Hypertension: A Natural Approach

A Natural Approach to Preventing Osteoporosis

Magnesium Taurate

Biochemistry
Magnesium plays a role in 300 enzyme reactions in the human body and is the most abundant divalent mineral cation in cells, second only in electrolyte quantity to potassium. Some examples of important enzyme reactions include hexokinase, which phosphorylates glucose by way of MgATP and other enzymes necessary for the glycolytic cycle. Magnesium is required for steps in the tricarboxylic acid cycle, and for 3 of the 4 steps in gluconeogenesis. It plays a role in fatty acid synthesis, amino acid activation via RNA and DNA polymerases, carboxylation reactions, and transketolase reaction involving thiamine. Magnesium plays a role in the formation of cyclic adenosine monophosphate (cAMP), which plays a role in asthma and the secretion of parathyroid hormone.

Antioxidant
Did you know the endogenous production of glutathione is dependant on magnesium? Low magnesium can induce a secondary glutathione deficiency. Many practitioners employ intravenous glutathione and oral absorbable forms of glutathione to increase antioxidant power in the body. However, a primary concern for these practitioners should be to increase magnesium in a highly absorbable form.

Energy Production
We are all familiar with the cellular energy currency of the body, adenosine triphophosphate (ATP). However, did you know that it exists in cells primarily as magnesium ATP (MgATP).

Ribose supplementation has become very popular for treating fatigue, fibromyalgia, heart disease and many other conditions. The negatively charged ribose has an affinity for magnesium.

Intestinal absorption studies indicate that the larger the supplemented dose, the lower the rate of absorption. It’s better to take a smaller supplemented dose of magnesium several times per day as opposed to one or two large doses.

Clinical Overview
Magnesium deficiency is associated with elevated triglycerides, initial elevations in PTH followed by low levels, refractory vitamin D deficiency as measured by 25 hydroxy-vitamin D blood test. Magnesium deficits elevate plasma concentrations of inflammatory cytokines such as IL-1, IL-6 and TNF alpha, which is associated with many disease states, including cancer and diabetes. An increase in histamine is to be expected, and all histamine sensitive conditions, from allergies, fatigue and irritable bowel deficiency will flare in the presence of a magnesium deficiency.

Taurine the Carrier
Taurine is the endproduct of cysteine catabolism. Taurine, 2-aminoethane sulfonate is formed from cysteine by removal of the carboxyl group and the oxidation of the sulfur to form a sulfonic acid group. Taurine is virtually void in strict vegetarianism.

Those who attend my neurobiology lectures know that I consider cysteine a conditionally essential amino acid, utilized in large quantities to assist detoxification pathways and support tissue growth and repair. From a neurobiological perspective, cysteine is responsible for starting and ending the catecholamine cycle. It begins the cycle as the core sulfur amino acid that drives heme thiolate – the ignition for tyrosine hydroxylase, the enzyme required for dopa production, and it ends the cycle by playing a major role in phenylethanolamine-N-methyl transferase conversion of norephinephrine into epinephrine.

Having said that, we can understand how cysteine can quickly deplete. Taurine synthesis requires both cysteine dioxygenase and cysteine sulfinate decarboxylase. S-Carboxymethl-L-cysteine has been used as a marker substrate for cysteine metabolism, by cysteine dioxygenase. About 20% of healthy individuals are poor s-oxydizers, based upon conversion of SCMC to urinary metabolites, SCMC sulfoxide or methylcysteine sulfoxide. A low capacity to oxidize SCMC has been observed in individuals with liver diseases and rheumatoid arthritis.

In clinical studies, taurine lowers elevated blood pressure, retards cholesterolinduced atherogenesis, prevents arrhythmias and stabilizes platelets--effects parallel to those of magnesium. The complex magnesium taurate may thus have considerable potential as a vascular-protective nutritional supplement. The effects of magnesium taurate in diabetes deserve particular attention, since both magnesium and taurine may improve insulin sensitivity, and also may lessen risk for the micro- and macrovascular complications of diabetes.

Because of its ability to travel intracellularly, and the similar characteristics it shares with the amino acid taurine, this reveals why magnesium taurate is the preferred form of supplemental magnesium, and a marriage made in heaven.

Clinical Use and Hypothesis in Medical Literature
Research papers have been written about the ability of magnesium taurate to reduce the incidence of preeclampsia, and along with fish oil to reduce the incidence of migraine headaches.

Clinical studies have found magnesium to play a major role in Insulin Action, Diabetes, and Cardio-Metabolic processes (Mol Aspects Med. 2003 Feb-Jun; 24 (1-3):39-52), and for hypertension (Hypertension, Vol 13, 227-232). The quantity of clinical studies in peer-reviewed journals is astounding. Type “magnesium” into medline search engine (an internet program that locates medical studies for health care professionals) and you will receive no less than 8000 hits!

By now, I’m sure you are aware why magnesium is an essential nutrient for health. Doctors categorize specific conditions that may benefit from magnesium in the following groups.

Cardiovascular/Endocrine*
Heart attack
High blood pressure
Diabetes
Stroke

Women's Health*
PMS
Pre-eclampsia
Pre-term labor
Osteoporosis

Pain Management/Energy/Respiratory*
Leg cramps
Migraines
Fatigue
Asthma

References
Med Hypotheses. 1996 Oct;47(4):269-72.
Med Hypotheses. 1996 Feb;46(2):89-100.
Med Hypotheses. 1996 Dec;47(6):461-6.
Mol Aspects Med. 2003 Feb-Jun; 24 (1-3):39-52
Diabetes Care. 2004 Jan;27 (1): 59-65
Diabetes Care. 2004 Jan;27 (1) 134-40.
Magnes Res. 1994 Mar;7(1):43-7.
Magnes Res 2000 Dec;13(4):275-84
Hypertension. 1998;32:260-265
Hypertension, Vol 13, 227-232
American Heart Journal 2000; 140: 212-8
Am Heart J 1998;136:480-90.

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Hypertension: A Natural Approach

Introduction: Blood Pressure Regulation and Hypertension
The body's ability to maintain its blood pressure is vital to life. Chronic hypertension is a major coronary heart disease risk factor. Hypertension contributes to half a million strokes and over a million heart attacks each year. The higher the blood pressure above the normal 120/80 mmHg, the greater the risk of heart disease. This condition is sometimes referred to as the silent killer, since people usually cannot feel the physical effects of high blood pressure.

There are two types of hypertension. Hypertension without an identifiable cause is categorized as essential or primary hypertension. When hypertension has a specific cause, such as in cases of kidney disease, it is considered secondary hypertension.

