Take a look at the American Heart Association statistics (6 mb file) here. You will recognize Drs. Seelig's and Rosanoff's figure on page 4. Perhaps the most startling finding in this data is the reduction in death rate for men in the last 20 years while the death rate for women has increased. I say the reason for this difference is because women supplement their diets with calcium to ward off osteoporosis, and men do not.
Look at what Dr. Mildred S. Seelig, MD, and Andrea Rosanoff PhD say about magnesium and statins in their 2004 article in the Journal of the American College of Nutrition article titled Comparison of mechanism and functional effects of magnesium and statin pharmaceuticals..
Here is the abstract: "Since Mg(2+)-ATP is the controlling factor for the rate-limiting enzyme in the cholesterol biosynthesis sequence that is targeted by the statin pharmaceutical drugs, comparison of the effects of Mg(2+) on lipoproteins with those of the statin drugs is warranted. Formation of cholesterol in blood, as well as of cholesterol required in hormone synthesis, and membrane maintenance, is achieved in a series of enzymatic reactions that convert HMG-CoA to cholesterol. The rate-limiting reaction of this pathway is the enzymatic conversion of HMG CoA to mevalonate via HMG CoA. The statins and Mg inhibit that enzyme. Large trials have consistently shown that statins, taken by subjects with high LDL-cholesterol (LDL-C) values, lower its blood levels 35 to 65%. They also reduce the incidence of heart attacks, angina and other nonfatal cardiac events, as well as cardiac, stroke, and total mortality. These effects of statins derive less from their lowering of LDL-C than from their reduction of mevalonate formation which improves endothelial function, inhibits proliferation and migration of vascular smooth muscle cells and macrophages, promotes plaque stabilization and regression, and reduces inflammation, Mg has effects that parallel those of statins. For example, the enzyme that deactivates HMG-CoA Reductase requires Mg, making Mg a Reductase controller rather than inhibitor. Mg is also necessary for the activity of lecithin cholesterol acyl transferase (LCAT), which lowers LDL-C and triglyceride levels and raises HDL-C levels. Desaturase is another Mg-dependent enzyme involved in lipid metabolism which statins do not directly affect. Desaturase catalyzes the first step in conversion of essential fatty acids (omega-3 linoleic acid and omega-6 linolenic acid) into prostaglandins, important in cardiovascular and overall health. Mg at optimal cellular concentration is well accepted as a natural calcium channel blocker. More recent work shows that Mg also acts as a statin." Why bother taking the pharmaceutical company junk when magnesium works better?
I am reminded of the story of the boiling frogs. In biology, there is a famous experiment using frogs. A frog suddenly dropped into hot water will jump out instantly! Saving his life. On the other hand, a frog placed in warm water will enjoy the warmth and not jump out. If the heat is slowly increased to higher and higher temperatures, the frog will unknowingly cook to death. In this respect, we are like boiling frogs, slowly dying of an unknown and unrecognized threat. We responded as a nation instantly to the Al Qaeda attack on America. We are very good at this, but we are dying at the rate of a 9/11 every day from high calcium/low magnesium and can't see it. Do you enjoy the warmth?
More. I am 68 years old and my blood pressure is 100/60. Who cares what the other cardiac risk are when one has this "teenager" blood pressure! I do keep my salt, carbohydrate and fat intake low and never smoke or drink. I do take 500 mg of magnesium as magnesium citrate (or glycinate) every day and I am not overweight, but can't stand to sweat, so I don't work out, although I regularly do manual labor on my central Texas ranch. Enough said?
If you are on cardiac drugs and decide to do nature's magnesium plan, then you need the help of a willing-physician (good luck) to do it carefully. However, the best thing to do first is read "The Magnesium Factor" by Mildred S. Seelig, MD, MPH and Andrea Rosanoff, PhD. On pages 77 through 84, they state the following (much abbreviated) plan:
- Read Dr. Seelig's book before taking any major action.
- Make certain that you have primary hypertension.
- Trust your doctor on the immediate need for drugs, but start with magnesium for the long term.
- Consider metabolic syndrome X (other low magnesium deficiency symptoms). They will likely vanish too.
- Be careful if you are using potassium sparing diuretics or beta-blockers, because potassium can go dangerously high (or low if on thiazide or some of the stronger loop diuretics).
- Determine your potassium and magnesium levels using red blood cell testing.
- Replenish your potassium and magnesium levels gradually.
