Anonymous ID: aebade April 20, 2024, 2:34 p.m. No.20753341   🗄️.is 🔗kun   >>3342

https://uoeldcu.org/site/uploads/docs/Dead%20Doctors%20Dont%20Lie%20by%20Joel%20Wallach%20(z-lib.org).pdf

 

Selenium Deficiency Diseases

Direct Results

Anemia

“Age spots” & “Liver spots” Fatigue

Muscular weakness

Myalgia (muscle pain and soreness)

Fibromyalgia

Scoliosis

Muscular dystrophy (MD, White Muscle Disease, Stiff Lamb Disease)

Cardiomyopathy (Keshan Disease, “Mulberry heart” Disease)

Heart palpitations

Atrial fibrilation

Liver cirrhosis

Pancreatitis

Pancreatic atrophy

Infertility

Low birth weight

High infant mortality

SIDS (Sudden Infant Death Syndrome)

Cystic Fibrosis (congenital)

Indirect Results

HIV (increased rate of conversion to AIDS and transmission to fetus) ALS

(Lou Gehrig’s Disease) MS (Multiple sclerosis) Alzheimer’s Disease

Cancer (increases cancer risk significantly)

Selenium deficiency can result in infertility in both men and women.

Congenital selenium deficiency during pregnancy can result in a wide

variety of problems ranging from miscarriage, low birth weight, high infant

mortality, cystic fibrosis, muscular dystrophy, cardiomyopathy, and liver

cirrhosis. Selenium deficiency in growing children can result in crib death

or SIDS (Sudden Infant Death Syndrome). Sixty-five percent of SIDS

deaths occur in children on canned infant formulas. Slow growth, small size

(failure to reach genetic potential for size and mass), muscular dystrophy,

scoliosis, cardiomyopathy (muscular dystrophy of the heart muscle or

Keshan Disease), anemia, liver cirrhosis, muscular weakness,

Appendix A-265

lowered immune capacity, and neuromuscular diseases are also linked to Se

deficiency.

In young adults, selenium deficiency appears as anemia, chronic fatigue,

muscular weakness, myalgia, fibromyalgia, muscular tenderness,

pancreatitis, infertility, muscular dystrophy, scoliosis, and cardiomyopathy.

Cardiomyopathy is quite common in young athletes such as basketball and

football players at the high school, college, university, and professional

levels because of Se deficiency, as are multiple sclerosis and liver cirrhosis.

Selenium deficiency in adults appears as reduced immune capacity, anemia,

infertility, “age spots” or “liver spots”, myalgia, fibromyalgia, muscle

weakness, MS, ALS, Parkinson’s Disease, Alzheimer’s Disease,

palpitations or irregular heart beat, cardiomyopathy, liver cirrhosis, and

cancer.

In a review of the anti-cancer effects of selenium, Dr. Gerhard N.

Schrauzer, head of the Department of Chemistry, UCSD, states:

Selenium is increasingly recognized as a versatile anticar-cinogenic agent.

Its protective functions cannot be solely attributed to the action of

glutathione peroxidase. Instead, selenium appears to operate by several

mechanisms, depending on dosage and chemical form of selenium and the

nature of the carcinogenic stress. In a major protective function, selenium is

proposed to prevent the malignant transformation of cells by acting as a

“redox switch” in the activation-inactivation of cellular growth factors and

other functional proteins through the catalysis of oxidation-reduction

reactions of critical -SH groups or -S-S- bonds.

The growth-modulatory effects of selenium are dependent on the levels of

intracellular glutathione peroxidase and the oxygen supply. In general,

growth inhibition is achieved by the Se-mediated stimulation of cellular

respiration (more oxygen, less cancer). Selenium appears to inhibit the

replication of tumor viruses in animals and the activation of oncogenes by

similar mechanisms. However, it may also alter carcinogen metabolism and

protect DNA against carcinogen-induced damage. In additional functions of

relevance to its anticar-cinogenic activity, selenium acts as an acceptor of

biogenic methyl groups, and is involved in detoxification of metals and

certain xenobiotics. Selenium also has immunopotentiating properties. It is

required for optimal macrophage and natural killer cell functions.