What is blood pressure? The pumping action of the heart must create enough force to push blood through the major arteries, into the smaller arteries, and finally into the tiny capillaries, where the porous walls permit fluid exchange between the blood and tissues.

Several common factors influence blood pressure. The nervous system helps maintain blood pressure by adjusting the size of the blood vessels, and by influencing the hearts pumping action. The kidneys assist in regulating blood pressure by adjusting mechanisms that change blood volume. For example, when blood flow to the kidneys is reduced, as would be the case in atherosclerosis, the kidneys set in motion actions that raise blood pressure by expanding blood volume, and constricting surrounding blood vessels. Obesity is a contributing factor because excess body fat, especially central fat, can precipitate hypertension. Another reason could stem from the extra miles of capillaries through which blood must be pumped. Insulin resistance, which is associated with obesity, triggers the pancreas to produce more insulin to move glucose into cells. High blood insulin may signal the kidneys to retain sodium, and may precipitate the development of hypertension. This may explain why hypertension is 2 to 3 times more likely to occur in people with Non Insulin Dependent Diabetes Mellitus (NIDDM), which is characterized by insulin resistance, than the rest of the population.

The treatment of hypertension often focuses on weight loss, dietary changes, exercise, and drug therapy. Aside from drug therapy, changes can be implemented by the individual as part of a therapeutic protocol.

For individuals with insulin resistance, consuming a consistent amount of carbohydrate, based on individual tolerance, as part of balanced meals, at regular times, is a good place to start. All simple sugars, refined foods, and processed carbohydrates must be avoided. The details of such a plan can be explained and designed by a Certified Nutritionist.

Now we will explore some natural approaches to address this condition.

Prior to addressing what can reduce blood pressure, we should briefly address often overlooked contributing factors to hypertension.

Other than a poor diet, obesity, certain diseases, sedentary lifestyle, and a genetic predisposition, there are several contributing factors to hypertension. Lifestyle factors, environmental factors, and stress management can all play a role in hypertension. Adjusting and addressing each of these factors can play a strong part in the nonpharmacological treatment of hypertension.

Lifestyle factors including smoking, alcohol, and coffee consumption, have been shown to increase blood pressure. Chronic alcohol consumption is a predictor of hypertension,(1) and nicotine has been found to increase blood pressure.(2) A study conducted in Paris, France, revealed higher systolic and diastolic blood pressure levels in coffee drinkers, compared to non drinkers, with levels rising in correlation to the amount of coffee consumed each day.(3)

Environmental factors such as lead contaminated drinking water and cadmium toxicity have been shown to promote hypertension. (4) Sources of lead exposure include lead paint, shooting ranges, water contamination via municipal water supplies or household lead pipes. Sources of cadmium include industrial commercial paints, and cigarettes. The best safe guard against lead and cadmium toxicity is to remain acutely aware of their sources and avoid them when possible. In the event of lead or cadmium toxicity, a Medical Doctor knowledgeable in the art of heavy metal poisoning can design a protocol to remove such metals. Mercury toxicity can also induce a rise in blood pressure. Common sources of mercury include specific fish such as shark, swordfish, king mackerel, tilefish, tuna steaks, canned tuna, sea bass, Gulf Coast Oysters, marlin, halibut, pike, walleye, white croaker, and largemouth bass (for more information on mercury in fish, please go to ewg.org). Essential fatty acids are essential for blood pressure regulation (33), and fish are terrific sources of these fats. Consuming low mercury content fish such as wild salmon from vitalchoice.com, as well as increasing the intake of nuts (walnuts especially), and supplementing with high quality omega-3 fats with EPA and DHA will cover your bases for essential fatty acid intake. A 24 hour urine collection test for toxic metals can reveal the presence of mercury. Personally, I like using captomer (DMSA) to chelate metals, along with intravenous therapy if lead and cadmium are present in toxic levels. Many readers are aware of intravenous chelation therapy. Keep in mind that intravenous chelation therapy will not remove mercury. It will remove lead and cadmium very effectively. To find a medical doctor knowledgeable in chelation therapies please contact the American College for Advancement in Medicine at acam.org.

How an individual handles stress can affect blood pressure. The ground work for the modern meaning of stress was laid by Walter B. Cannon, a physiologist at Harvard University around the turn of the century. He described the fight or flight response as a series of biochemical changes that prepare one to deal with threats of danger. Hans Selye, one of the first major researchers on stress, described what happens in the body during the fight or flight response. He found that any problem, imagined or real, can initiate the fight or flight response, which results in an increase in heart rate, breathing rate, muscle tension, and blood pressure. Stress reduction techniques from various disciplines of mind/body medicine such as biofeedback, meditation, yoga, and relaxation exercises, have all shown success in reducing blood pressure.(5)

Exercise, diet, supplements, and certain herbs can produce a hypotensive effect.

Reduction in body fat is one of the most effective and long lasting treatments for hypertension. In fact, individuals on medication for hypertension may be able to have their doctor reduce the dose, or in some cases, discontinue the drugs if they lose weight. Weight control reduces the risk of hypertension, and even a modest reduction in body weight may significantly lower blood pressure. Not only does physical activity help with weight control, but also moderate exercise, specifically aerobics, helps lower blood pressure directly. Back in 1990, a study in the Journal of the American Medical Association stated that those who engage in regular aerobic activity might not need medication for mild hypertension (263; 2766-2771).

Diet can be a powerful strategy to combat hypertension. An ideal diet would be one that is designed specifically for a patient. However, in general an anti hypertension diet should include all essential nutrients, be rich in fiber, high in potassium, calcium, and magnesium from vegetables, fruits, legumes, whole grains, low fat dairy or dairy substitutes fortified to match the nutritional profile of dairy, low in sodium and saturated fat, with total fat from monounsaturated and polyunsaturated sources totaling 30% of calories, and conducive to weight loss. Such a diet supports, the 1997 recommendations of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. This diet, which was rigorously evaluated in the Dietary Approaches to Stop Hypertension (DASH) clinical trial, substantially lowered blood pressure in normotensive and hypertensive individuals.(6) As noted in this diet, sodium is reduced. The association of a high sodium diet and high blood pressure has been established. However, there may be an even stronger incentive to reduce dietary sodium levels. In the December 1, 1999 issue of the Journal of the American Medical Association, researchers studied the relationship between dietary sodium and cardiovascular disease risk in overweight and nonoverweight individuals. They concluded that high sodium intake is strongly and independently associated with an increased risk of cardiovascular disease and all cause mortality in overweight individuals (282: 2027-2034). However, remember that we are all biochemically unique, and one person’s food may actually be another person’s poison. It is important to consult a certified nutritionist to design an individualized diet.