- Over the following few weeks, gradually lower your medication.
- Consider a good multi-vitamin, multi-mineral supplement, and increase magnesium and potassium intake to high doses gradually.
- If this works, but insufficiently, try alternate methods of magnesium administration.
- If diarrhea develops, control it immediately using these tips.
- Again, read Dr. Seelig's book before taking any major action.
Add to that the following lesser known facts. Inflammation is a silent killer. One of the most significant markers, or indicators, predictive of who will get a heart attack is a substance known as C-reactive protein. C-reactive protein is a marker of chronic inflammation, which is a primary indicator of heart attack and diabetes risk. C-reactive protein management is a major goal of pharmaceutical drug pushers. It is a marker of "inflammation", not a cause of heart attacks. Clearly, inflammation and fibrosis are involved. That high magnesium blood levels is associated with low C-reactive protein and reduced cardiac inflammation is one of the most carefully guarded secrets of health. The effect of magnesium on reducing C-reactive protein and inflammation could only have been reported by researchers having a vested interest in improving peoples' health, and not improving corporate income. This is exactly what happened, and this critically important work was first published in 2002 by the team of F. Guerrero-Romero and M. Rodriguez-Moran working at the Medical Research Unit in Clinical Epidemiology, General Hospital of the Mexican Social Security Institute, Durango, Mexico. Do you really believe that Pfizer would support and publish such research? Not me! The abstract for the Guerrero-Romero and M. Rodriguez-Moran article reads:
"OBJECTIVE: To examine the association between serum magnesium levels and C-reactive protein (CRP) in non-diabetic, non-hypertensive obese subjects. DESIGN: Cross-sectional study. SUBJECTS: A total of 371 subjects, 101 men and 270 women. Of them 138 lean (37.2%), 133 (35.9%) overweight, and 100 (26.9%) were obese, matched by age. MEASUREMENTS: Fasting and 2 h serum glucose following a 75 g oral glucose load. Fasting serum total cholesterol, HDL- and LDL-cholesterol, triglycerides, C-reactive protein (CRP), albumin; and magnesium levels; urinary protein excretion; body mass index (BMI), waist-to-hip ratio (WHR), and blood pressure. RESULTS: The presence of CRP was documented in four (2.9%) lean, 13 (9.8%) overweight, and 20 (20.0%) obese subjects, and decreased magnesium levels (equal or less than 1.8 mg/dl), in 2 (1.45%) lean, 7 (5.2%) overweight, and 19 (19%) obese subjects. The lowest serum magnesium levels and the highest CRP concentrations were documented in the obese subjects. Twenty-three (82.1%) of the subjects with low serum magnesium (five overweight and 18 obese) showed CRP concentration equal or more than 10 mg/l. There was a graded significant decrease between CRP concentration and serum magnesium levels (r = -0.39, P = 0.002). The odds ratio (CI95%) between magnesium and CRP adjusted by age, sex, BMI and glucose tolerance status for the subjects within the low quartile of magnesium distribution was 2.11 (1.23-3.84). CONCLUSION: The results of this study show that low serum magnesium levels are independently related to elevated CRP concentration, in non-diabetic, non-hypertensive obese subjects."
More. You know what mitochondria are? They are the energy source of the cell. Without functional cellular mitochondria, the cell cools to room temperature and dies. If too many cells die, the organ dies. Consider the human heart. We need to do everything possible to keep our heart cells' mitochondria healthy. Certainly we shouldn't purposefully spear them with tiny daggers to kill them. Right? Low magnesium and high calcium creates tiny spears that kill the mitochondria from within. Dr. Burt Silver showed in 1975 in this original report that this exact situation occurred. Too much calcium in the presence of too little magnesium forms crystals that are mitochondria-killing spears. In the 3,000 reference 1980 book "Magnesium in Health and Disease" by Dr. Mildred S. Seelig, MD, (soon to be featured at the Magnesium Water site by Paul mason), Bert Silver and L. A. Sordahl shows microphotographs of these tiny calcium "spears", and that article is here. How about a tasty double cheese pizza for supper? Served hot with hundreds of billions of tiny heart-killing mitochondria-killing calcium spears! Sounds delicious to me!
