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Posted January 28, 2010: by Bill Sardi
His name: Dr. Lester Morrison.
His qualifications: Director and Research Professor, Institute for Arteriosclerosis Research, Loma Linda University, School of Medicine
Author: Coronary Heart Disease and the Mucopolysaccharides (1974, Charles C. Thomas)
In 1982 Dr. Morrison wrote: “I am Lester Morrison MD, and I have been a doctor for over 50 years. Much of that time has been devoted to finding a way to stop heart disease, which killed my mother, my father and several other members of my family and remains the number one killer in the U.S. and other developed countries.”
Dr. Morrison provided compelling evidence in the 1960s that heart and blood vessel disease could be reversed and prevented with natural molecules, particularly chondroitin sulfate. This was over 20 years prior to the advent of the first cholesterol-reducing statin drug, Mevacor (1987).
Dr. Morrison writes that his ideas involving heart disease went back as far as 1942. He first began is his research using natural molecules to heal damaged hearts and arteries.
Dr. Morrison’s research was published in no less than 8 different medical journals. He began his studies in the 1940s, working with choline, a natural component of lecithin.
Here are the results (below) of an early study published in the American Heart Journal. Lecithin was later to become an important component in Dr. Morrison’s Heart Saver Program. (Dr. Morrison’s book for the lay public by this title can still be purchased.)
He later conceived of the idea that gelatinous material, then known as mucopolysaccharides, today known as glycosaminoglycans, could heal damaged hearts and arteries. His work involved chondroitin sulfate, a molecule that is a normal component of the connective tissue in the body. Dr. Morrison calls it “the glue of life.”
He noted that chondroitin is the “coronary artery’s first line of defense against invasion by foreign substances,” such as cholesterol, bacteria and tumor cells. Chondroitin contributes to the elasticity of the blood vessels.
In cross section photos of coronary arteries, Dr. Morrison showed what a coronary artery looked in when an animal was fed a high-fat/cholesterol diet (left), revealing almost complete obstruction of the artery, and then when chondroitin sulfate was added to animal diets. The artery appears normal (right).
Left: Heart from rodent following heart attack (white area is scar tissue).
Right: Heart from rodent fed chondroitin sulfate, following heart attack.
Heparin is often administered to fresh heart attack patients to inhibit blood clots. The above photos demonstrate the superiority of chondroitin sulfate over heparin. Dr. Morrison said, “chondroitin did the job just as well as heparin, and the effect lasted longer. The anti-clotting property of heparin only lasts about 5 hours. In animal studies, chondroitin prolonged anti-clotting for up to two full days.”
It was time for Dr. Morrison to begin treating live human subjects with chondroitin. Here are the startling results of his first studies.
|IMPACT OF CHONDROITIN — HEART ATTACK PREVENTION
Heart attacks among patients over 6-year period
|60 patients||60 patients||60 patients||60 patients|
|Heart attack: fatal- with chondroitin||Heart attack/ fatal no chondroitin||Nonfatal heart attack- with chondroitin||Nonfatal heart attack- no chondroitin|
Total Risk Reduction
|Dr. Morrison treated 134 patients with chondroitin between 1942 and 1955
“The results were more than good, they were marvelous.”
Group 1: coronary arteriosclerotic heart disease
Group 2: arteriosclerosis of the brain arteries
Group 3: hardening of the arteries of the legs
More recent studies confirm Dr. Morrison’s earlier findings, that chondroitin sulfate is important in healing following a heart attack. Yet nothing is said of Dr. Morrison’s incredible discoveries decades prior.
Convincing evidence is also provided by Dr. Morrison with the presentation of individual cases, treated with chondroitin sulfate. Here is the data presented in three individual subjects.
Male, age 68
Previous heart attack 1949
Diagnosis in 1965: artery disease, high blood pressure, coronary artery (heart) disease
Multiple cerebro-vascular incidents (impairment of oxygen to the brain, “mini strokes”); visual impairment; disorientation; exhaustion; difficulty speaking; needs assistance to walk or stand; severe vertigo (imbalance); fainting (black outs); blood pressure 170/125; takes 5 drugs and a vitamin pill.
Began 10,000 milligrams of oral chondroitin sulfate in May, 1966, tapered to 3000 mgs after 4 months and 1500 mgs after 5 months. After 2 months, “dramatic persistent improvement noted.” All black-outs ceased; remarkable improvement in vision; able to walk without assistance; able to walk 6 miles each morning; notable hair growth.
Female, age 59
Diagnosis in 1966: coronary artery disease with angina (chest pain); rheumatoid and osteoarthritis
Chest pain radiating to right shoulder for 3 years accompanied by shortness of breath, exhaustion, fright; symptoms relieved by rest; blood pressure 118/74; ankle swelling. Takes vitamin E, lecithin, valium, nitroglycerine, multivitamin, thyroid, arthritis drug.
Began 6000 milligrams of oral chondroitin sulfate in June of 1966, tapered to 1500 mg by December, 1966.
Two months following chondroitin: “very marked clinical improvement; complete disappearance of angina chest pain; began swimming, walking. Remarkable increase in vitality.”
Male, age 77
Diagnosis: Heart attack (healed), general artery disease, high blood pressure, prostate enlargement, “heart pounding” and skipped heartbeats; weakness, shortness of breath on exertion, loss of memory, insomnia, nervousness; blood pressure 160/100.
Previous treatments: Digitalis, blood pressure drugs, lecithin, vitamin supplements.
Began 6000 milligrams of oral chondroitin sulfate in June of 1966, tapered to 1500 mgs by Oct. 1966.
By Sept. 1966 patient reported he “feels wonderful”; disappearance of fatigue, debility, nervousness, weakness on exertion; no skipped heart beats; bushy hair growth on head, black hair replacing white hair; cancellation of planned prostate surgery.
Two recent experiences come to mind in regard to chondroitin sulfate and post-heart attack patients.
A man living in a remote part of eastern Washington State was reported to have experienced crushing persistent chest pain, with swelling of his ankles, evidence of heart failure following a heart attack. The man was averse to seeking medical treatment. He was advised to take 1500 milligrams of chondroitin sulfate with other dietary supplements. Months later he was finally coaxed to undergo examination by a cardiologist who explained, by his past history, he had experienced some sort of serious cardiac event, but that there was no remaining evidence of the event.
In another instance, a 64-year-old man, who had experienced four prior heart attacks, which were evident on his electrocardiogram (EKG), took 1500 milligrams of chondroitin sulfate for a few months, then returned to a follow-up EKG in preparation for hernia surgery. Surprisingly, his EKG showed no evidence of a prior heart attack. The EKG technician thought his name had mistakenly been marked on an EKG of a healthy patient, so the EKG test was repeated, with the same result. This man has no more chest pain and is bicycling and hiking at a performance level uncharacteristic of a person his age.
The heart is slow to heal following a heart attack. Cell renewal is slow. Heart muscle tissue remains scarred (fibrotic). The provision of supplemental chondroitin sulfate appears to accelerate healing following a heart attack and would be a simple and unproblematic approach to regaining heart health following a heart attack. For the healthy, supplemental chondroitin sulfate would keep arterial plaque from developing altogether.
Since chondroitin also inhibits arterial calcification and cholesterol plaque as well as formation of blood clots, it becomes a comprehensive plaque and clot buster, proven in forgotten human studies. Chondroitin sulfate alone should be preferred over glucosamine, which requires a number of nutritional precursors before it can be converted to chondroitin.
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