The supplement coenzyme Q10 has been utilized to treat hypertension. Almost ten years ago, the department of medicine, Mt. Sinai Hospital and Medical Center in New York, reported in the Journal of Clinical Pharmacology that its cardiovascular importance is now being realized in clinical trials worldwide.(7) In humans, a deficiency of coenzyme Q10 was found in 39% of patients with hypertension, compared to 6% of those with normal blood pressure. Providing these patients with 60 mg of coenzyme Q10 for eight weeks resulted in a 10% or greater decrease in blood pressure.(8)

In a double blind study, 20 hypertensive subjects with low serum coenzyme Q10 levels receiving 100 mg of coenzyme Q10 per day for 12 weeks, showed a significant reduction in systolic and diastolic blood pressure. (9)

In a 1994 study, 109 patients with known hypertension were given 225 mg of coenzyme Q10 daily, achieving a serum level of at least 2 mcg/ml. There was a decrease in systolic blood pressure from an average of 159 mmHg to 147 mmHg, while mean diastolic pressures dropped from 94 to 85 mmHg. Fifty percent of patients were able to decrease or eliminate their medication.(10)

The mechanism by which coenzyme Q10 reduces blood pressure is not fully understood. However, in 1990, Digiesi and Cantini demonstrated a decrease in resistance of blood vessel walls.(11) Further, clinical cardiologist Stephen Sinatra, MD, FACC, believes this action may be secondary to an improvement in the metabolic function of the cells, and that the antioxidant properties of coenzyme Q10 may help normalize cellular chemistry and promote optimal tone and compliance of the elastic vessel walls.(12)

Magnesium levels have been found to be consistently low in individuals with hypertension.(13) In one study, supplemental magnesium lowered blood pressure in 19 out of 20 hypertensives.(14)

At the division of Hypertension and Nephrology, National Cardiovascular Center, Suita, Osaka, Japan, a study was conducted on the effects of magnesium supplementation on office, home, and ambulatory blood pressure in patients with essential hypertension. Sixty untreated or treated patients (34 men and 26 women, aged 33 to 74 years) with office blood pressure greater than 140/90 mmHg were assigned to an 8-week magnesium supplementation period (400 mg), or an 8-week control period in a randomized crossover design. All of the blood pressures were lower during the magnesium supplemented period than in the control period. The results indicate that magnesium supplementation lowers blood pressure in hypertensive subjects, and this effect is greater in subjects with higher blood pressure.(15)

Practically identical to the above study, the same researchers repeated the parameters using 1 gram of calcium per day. The results revealed a small decrease in home, office, and ambulatory blood pressures during the calcium supplemental period.(16)

Another study examined the possible hypotensive effects of calcium supplementation. Fifty-seven borderline and mild-to-moderate hypertensive patients received 1 gram of calcium carbonate in a randomized, double-blind, placebo-controlled study for 14 weeks. The high calcium intake lowered systolic blood pressure by an average of 17 mmHg , and diastolic blood pressure by 11 mmHg.(17)

The mineral potassium was also found to reduce blood pressure. A 15 week randomized double-blind placebo controlled trial of oral potassium supplements was conducted on 37 patients who had mildly increased blood pressure and a normal dietary intake of sodium. The results revealed that moderate oral potassium supplements are associated with a long term reduction in blood pressure in patients who have mild hypertension.18 Other studies yield similar results.(19)

In a 1994 study in the British Medical Journal focused on 100 middle aged and elderly men and women, the combination of dietary fiber, potassium, and magnesium lowered the risk of high blood pressure.(20)

The non-essential amino acid L-Taurine may exhibit hypotensive properties. However, the doses utilized to reap hypotensive results vary widely in the studies. One study suggests 6 grams of taurine per day in divided doses 21, while N. Kohashi, et al., suggested 1 to 3 grams per day back in 1983 in the Japan Heart Journal. Some researchers suggest that the reduced blood pressure may be due to taurine’s blunting of epinephrine levels, and thus a reduction in signals from the nervous system. Others believe that taurine has been shown to assist in the cellular uptake of insulin, suggesting that this is a mechanism by which it may help reduce blood pressure. (22)

Several herbs have been found to reduce blood pressure. Garlic has a mild blood pressure lowering effect.(23) Forty-seven non-hospitalized patients with mild hypertension took part in a randomized, placebo-controlled, double-blind trial conducted by 11 general practitioners. The patients who were admitted had diastolic blood pressures between 95 and 104 mmHg. The patients then took either a preparation of garlic powder (Kwai) or a placebo of identical appearance for 12 weeks. Significant differences between the placebo and the garlic group were found during the course of therapy. For example, the diastolic blood pressure in the group having garlic treatment fell from 102 to 91 mmHg after eight weeks, and to 89 mmHg after twelve weeks. Serum cholesterol and triglycerides were also significantly reduced after eight and twelve weeks of treatment. In the placebo group, on the other hand, no significant changes occurred.(24)

Hawthorn (crataegus oxycantha) may have a mild blood pressure lowering effect.(25) According to studies, it may dilate coronary vessels, inhibit angiotensin-converting enzyme, increase the functional capacity of the heart, and possess mild diuretic activity.(26)

The herb Coleus Forskohlii has a long history of use in Ayurvedic systems of medicine. Its primary active chemical component, forskolin, was discovered in 1974 by the Indian Central Drug Research Institute.(27) Possible cardiovascular effects of the herb Coleus Forskohlii involve the lowering of blood pressure by increasing cAMP levels throughout the cardiovascular system, which results in relaxation of the arteries.(28) Here is an example of how that may work. Forskolin may cause the activation of an enzyme called adenylate cyclase, which increases the amount of an important cell regulating chemical called cAMP (cyclic adenosine monophosphate) in cells.(29) Normally, a stimulatory hormone, such as adrenaline (epinephrine) binds to a receptor site on a cell membrane and stimulates the activation of adenylate cyclase. However, it has been postulated that forskolin bypasses this need for direct hormonal activation, and as a result cAMP cellular levels rise. Such an increase in cAMP can result in relaxation of the arteries and other smooth muscles. Further studies have demonstrated its blood pressure lowering characteristics.(30)

Animal studies regarding maitake (Grifola frondosa) have shown the powerful hypotensive and cholesterol lowering actions of this dietary mushroom.(31) After a cursory review of some studies, the Department of Medicine, Memorial Sloan-Kettering Cancer Center, in New York, called for further epidemiological evidence of the role of this functional food class (edible mushrooms).(32) They concluded that Grifola (maitake) mushrooms have various degrees of immunomodulatory, lipid-lowering, antitumor, and other beneficial or therapeutic health effects without any significant toxicity.