More on what causes a lethal heart attack, at least the calcification of heart and arterial tissues that leads to most lethal heart attacks. Fibrosis is another factor. In 1997, Emile Mohler MD, et al. at the University of Pennsylvania, published an article concerning a "bone building" protein found in calcified aortic valves. Mohler and colleagues found "osteopontin", a protein that makes up the molecular scaffolding to which calcium sticks in the formation of bone, in calcified hearts. "We're the first group, to my knowledge, to directly isolate osteopontin in calcified valves," notes Mohler. "Identifying the molecular mechanisms underlying ossification of valves could lead to novel therapies to prevent or treat valve disease." In addition, the work may help to determine how calcium deposits form in the arteries of people with atherosclerosis and other vascular diseases. Cardiac valve calcification often results in obstruction of blood flow, which eventually leads to valve replacement. Collagen and specific bone matrix proteins are thought to provide the framework for ectopic tissue calcification. Osteopontin was present in both heavily and minimally calcified aortic valves and absent in noncalcified aortic valves. Osteopontin also localized with valvular calcific deposits, and macrophages were identified in the vicinity of osteopontin. These results, in addition to showing that osteopontin is present in calcified human aortic valves, suggest that osteopontin is a regulatory protein in pathological calcification. OK. Sounds interesting. George says, I wonder if magnesium... So, I searched PubMed. If we go to this Japanese group's work on osteopontin formation in kidneys, we find that osteopontin is eliminated when magnesium supplements are given. This should not be too difficult to understand and interpret in terms of cardiology too. Although osteopontin is absolutely necessary for bone formation, osteopontin formation in soft tissues, like in the heart and arteries as well as the kidneys, leads to deposition of calcium, which leads to narrowing of arteries, heart attacks, kidney disease and a wide variety of calcification health issues. A very popular book is The Calcium Bomb which proposes nanobacteria as cause of calcium buildup in cardiac tissue. Perhaps this is true, but is osteopontin buildup the mechanism by which nanobacteria construct their calcium shells? If yes, then magnesium may likely prevent their buildup.
The only other agent that I know of that inhibits osteopontin formation in soft tissue (but annihilates hypercalcemia, restores bone and generally heals tissue injuries) is gallium, an element that is normally found in the human to the extent of less than 0.2 milligrams. Gallium has clinical use in treating some serious bone loss diseases. I use a lot of gallium nitrate in the treatment of a bone/joint condition in horses called "navicular disease" with great effect. I have also postulated that gallium is an essential nutrient for survival of the 21st century. Gallium nitrate is effective in treating an otherwise incurable horse disease. I also give my horses large amounts of magnesium dietary supplements. My old horses run around like spring chickens! Magnesium and gallium really make them act young. Late in 2006, I published a veterinary journal article on gallium and the cure for navicular disease, which is located on the web here.
Getting back on track, we remember that mitral valve prolapse can be totally reversed in about one year with daily supplements of 1,000 mg of magnesium as magnesium orotate (probably any other form of biologically available magnesium too). Also, look at these graphics of "calcified hearts" on Google. To me, if your physician has told you that you have calcium deposits in your arteries and/or heart, you would be totally insane not to take about 1,000 mg of magnesium every day, twice what I must take, in hope that in about a year you might become free of this silent killer. The benefits are believed to start immediately, but complete clearance will take a while, perhaps a long while. If you must take that much supplemental magnesium, be prepared for gut problems, and study tips on this page on how to deal with magnesium-induced diarrhea.
Here is an example of a mouse poison made by Tomcat, which uses Vitamin D3 as a mouse poison. Still think lots of vitamin D3 is good for you? Dr. Mercola adds, "This is a major point: excess vitamin D will cause, not prevent, osteoporosis and hardening of your arteries. Please be very careful with cod liver oil. If you are unable to obtain vitamin D testing, then please do not exceed one to two teaspoons of cod liver oil or switch to plain fish oil (no vitamin D) immediately." According to this Wikipedia article, the exact long-term safe dose of bottled (supplemental) vitamin D is not entirely known, but dosages up to 250 micrograms (10,000 IU) /day in healthy adults are believed to be safe, and all known cases of bottled vitamin D toxicity with hypercalcemia have involved intake of or over 1,000 micrograms (40,000 IU)/day[37] of bottled Vitamin D. The U.S. Dietary Reference Intake Tolerable Upper Intake Level (UL) of vitamin D for children and adults is 50 micrograms/day (2,000 IU/day), with evidence that this value is too low by a factor of 5. In adults, sustained intake of 2500 micrograms/day (100,000 IU) can produce toxicity within a few months. For infants (birth to 12 months) the tolerable UL is set at 25 micrograms/day (1000 IU/day), and vitamin D concentrations of 1000 micrograms/day (40,000 IU) in infants has been shown to produce toxicity within 1 to 4 months. In the United States, overdose exposure of vitamin D was reported by 284 individuals in 2004, leading to 1 death.[39] The Nutrition Desk Reference states "The threshold for toxicity is 500 to 600 micrograms [vitamin D] per kilogram body weight per day." One point universally agreed, is that sunlight-derived vitamin D is harmless since the body shuts off production before it can become toxic. This is why sunlight is the best source of vitamin D.