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The school of pharmacy from the University of Georgia released a report in

August of 1994 that concludes that a human selenium deficiency is related

to the clinical onset of full blown AIDS in chronically infected HIV

patients. According to their report, HIV requires large amounts of selenium

for replication. In selenium deficient patients, the virus competes with the

patient for the limited amounts of available selenium. The HIV patient

actually dies of a chronic selenium deficiency encephalopathy, liver

cirrhosis, or cardiomyopathy. Long-term HIV patients (20 years or more)

that never developed full blown clinical AIDS had supplemented with large

amounts of selenium.

 

Clinical Diseases Associated with Vanadium Deficiency

Slow growth

Increased infant mortality Infertility

Elevated cholesterol

Elevated triglycerides

Hypoglycemia

Hyperinsulinemia

Narcolepsy

Prediabetes

Diabetes

ADD, ADHD

Depression

Manic depression, Bi-polar disease Tourette’s syndrome Cardiovascular

disease Obesity

 

Symptoms of Nickel Deficiency

( Poor growth

< Anemia

< Depressed oxidative ability of the liver

< Increased newborn mortality ( Rough/dry hair

( Dermatitis

( Delayed puberty

( Poor zinc absorption

Appendix A - 255

Less than 10 percent of ingested metallic nickel is absorbed. Nickel

deficiency was first reported in 1970. Nickel functions as a cofactor for

metalloenzymes and facilitates gastrointestinal absorption of iron and zinc.

Optimal tissue levels of vitamin B12 are necessary for the optimal

biological function of nickel. Vitamin B12 deficiency results in an increased

need for nickel by animals and man.

 

Deficiency Diseases of Manganese

Congenital ataxia

Deafness (malformation of otolithes) Asthma

Chondromalacia Chondrodystrophy “Slipped Tendon”

Defects of chondroitin sulfate metabolism (poor cartilage

formation) TMJ

Repetitive motion syndrome Carpal tunnel syndrome Convulsions

Infertility (failure to ovulate, testicular atrophy)

Still births/spontaneous abortions (miscarriages)

Loss of libido in males and females

Retarded growth rat

Anonymous ID: aebade April 20, 2024, 2:34 p.m. No.20753342   🗄️.is 🔗kun

>>20753341

Magnesium Deficiency Diseases

Asthma Anorexia

Menstrual migraines

Growth failure

ECG changes

Neuromuscular problems

Tetany (convulsions)

Depression

Muscular weakness

Muscle “ties”

Tremors

Vertigo

Calcification of arterial media “Malignant calcification” of soft tissue

The rate of absorption of Mg ranges from 24 to 85 percent. The lesser

absorption rate is for metallic sources of Mg, the higher rates of absorption

are associated with plant derived colloidal mineral sources. Vitamin D has

no effect on Mg absorption. The presence of fat, phytates, and calcium

reduces the efficiency of absorption. High performance athletes lose a

considerable amount of Mg in sweat.

The RDA for Mg is 350 mg/day for adult males, 300 mg/day for adult

females, and 450 mg/day for pregnant and lactating females. If the kidneys

are healthy there is no evidence of toxicity at up to 6,000 mg/day

 

Symptoms of Hypothyroidism

Hashmoto’s disease Fatigue

Cold intolerance

Muscle aches and pains

Heavy or more frequent periods

Low sex drive

Brittle nails

Weight gain

Hair loss

Muscle cramps

Depression

Constipation

Elevated blood cholesterol

Puffy face

Dry skin and hair

Inability to concentrate

Poor memory

Goiter

Symptoms of Hyperthyroidism

Grave’s disease

Insomnia

Heat intolerence

Excessive sweating

Lighter/less frequent periods

Hand tremors

Rapid pulse

Exophthalmos (“bug-eyes”) Weight loss

246 - DEAD DOCTORS DON’T DE

Increased appetite

Muscle weakness

Frequent bowel movements

Irritability

Nervousness

Goiter

Many foods and food additives are known as “goitrogens” because they

interfere with the thyroid metabolism and produce thyroid disease. These

foods and food additives are nitrates, broccoli, cabbage, Brussels sprouts,

etc.