In the final analysis, it is quite evident that alternatives to the pharmacological treatment of hypertension abound. However, it is important to note that all of the aforementioned substances should be discussed with your primary care physician prior to ingestion. Herbs for example, can potentate the antihypertensive action of blood pressure medication, promoting complications. It is important to have regular blood pressure screenings, and follow the advice of a primary care physician when confronted with the diagnosis of hypertension.

Current dose chart for some of the supplements in this article:

Coleus Forskohlii: The forskolin content of coleus root is typically 0.2-0.3%, therefore, the forskolin content of crude coleus products may not be sufficient to produce a pharmacological effect. To circumvent this, I recommend standardized extracts with a concentrated forskolin content. The current recommendation is 18% forskolin per 50mg capsule (= 9mg of forskolin), 2 to 3 times per day.

Hawthorn: standardized to contain 1.8% vitexin-4`-rhamnoside or 20% procyanidins, 100 to 250mg, three times per day.

Hawthorn in the dried capsule form (non-standardized), 3 to 5 grams, 3 times per day.

Freeze dried berries: 1 to 1.5 grams, three times per day.

L-Taurine is between 3 and 6 grams in divided doses per day, between meals (to avoid amino acid competition, as caused by proteinaceous molecules of food).

Garlic: total allicin potential of 4,000 mcg. (which is equal to approximately 1 clove of fresh garlic).

Coenzyme Q-10: < 60 to 250 mg.

Magnesium: 400 mg to 600 mg.

Calcium: 1000 mg.

Maitake: 3 to 7 grams.

EPA/DHA: 420 mg of EPA (eicosapentaenoic acid), two to three times daily).

References:

1. Fortman, S. P., et al., "The Association of Blood Pressure and Dietary Alcohol: Differences By Age, Sex, and Estrogen Use." American Journal of Epidemiology, 118 no.4 (Oct, 1983): 497-507.

2. Schroeder, K. L.; and CHen, M.S., Jr. "Smokeless Tobacco and Blood Pressure." New England Journal of Medicine 312 no.14 (April 1985): 919.

3. Lang, T., et al. "Relation Between Coffee Drinking and Blood Pressure: Analysis of 6,321 Subjects in the Paris Region." American Journal of Cardiology, 52 no.10 (Dec, 1983): 1238-42.

4. Pirkle, J.L., et al., "The Relationship Between Blood Lead Levels and its Cardiovascular Risk Implications", American Journal of Epidemiology, 121 no.2 (Feb, 1985): 246-258. Glauser , S.C., Bello, C. T., and Glauser, E.M., "Blood Cadmium Levels in Normotensive and Untreated Hypertensive Humans." Lancet, April 3, 1976, pp. 717-718. Ostergaard, Karen, "Cadmium and Hypertension." Lancet, March 26, 1977, pp. 677-678.

5. Goldstein, I. B., et al, "Home Relaxation Techniques for Essential Hypertension", Psychosomatic Medicine 46 no. 5 (Sept-Oct, 1984): 398-414. Brassard, C; and Couture, R.T., "Biofeedback and Relaxation for Patients with Hypertension", Canadian Nurse 89 no.1 (Jan, 1993): 49-52. Whyte, H.M., "NHMRC Workshop on Non-Pharmacological Methods of Lowering Blood Pressure", Medical Journal of Australia 2 no. 1 supplement (July, 1983): s13-s16.

6. Appel LJ, "Nonpharmacologic Therapies That Reduce Blood Pressure: A Fresh Perspective", Clin Cardiol 1999 Jul;22(7 Suppl):III1-5.

7. Greenberg S. Frishman, WH, "Coenzyme Q10 - A New Drug For Cardiovascular Disease", J Clin Pharmacol, 1990 July; 30 (7): 596-608.

8. Yamagami, T, Shibata, N, and Folkers, K, "Bioenergetics in Clinical Medicine: Studies on Coenzyme Q10 and Essential Hypertension", Res Commun Chem Pathol Pharmacol 11: 273; 1975. Folkers, K, et al., "Bioenergetics in Clinical Medicine, XVI: Reduction of Hypertension in Patients by Therapy with Coenzyme Q10", Res Commun Chem Pathol Pharmacol 31: 129; 1981.

9. Yamagami, T., Takagi, M., Akagami, H., Kubo, H., et al., "Effect of Coenzyme Q10 on Essential Hypertension: A Double-blind Controlled Study" In: Folkers, K, Yamamura, Y., (eds) Biomedical and Clinical Aspects of Coenzyme Q10. Vol. 5, Elsevier Sci Publ B. V., Amsterdam, 1986; 337-343.

10.Langsjoen, P. Willis, R., Folkers, K., "Treatment of Essential Hypertension with Coenzyme Q10", Mol Aspects Med, 1994: 15 (suppl): 265-272.

11. Digiesi, V, Cantini, et al, "Effect of Coenzyme Q10 on Essential Arterial Hypertension", Curr Ther Res, 1990; 5: 841-845.

12. Sinatra, Steven, The Coenzyme Q10 Phenomenon, Keats Publishing, New Canaan Connecticut, 1998)

13. Pizzorno, J.E., Murry, M. T., eds. A Text Book of Natural Medicine. Chapter VI: "Hypertension", Seattle, WA: John Bastyr Publications, 1988.

14. Dyckner, T., and Wester, P., "Effect of Magnesium on Blood Pressure", BMJ 286 no. 6381 (Jan, 1983) 1847-1849.

15. Kawano Y, Matsuoka H, Takishita S, Omae T, "Effects of Magnesium Supplementation in Hypertensive Patients: Assessment by Office, Home, and Ambulatory Blood Pressures", Hypertension 1998 Aug;32(2):260-5.

16. Kawano Y, Matsuoka H, Takishita S, Omae T, "Calcium Supplementation in Patients with Essential Hypertension: Assessment by Office, Home and Ambulatory Blood Pressure", J Hypertens 1998 Nov;16(11):1693-9.

17. Zhou C, Fan S, Zhou L, Ni Y, Huang T, Shi Y, "Clinical Observation of Treatment of Hypertension with Calcium", Am J Hypertens 1994 Apr;7(4 Pt 1):363-7.

18. Siani A, Strazzullo P, Russo L, Guglielmi S, Iacoviello L, Ferrara LA, Mancini M, "Controlled Trial of Long Term Oral Potassium Supplements in Patients with Mild Hypertension", Br Med J (Clin Res Ed) 1987 Oct 17;294(6604):961.