Even snake keepers know too much calcium and bottled vitamin D will cause heart failure. Here is Fred's story. He was a python that died of a calcified heart. Apparently, some snakes are extremely sensitive to even small amounts of supplemental calcium, and bottled vitamin D.
The Lethal Hypothyroid - Low Magnesium Axis

Near the beginning of this essay, I reported that hypothyroidism can cause depression and that it must be treated and/or ruled out as cause of depression. Now there is clear evidence as shown in this figure that one of the thyroid hormones (T4) is directly related to magnesium serum levels in major depression, particularly in women. For more information see this clinical report. Levels below 0.9 mMol magnesium are considered low. We can extend this observation to say that hypothyroidism causes low serum magnesium, which appears to be the actual mechanism by which hypothyroidism causes depression. Interestingly, hypothyroidism does not affect calcium blood levels. Low magnesium caused by hypothyroidism also contributes heavily to cardiovascular disease and it must be corrected for longevity.
The simplest of all clinical tests, the use of a glass (not digital) thermometer held in the mouth far back under the tongue remains the gold standard for detecting hypothyroidism. The temperature should be taken over a full ten minute time and repeated for about a week each morning before warming up. An oral temperature below 97.5 degrees should be considered an 80% probability of hypothyroidism. While men can check their temperature any day of the month, women have a menstrual cycle that must be considered. The only accurate time of the month for determining true body temperature (as it relates to hypothyroidism) in women is while they are not menstruating. Some of the signs of hypothyroidism include: Fatigue, depression, difficulty concentrating, difficulty getting up in the morning, cold hands and feet or intolerance to cold, constipation, loss of hair, fluid retention, dry skin, poor resistance to infection, high cholesterol, psoriasis, eczema, acne, premenstrual syndrome, loss of menstrual periods, painful or irregular menstrual periods, excessive menstrual bleeding, infertility, fibrocystic breast disease, and ovarian cysts. There are many good web pages on thyroid disease, and I encourage you to examine them. The Father of thyroid disease research is Broda O. Barnes, MD and his web site is at http://www.brodabarnes.org/. His book "Hypothyroidism: The Unsuspected Illness" is both a standard and a classic, and it reports that untreated hypothyroidism is the cause of enormous amount of morbidity and mortality, often through heart attacks.
In fact, Dr. Barnes' research suggested that many heart attacks have a hypothyroid component, apparently via lowering magnesium serum levels, strongly suggesting that the American Heart Association figure cited by Seelig and Rosanoff is, while accurate, it and its many derivatives are misleading. The point that Dr. Barnes made in his Chapter 11 is that although few people died of heart attacks pre-1900 (as is clearly shown by the misleading American Heart Association figure), they died of infectious diseases, usually tuberculosis, before they had a chance to die of heart failure. His review of 70,000 autopsy records of Graz, Austria showed that a very large number of people dying early of non-cardiac deaths also had the same cardiovascular lesions and cholesterol buildup that are known to cause heart attacks and death. They simply died of something else earlier, and theoretically would have died of heart failure later.

Since Dr. Barnes' practice primarily addressed thyroid issues, he was baffled as to why his patients did not develop heart disease. He looked into his patients records and discovered the cause of many heart attacks! On his page 180, he showed that it was easy to prevent heart attacks in his patients - if and only if - hypothyroid issues were solved. His Table 1 shows the number of heart attacks in two different but essentially equivalent populations. The groups showed sex and age of patients, number of his patients treated with thyroid, total man-years patients were treated with thyroid, the resultant expected coronary cases (heart attacks) according to the Framingham study (not treated with thyroid) and coronary cases in the thyroid-treated patients of Dr. Barnes. He also showed that if hypothyroidism were corrected, high cholesterol issues would also go down. Further, he showed that hyperthyroidism would even further lower cholesterol! He strongly emphasized that only whole thyroid (