynert), locus caeruleus, and nucleus raphae dorsalis.
Cerebral glucose use and perfusion is reduced in some areas of
the brain (parietal lobe and temporal cortices in early-stage
disease, prefrontal cortex in late-stage disease), as determined by
positron emission tomography; whether this reduction precedes or
follows cell death is not known. The microvasculature may also be
affected, as seen in congophilic angiopathy.
Neuritic or senile plaques (composed of neurites, astrocytes, and
glial cells around an amyloid core) and neurofibrillary tangles
(composed of paired helical filaments) play a role in the
pathogenesis of Alzheimer's disease. Senile plaques and
neurofibrillary tangles occur with normal aging, but they are much
more prevalent in persons with Alzheimer's disease
82
Symptoms and Signs
Alzheimer's disease can be divided into clinical stages. However, patients vary
greatly, and disease progression often is not as orderly as the following
description implies. The disease progresses gradually, although sometimes
symptoms seem to plateau for a time.
The early stage is characterized by loss of recent memory, inability to learn
and retain new information, language problems (especially word finding), mood
swings, and personality changes.
In the intermediate stage, patients become unable to learn and recall new
information. Memory of remote events is affected but not totally lost. Patients
may require assistance with bathing, eating, dressing, or toileting. Although they
remain ambulatory, they are at risk for falls or accidents secondary to
confusion.
In the severe stage, patients are unable to walk or to perform any activity of
daily living and usually are totally incontinent. Recent and remote memory is
completely lost. Patients may be unable to swallow and eat and are at risk of
malnutrition, pneumonia (especially from aspiration), and pressure sores.
Placement in a long-term care facility often becomes necessary because they
are totally dependent on others for care.
The end stage of Alzheimer's disease is coma and death, usually from
infection.
Prognosis and Treatment
Cognitive decline is inevitable, but the rate of progression is unpredictable.
Survival ranges from 2 to 20 yr, with an average of 7 yr.
General treatment principles for Alzheimer's disease are the same as those for
all dementias.
Some drugs that enhance cholinergic neurotransmission, such as donepezil,
can at least temporarily improve memory during the early stages of Alzheimer's
disease. However, they do not modify the steady worsening of the underlying
pathology. Tacrine produces more unwanted side effects. A trial of donepezil
starting with 5 mg once daily in the evening and, after 4 to 6 wk, increasing to
10 mg may be considered; it should be continued for several months to assess
effectiveness. Antioxidants (eg, vitamin E), estrogen therapy, and NSAIDs are
under study.
Many drugs adversely affect the CNS, increasing confusion and lethargy.
Sedatives, such as benzodiazepines, should be avoided when possible.
Anticholinergic drugs, such as some tricyclic antidepressants, antihistamines,
antipsychotics, and benztropine, should be avoided.
An extract of Ginkgo biloba called EGb may slow down or modestly reverse
memory loss and other symptoms in patients with Alzheimer's disease or
vascular dementia. The extract may act as a free-radical scavenger.
Complications appear to be minor, but further studies are needed.
83
Protocol:
Neuroplex®: 2
OPC Synergy®: 2
Niacinamide-B6: 3-6
Ribonucleic Acid: 3
Folic Acid-B12: 2
Ginkgo tabs: 4
Bacopa Complex: 3
Mayo Clinic Health Threat #10 for Women: Blood Poisoning (septicemia/sepsis)
84
•Sepsis is a serious medical condition characterized by a whole‐body inflammatory state (called a systemic inflammatory response syndrome or SIRS) and the presence of a known or suspected infection. The body may develop this inflammatory response to microbes in the blood, urine, lungs, skin, or other tissues. An incorrect layman's term for sepsis is blood poisoning, more aptly applied to Septicemia, below.
•Septicemia is a related term referring to the presence of pathogenic organisms in the blood‐stream, leading to sepsis. The term has not been sharply defined. It has been inconsistently used in the past by medical professionals, for example as a synonym of bacteremia, causing some confusion. The present medical consensus is therefore that the term "septicemia" is problematic and should be avoided.
•Sepsis is usually treated in the intensive care unit with intravenous fluids and antibiotics. If fluid replacement is insufficient to maintain blood pressure, specific vasopressor drugs can be used. Artificial ventilation and dialysis may be needed to support the function of the lungs and kidneys, respectively. To guide therapy, a central venous catheter and an arterial catheter may be placed. Sepsis patients require preventive measures for deep vein thrombosis, stress ulcers and pressure ulcers, unless other conditions prevent this. Some patients might benefit from tight control of blood sugar levels with insulin (targeting stress hyperglycemia), low‐dose corticosteroids or other drugs.
• In addition to symptoms related to the provoking infection, sepsis is characterized by evidence of acute inflammation present throughout the entire body, and is, therefore, frequently associated with fever and elevated white blood cell count (leukocytosis) or low white blood cell count and lower‐than‐average temperature. • The modern concept of sepsis is that the host's immune response to the infection causes most of the symptoms of sepsis, resulting in hemodynamic consequences and damage to organs. This host response has been termed systemic inflammatory response syndrome (SIRS) and is characterized by hemodynamic compromise and resultant metabolic derangement. • Outward physical symptoms of this response frequently include a high heart rate (above 90 beats per minute), high respiratory rate (above 20 breaths per minute), elevated WBC count (above 12,000) and elevated or lowered body temperature (under 36 °C or over 38 °C). • Sepsis is differentiated from SIRS by the presence of a known pathogen. For example SIRS and a positive blood culture for a pathogen indicates the presence of sepsis. Without a known infection you can not classify the above symptoms as sepsis, only SIRS.
• This immunological response causes widespread activation of acute‐phase proteins, affecting the complement system and the coagulation pathways, which then cause damage to the vasculature as well as to the organs. Various neuroendocrine counter‐
regulatory systems are then activated as well, often compounding the problem. Even with immediate and aggressive treatment, this may progress to multiple organ dysfunction syndrome and eventually death.
85
Our protocol:
Transport!! Later:
Depends on cause, if identified, and location of damage.
Possibly: Immuplex, Renafood, Livaplex, Echinacea as general considerations.
We have solved all health problems!
86

Session 105 Notes - Alaska Chiropractic Society

Transcription

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