19. Patki PS, Singh J, Gokhale SV, Bulakh PM, Shrotri DS, Patwardhan B, "Efficacy of Potassium and Magnesium in Essential Hypertension: A Double-blind, Placebo Controlled, Crossover Study", BMJ 1990 Sep 15;301(6751):521-3.

20. Geleijnse, J.M, Witteman, J. C., et al., "Reduction on Blood Pressure with a Low Sodium, High Potassium, High Magnesium Salt in Older Subjects with Mild to Moderate Hypertension", Br. Med J (1994) 309 (6952): 436-40.

21. T. Fujuta, et al, "Effects of Increased Adrenomedullary Activity and Taurine in Young Patients with Borderline Hypertension", Circulation 75 (1987): 525.

22. W.G., Lampson, et al., "Potentiation of the Actions of Insulin by Taurine" J Physiol Pharmacol, 61: 457-62, 1983.

23. Silagy C, Neil AW, "A Meta-analysis of the Effect of Garlic on Blood Pressure". J Hypertens 1994; 12: 463-68.

24. Auer W, Eiber A, Hertkorn E, Hoehfeld E, Koehrle U, Lorenz A, Mader F, Merx W, Otto G, Schmid-Otto B, et al, "Hypertension and Hyperlipidaemia: Garlic Helps in Mild Cases", Br J Clin Pract Suppl 1990 Aug;69:3-6.

25. Blesken, V.R., "Use of Crataegus in Cardiology", Fortschr Med 1992; 15: 290-92.

26. Petkov, V., "Plants with Hypotensive, Antiatheromatous and Coronarodilating Action". Am J Chin Med 7, 1979, 197-236.

27. Ammon HPT and Muller AB, "Forskolin: From Ayurvedic Remedy to a Modern Agent" Planta Medica, 51, 473-477, 1985.

28. Seamon, KB, and Daly, JW, "Forskolin: A Unique Diterpene Activator of cAMPgenerating Systems". J Cyclic Nucleotide Res 7, 201-224, 1981.

29. Christenson JT, Thulesius O, Nazzal MM, Department of Surgery, Faculty of Medicine, Kuwait University. "The Effect of Forskolin on Blood Flow, Platelet Metabolism, Aggregation and ATP Release". Vasa 1995;24(1):56-61.

30. Dubey, MP, et al, "Pharmacological Studies on Coleonol, a Hypotensive Diterpene From Coleus Forskohlii", J. Ethnopharmacol 3, 1-13, 1981.

31. Kabir Y, Kimura S, "Dietary Mushrooms Reduce Blood Pressure in Spontaneously Hypertensive Rats (SHR)", Department of Food Chemistry, Faculty of Agriculture, Tohoku University, Sendai, Japan. J Nutr Sci Vitaminol ( Tokyo) 1989 Feb;35(1):91-4. Kabir Y, Yamaguchi M, Kimura S Department of Food Chemistry, Faculty of Agriculture, Tohoku University, Sendai, Japan, "Effect of Shiitake (Lentinus edodes) and Maitake (Grifola frondosa) Mushrooms on Blood Pressure and Plasma Lipids of Spontaneously Hypertensive Rats", Nutr Sci Vitaminol (Tokyo) 1987 Oct;33(5):341-6

32. Chang R, "Functional Properties of Edible Mushrooms", Nutr Rev 1996 Nov;54(11 Pt 2):S91-3.

33. Artemis P Simopoulos , “Essential fatty acids in health and chronic disease”, American Journal of Clinical Nutrition, Vol. 70, No. 3, 560S-569S, September 1999

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A Natural Approach to Preventing Osteoporosis

Introduction: Blood Pressure Regulation and Hypertension
Osteoporosis, one of the most common conditions associated with aging, is characterized by excessive loss of calcified matrix and collagenous fibers of bone. Holes or pores are formed as bone tissue is lost, increasing the risk of fracture.

Osteoporosis may be primary or secondary. Primary osteoporosis as defined by western medicine, is of unknown origin, occurs with aging, accelerates with menopause, and has no direct or singular cause. There are two types of primary osteoporosis, Type I, which involves losses of trabecular bone, and Type II, which involves losses of cortical and trabecular bone. Secondary osteoporosis has a direct cause. It can be due to endocrine abnormalities, bone marrow disorders, connective tissue disorders, gastrointestinal disorders, renal disorders, and due to some prescription drugs. An effort should be made to rule out the above anytime excessive bone loss occurs.

Nutrition, lifestyle and genetics contribute to the pathogenesis of osteoporosis. Primary osteoporosis can be prevented through proper diet, supplementation, and lifestyle modifications. Many nutrients are required to build bone. The minerals boron, calcium, copper, magnesium, manganese, phosphorus, silica, and zinc; the vitamins A, B6, B12, C, D, folic acid, K; and essential fatty acids are all involved in the bone building process.

The Standard American Diet is deficient in many of the above nutrients, and thus conducive to poor bone health. This diet also contains many excesses that can be considered as bone robbing. The high phosphoric acid content of many American diets due to the consumption of excess soda and other carbonated beverages has been linked to a higher rate of bone fractures. The high content of sodium from consuming processed foods results in a 20% increase in urinary calcium. High sugar intake increases urinary excretion of calcium, magnesium, chromium, copper and zinc. Diets high in the wrong types of fat (trans-fatty acids, hydrogenated, high quantity of saturated) may result in an increased incidence of osteoporotic fracture. To the contrary, essential fatty acids are important for bone health. In some cases, excess protein consumption may induce a condition called acidosis. The effects of which include increased leaching of calcium from bone.

Protein Controversy
Research has pushed to and fro regarding protein intake and bone loss. Some studies show that a high intake of protein from animal sources (milk, eggs, meat) increases calcium loss in the urine, threatening bone health. While other studies indicate that protein intake from food sources (particularly meats) have a negligible affect on calcium status, and argue that the studies that find high protein intakes increase urinary calcium excretion are based on protein powders and not animal foods. Furthermore, diets very low in protein, such as vegan diets, or strict vegetarian diets, have been shown to promote bone loss over time.

Let’s look to the past to learn more about the present association of calcium and protein. The question of high levels of protein in the diet and the issue of calcium excretion is of particular interest in light of Paleolithic diet research for two reasons. First, because estimates of the levels of protein--and specifically animal protein--in the human diet during at least the last 1.7 million years of human evolution (from the time of Homo erectus) are much higher than considered prudent in some sectors of the nutritional research community today. Secondly, at the very same time, the fossil evidence shows Paleolithic humans to have had high bone mass that would have been robust and fractureresistant compared to that of modern Western humans: in exact opposition to some of current nutritional theory about the alleged role of protein in causing osteoporosis. Let’s examine this apparent paradox.