 

Copper Deficiency Symptoms and Diseases

< White, grey, and silver hair

( Dry britde hair (“steely wool” in sheep)

( Ptosis (sagging tissue—eye lids, “crow’s feet,” skin, breasts,

stomach, etc.) ( Hernias (congenital and acquired) ( Varicose veins

(including hemorrhoids) ( Spider veins

( Aneurysms (cerebral artery, coronary artery, and large artery blowouts)

( Kawasaki disease (congenital aneurysms with streptococcal infection)

( Anemia (especially common in high milk and vegan diets)

< Hypo and Hyperthyroid dysfunction

( Arthritis (especially where bone growth plates are involved) ( Ruptured

vertebral discs

< Liver cirrhosis

( Violent behavior, blind rage, explosive outbursts, and

“criminal behavior” ( Learning disabilities

( Cerebral palsy and hypoplasia of the cerebellum (congenital

ataxia in sheep) ( High blood cholesterol ( Iron storage disease

(hemosiderosis) ( Reduced carbohydrate tolerance ( Neutropenia (low

neutrophil count)

Copper is required in many physiological functions: RNA, DNA, Lysil

oxidase cofactor, melanin production (hair and skin pigment), electron

transfer for subcellular respiration, tensile strength of elastic fibers in blood

vessels, skin, vertebral discs, etc. Neonatal enzootic ataxia (sway back,

lamkruis) was recognized as a clinical entity in 1937 as a copper deficiency

in pregnant sheep. Copper supplements prevented the syndrome, which was

characterized by demyelination of the cerebellum and spinal cord.

Cavitation or gelatinous lesions of the cerebral white matter, chromatolysis,

nerve cell death and myelin aplasia (failure to form during embryonic life)

were also identified as copper deficiency diseases in sheep. These are

identical to the classical changes of human cerebral palsy.

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Famous people affected or dying of an obvious copper deficiency include:

Albert Einstein (ruptured aneurysm), Paavo Airola (ruptured cerebral

aneurysm), Conway Twitty (ruptured abdominal aneurysm), and George

and Barbara Bush (thyroid disease and white hair). Four to six of every 100

Americans autopsied have died of a ruptured aneurysm. An additional 40

percent have aneurysms that had not ruptured.

The average well-nourished adult human body contains between 80 and 120

mg of copper. Concentrations are higher in the brain, liver, heart, and

kidneys. Bone and muscle have lower percentages of copper but contain 50

percent of the body total copper reserves because of their mass. It is of

interest that the greatest concentration of copper is found in the newborn.

Their daily requirement is 0.08 mg/kg, toddlers require 0.04 mg/kg and

adults only 0.03 mg/kg.

The average plasma copper of women ranges from 87 to 153 mg/dl. For

men it ranges from 89 to 137 mg/dl. About 90 percent of the plasma copper

is found in ceruloplasmin.

Copper functions as a cofactor and activator of numerous cupro-enzymes

that are involved in the development and maintenance of the cardiovascular

system. Deficiency of Cu in the pregnant female results in congenital

defects of the heart and brain, and Kawasaki disease, cerebral palsy, and

hypoplasia of the cerebellum. Deficiency of Cu also results in reduced lysyl

oxidase activity causing a reduction in conversion of proelastin to elastin

causing a decrease in the tensile strength of arterial walls and ruptured

aneurysms. Deficiency of copper also results in lower skeletal integrity

including a specific type of arthritis in children that forms bone spurs in the

bone growth plate. Lack of Cu can result in myelin defects, anemia, poor

hair keratinization, and loss of hair color. Nutropenia (reduced numbers of

neutrophillic WBC’s or white blood cells) and leukopenia (reduced total

WBC count) are the earliest indications of a copper deficiency in an infant.

Infants whose diets are primarily cows milk frequently develop anemia

and/or iron storage disease.

Menkes’ Kinky Hair Syndrome is thought to be a sex-linked recessive

defect of copper absorption. The affected infants exhibit retarded growth,

defective keratin formation of the hair, loss of hair pigment, low body

temperature, degeneration and fractures of aortic elastin (aneurysms),