Our hunter-gatherer ancestors certainly consumed a high intake of animal protein. However, they also had low intakes of sodium, higher magnesium, higher boron and higher vitamin K intakes than their modern counterparts. Estimates of calcium intake show that our hunter-gatherer ancestors consumed a diet rich in calcium from plant sources. Plant sources of calcium, such as collard greens and kale, can provide as much as a 55% absorption rate, compared to only 30% absorption rate from dairy. So, while our ancestors consumed large amounts of protein, yet had strong bones, we must note that their diet was better for bone health than our current standard American diet.

Although dietary calcium intake is most often the focus of nutritional recommendations for osteoporosis, what's important is the calcium balance, not just calcium intake. This is another case in which just looking at a single nutrient does not tell the whole story. Rather, you have to consider the entire diet. Whether planning an osteoporosis prevention program, or treating the condition, always work with a certified nutritionist to find your ideal intake of all essential nutrients, including protein.

The Caffeine Connection
America ’s love affair with caffeine can have profound negative consequences on skeletal health. Recent research in the American Journal of Clinical Nutrition examined the role of caffeine as a risk factor for bone loss. Women with high caffeine intakes had significantly higher rates of bone loss at the spine than did those with low intakes of caffeine. The researchers concluded that intakes of caffeine in amounts up to 300 mg (equivalent to 18 oz. of brewed coffee) accelerate bone loss at the spine in elderly postmenopausal women. Interestingly, women with a genetic variant of the vitamin D receptor gene appear to be at a greater risk for this deleterious effect of caffeine on bone.

According to the National Coffee Association and the US Department of Agriculture, a 6 oz. cup of brewed coffee contains 103 mg of caffeine. Coffee is not the only caffeine culprit. Soda, tea and medications contribute to the daily caffeine total.

Caffeine Content of Beverages, Foods, and Medications

• Dark chocolate, semi-sweet - 1 oz. serving = 20 mg of caffeine.
• Baker’s chocolate - 1 oz. serving = 26 mg of caffeine.
• Soft Drinks (various brands) - 12 oz. serving = 44.5 to 55 mg of caffeine.
• Aqua Ban (diuretic) - 1 standard dose = 200 mg of caffeine.
• Anacin, Excedrin, Midol (analgesics) - 1 standard dose = 33 to 65 mg of caffeine.
• Tea, major US brands - 6 oz. serving = 40 to 70 mg of caffeine (it seems that theanine, a component in tea, prevents the negative effects of caffeine – please read the article on theanine on this site).

Skeletal Health and Nutrient Deficiency Nutrient deficiencies must be addressed. One example of how a single nutrient lacking in the diet can result in weakening the skeletal system can be provided by magnesium. Magnesium stimulates the thyroid’s production of the bone preserving hormone calcitonin, which is necessary for the conversion of vitamin D into its active form, and is required by an enzyme necessary for the formation of new calcium crystals. It is easy to understand why a deficiency of this one mineral can result in vitamin D resistance syndrome, hyperparathyroidism (in which excess parathyroid hormone is produced, causing the withdrawal of calcium from bone), and thus is a causative factor in osteoporosis. Hypochlorhydria (low stomach acid) may also lead to deficiencies, since an acid medium is required for the absorption of certain minerals, especially calcium. Calcium citrate or citrate malate may circumvent low stomach acid production as a route to absorption. However, it is better to correct the underlying problem as it can lead to other chronic conditions.

Vitamin D
Without vitamin D, the small intestine absorbs no more than 10 to15% of dietary calcium. In a person with vitamin D insufficiency, the small intestine absorbs, on average, 30% of dietary calcium; during growth, lactation, and pregnancy, the efficiency increases to 80%. Vitamin D deficiency during bone development and growth causes the bone-deforming disease rickets. In adults bone growth stops and bone remodeling continues. Vitamin D deficiency in adults causes secondary hyperparathyroidism that can precipitate and exacerbate osteoporosis. How common is vitamin D deficiency? Surprisingly, it has made a resurgence in neonates and young children, in part because of the campaign to encourage all women to provide all of their infants’ nutrition through breastfeeding. Because there is very little, if any, vitamin D in human milk, infants, especially infants of women of color, are at high risk of developing vitamin D deficiency and rickets if they are not given a vitamin D supplement. Breastfeeding provides excellent nutrition, but truth be told, a vitamin D supplement is imperative to prevent deficiency.

The elderly are at risk for vitamin D deficiency because of poor dietary vitamin D intake and decreased exposure to sunlight. Dr. Michael Holick observed that 30%, 42%, and 84% of free-living white, Hispanic, and African American elderly women respectively, were vitamin D deficient at the end of August in Boston.

It has always been assumed that young and middle-aged adults are not at risk of vitamin D deficiency because of their outdoor activities and dietary intake. However, it was recently recognized that 42% of African American women throughout the United States were vitamin D deficient at the end of winter. Hard-working young and middle-aged adults who seldom spend any time outdoors or always wear sun protection outdoors are also at high risk of vitamin D deficiency. Holick observed that 32% of healthy adults 18 to 29 years of age were vitamin D deficient at the end of the winter in Boston. Obesity is often associated with vitamin D deficiency. It is now recognized that, whether vitamin D is ingested in the diet or obtained from exposure to sunlight, it is efficiently deposited in the large body fat stores and is not bioavailable. This is probably the reason that obese persons are chronically vitamin D deficient.

Dr. Holick feels there are 3 reasons for the increase in vitamin D deficiency. First, it is believed that either exposure to sunlight or dietary intake of vitamin D is adequate, or, therefore, that Americans and Europeans are not at risk of vitamin D deficiency. Second, physicians who perform routine blood work-ups often obtain a blood calcium value. If they find it to be normal, they assume that the patient is vitamin D sufficient, which is not correct. Third, the wise physician that wants to test for vitamin D, erroneously orders an analysis for the active form of vitamin D, 1,25-dihydroxyvitamin D know as (1,25(OH)2D), to determine the vitamin D status of a patient. Unfortunately, the test 1, 25(OH) 2D not only is not a measure of vitamin D status. The appropriate test is 25(OH) D. This blood test done through many labs, including Quest, is an accurate measure of vitamin D status.

The simplest way to obtain vitamin D is from moderate exposure to sunlight. Dr. Holick recommends exposure of hands, face and arms, or arms and legs to sunlight for a period equal to 25% of the time that it would take to cause a light pinkness to the skin (1 minimum erythemal dose). This is sufficient not only to satisfy the body’s requirement, but also to make sufficient amounts of vitamin D to store in the body for use on rainy days and during times when sun exposure is inadequate to produce enough vitamin D in the skin. Granted this is a very controversial position to take. I have attended numerous lectures given by Dr. Holick, and lectured at the same medical conference for the American College for Advancement in Medicine in May 2004. Holick is certain that he worked out the details to guidelines for the amount of sun exposure needed by people of all skin types to achieve their vitamin D requirement without significantly increasing the risk of skin damage and skin cancer. I’m not currently aware of any dermatologists that endorse this belief, but I can tell you that it has made a big difference in patients that I see in clinical practice. However, if a patient is at risk for, or had skin cancer, I will only recommend oral vitamin D supplementation. Please consult with your physician prior to attempting any sun exposure to replenish vitamin D stores.

Food Allergies/Sensitivities and Intolerances
A food allergy, defined as an immune response to a normally innocuous substance in the diet, can prevent absorption of some important bone building nutrients. The reason is that food allergies can induce micro inflammation in the small intestine where many bone building nutrients are absorbed, thus reducing surface area of absorption, resulting in a secondary deficiency. Food allergies/sensitivities and intolerances play a major role in health and disease. One fact that you should remember is that approximately 65% of the human immune system is in the intestines. It is called the gut associated lyphoid tissue or GALT. Can you imagine having an immune response to a food (a food allergy)? How could that not affect how you feel, and absorb nutrients.

Lactose intolerance can induce diarrhea in sensitive individuals which can result in loss of important bone building nutrients, especially magnesium.

Gluten intolerance or celiac disease (two completely separate conditions) definitely induces mineral deficiencies that will affect bone health. The only treatment known to date is a strict gluten free diet. Diagnosis of either condition is made by a medical doctor and the patient is routinely sent to a clinical nutritionist to eliminate the offending foods.

Anaerobes and Bone Health
Bacterial overgrowth of the small intestine is a serious digestive disorder that can inhibit nutrient absorption and lead to many health problems. Although widespread, it is frequently unsuspected in cases of chronic bowel problems and carbohydrate intolerance because its symptoms often mimic other disorders. What does this have to do with bone health? According to a new study by gastroenterologists at the University of Pavia in Italy, bacterial overgrowth of the small bowel may significantly increase the risk of progressive bone thinning. Using hydrogen breath testing, researchers identified fourteen patients with bacterial overgrowth of the small intestine. Researchers also measured bone density in these patients and in healthy controls. Based on World Health Organization criteria, researchers found that 86% and 93% of patients with small intestine bacterial overgrowth had significant bone loss near the hip (proximal femur) and lower back (lumbar spine), respectively. In fact, these patients were more than twice as likely to have bone loss than healthy controls. Their bone loss also tended to be more severe (Am J Gastroenterol 2000; 95(12)). Although underlying mechanisms are still unclear, researchers postulated that bacterial overgrowth in the small bowel could trigger bone loss by promoting calcium malabsorption as well as the loss of key enzymes in the small intestine.

Diet and Supplementation
Since each individual has a unique biochemistry, a proper bone building diet must incorporate healthy foods that contain all essential nutrients, specifically tailored and adjusted for food sensitivities, allergies, carbohydrate sensitivity, level of activity, and current state of health. One’s diet should be based on fish, poultry, lean meats, eggs, low fat dairy (if not allergic), or dairy substitutes formulated to match the nutritional profile of dairy (soy milk, rice milk, etc.), legumes (especially those containing isoflavones), whole grains, seeds, nuts, cold pressed oils (such as flax), and vegetables (especially dark leafy greens).

Supplementation should be considered to ensure that all essential nutrients are acquired in optimal amounts. Totals from food should be factored in prior to choosing a dosage. Doses should be adjusted for each individual by a certified nutritionist.

Adult recommendations:
Boron - 5mg
Calcium- 1200mg to 1500mg
Copper- 2mg
Magnesium- 400mg to 800mg
Manganese- 2mg to 5mg
Zinc- 15mg
B6- 50mg
B12- 50mcg to 5000mcg
C- 1000mg to 2000mg
D- 1000IU to 4000IU (extreme vitamin D deficiencies require a prescription dose).
Folic acid- 800mcg to 1mg
Ipriflavone – 600mg
K - 45mg
Strontium citrate – 680mg (taken away from any other mineral, especially calcium, preferably before bed).

Ipriflavone: the good, the bad, and the ugly
Isoflavones are compounds found in some plants that are analogous in structure to the estrogens found in animals and humans. Ipriflavone is a synthetic isoflavone synthesized from daidzein, an isoflavone of soy. Many researchers are increasingly touting the benefits of ipriflavone for prevention and treatment of osteoporosis, and other metabolic bone diseases including Paget’s disease, and hyperparathyroidism. But what are the facts?

The isoflavone ipriflavone has been found to stimulate the activity of bone building osteoblasts in several studies, and inhibit the effects of osteoclasts, the cells responsible for bone resorption.

Preliminary studies have also found ipriflavone effective in preventing bone loss associated with chronic steroid use, immobility, oophorectomy, and renal osteodystrophy. While ipriflavone appears to enhance estrogen's effect, it does not possess intrinsic estrogenic activity, making it an attractive adjunct or alternative to conventional hormone replacement therapy.

In one study, researchers who previously found that 0.625mg per day of conjugated equine estrogen (CEE) did not prevent bone loss the first year after oophorectomy, discovered that adding 600mg of ipriflavone to the same treatment resulted in inhibitory action of CEE and ipriflavone on the turnover of bone metabolism, and stimulatory action of ipriflavone on bone formation. They concluded that concomitant use of ipriflavone with CEE at an early stage after oophorectomy inhibited bone loss, and was considered to be effective in maintaining bone mass after oophorectomy.

In a study to assess the effects of ipriflavone administration in the prevention of the rapid bone loss that follows oophorectomy in women, patients received either 500mg of elemental calcium or 600mg of ipriflavone in addition to the same daily calcium supplement for 12 months. At the conclusion of the study the data indicated that ipriflavone can restrain the bone remodeling processes, and radial bone density showed no significant modification during the 12- month study period. The researchers concluded that these results demonstrate that ipriflavone administration may prevent the rapid bone loss that follows oophorectomy. In addition, they suggested that ipriflavone might represent an attractive alternative for the prevention of osteoporosis in postmenopausal women with contraindications to estrogen replacement therapy.

In a randomized controlled trial designed to see whether oral administration of ipriflavone could prevent bone loss occurring shortly after menopause, fifty-six women with low vertebral bone density, and with a postmenopausal age less than five years, were randomly allocated to receive either ipriflavone, 200 mg three times daily, or a placebo. All subjects also received 1,000 mg of elemental calcium daily. At the conclusion of the study, vertebral bone density declined after two years in women taking only calcium, but it did not change in those receiving ipriflavone. The researchers concluded that ipriflavone prevents the rapid bone loss following early menopause by reducing bone turnover rate.

The aim of a study at Cattedra di Medicina Interna, University of Rome, was to evaluate the effects of ipriflavone treatment on bone remodeling in primary hyperparathyroidism. Upon completion of the study, the researchers concluded that ipriflavone is indicated in the treatment of metabolic bone diseases characterized by a high bone turnover, since the data suggest that ipriflavone affects bone remodeling by inhibiting bone resorption without affecting bone formation.

In two double-blind studies, 149 osteoporotic women with vertebral fractures, age 65-79, received either 600mg of ipriflavone or a placebo. Both groups received 1000mg of elemental calcium. Urinary hydroxyproline was significantly decreased in ipriflavone treated patients, suggesting a reduction in bone turnover rate. A reduction of incident vertebral fractures was observed in ipriflavone treated women compared with control subjects. The data indicated that long-term treatment with ipriflavone may be considered safe, and may increase bone density, and possibly prevent fractures in elderly patients with established osteoporosis.

However, not all studies are favorable. According to a study in The Journal of the American Medical Association (March 21, 2001;285:1482-1488), ipriflavone appears ineffective, based on the results of a 3-year study in Denmark. Researchers studied a group of 474 postmenopausal women. The women received either 600 mg of ipriflavone daily or a placebo daily for 3 years. In addition, all women took 500 mg of calcium daily. Researchers measured the women's bone density at three different sites (spine, hip and forearm) every 3 months. No difference in bone density was seen between the two groups.

Researchers even found some women who took the supplement experienced a drop in their white blood cell counts, a condition that can impair the immune system. About 13% of women on ipriflavone developed lymphocytopenia, a drop in white blood cells that, in most of these cases, resolved after the women stopped taking ipriflavone. A drop in white blood cells can suppress immune function.

According to the researchers, although earlier studies have suggested ipriflavone does fight bone thinning, these findings suggest that compared with other osteoporosis treatments, ipriflavone offers little benefit. Discuss this issue with your doctor prior to supplementing with ipriflavone.

Hormones and Bone Health
I already discussed the role of the parathyroid in bone health. There are other major endocrine glands that are major factors in skeletal health. The pituitary gland secretes growth hormone stimulates cell division and protein development in bone and cartilage. This is why children with a low production of growth hormone develop growth abnormalities including short stature. If the adrenal glands are stressed, excess cortisol is produced which is a catabolic hormone (tissue breakdown hormone), and may result in poor bone health. The female sex hormones estrogen and progesterone enhance bone health. You can see in the above section on ipriflavone, that low estrogen can equal bone loss. However, researchers are also looking at the importance of progesterone in bone health. Many women might fit the mold of estrogen dominance set by Dr. Lee. It is thought that progesterone promotes bone formation and increases bone regeneration, possibly by enhancing the function of bone-generating osteoblast cells. The male hormone testosterone has been shown to enhance bone health. Men with low levels of this vital hormone are more prone to getting osteoporosis.

Strontium for Bone Health
Other than while studying the periodic table of elements, my first knowledge of strontium occurred while reading Dr. Wright’s Guide to Healing with Nutrition, a wonderful book written in 1971 as a treatise for medical students that ended up being a popular press book. Dr. Jonathan Wright discussed how radio active strontium 90 could be found in human bone, and could prevent the absorption of calcium in bone, and lead to cancer. Of course this was of concern in the 1950’s when above ground nuclear testing was in vogue. As a young student in nutrition 10 years ago, I actually pondered while reading that information “I wonder what non-radioactive strontium would do to bone?”

Strontium has been safely used as a medicinal substance for more than a hundred years. It was first listed in Squire’s Companion to the British Pharmacopoeia in 1884. Subsequently, strontium was used therapeutically in the United States and Europe. As late as 1955, strontium compounds were still listed in the Dispensatory of the United States of America.

The processes of bone resorption and formation are tightly governed by a variety of systemic and local regulatory agents. In addition, minerals and trace elements affect bone formation and resorption through direct or indirect effects on bone cells or bone mineral. Some trace elements closely chemically related to calcium, such as strontium have pharmacological effects on bone when present at levels higher than those required for normal cell physiology. The human body contains approximately 320 to 400 mg of strontium in bone, and connective tissue. If we look at clinical studies, indeed, strontium was found to exert several effects on bone cells. In addition to its antiresorptive activity, strontium was found to have anabolic activity in bone, and thus may have significant beneficial effects on bone balance in normal and osteopenic animals. Accordingly, strontium has been thought to have potential interest in the treatment of osteoporosis.

In a three-year, randomized, double-blind, placebo controlled study using 680 milligrams of strontium daily, women suffering from osteoporosis experienced a 41 percent reduction in risk of a vertebral fracture, compared with placebo. And, overall vertebrae density in the strontium group increased by 11.4 percent but there was a 1.3 percent decrease in the placebo group.

In a second study, 353 women who had suffered at least one vertebral fracture due to osteoporosis took varying levels of a prescription for of strontium referred to as strontium ranelate or a placebo. The women who took 680 milligrams of strontium daily had an increase in lumbar bone mineral density of approximately 3 percent per year, significantly greater than placebo. By the second year of the study, there was a significant decrease in additional fractures in the strontium group as compared with the placebo group.

These studies, the benefits of strontium ranelate (reducing fracture risk by as much as 50%) and the history of strontium in medical practice were discussed as an Editorial in the New England Journal of Medicine, January 29 th, 2004.

Further, scientists are looking into the benefits of strontium for osteoarthritis because researchers hypothesized that strontium might also improve cartilage metabolism, and for dental carries since 10% of subjects that had no dental carries in a 10 year study sponsored by the US Navy, resided in a small town that had unusually high levels of strontium in the municipal water supply. Strontium is available as strontium carbonate, strontium chloride, strontium sulfate, strontium gluconate and strontium citrate. In clinical research strontium gluconate was absorbed better than strontium carbonate. It is my clinical opinion that strontium citrate is absorbed better than the other forms of this metal.

Remember that strontium is very closely related to calcium. They both utilize the same carrier protein for transport. Calcium will win this tug of war effortlessly. The take home message is to take strontium 4 hours away from calcium (preferably other minerals as well) before bed. Currently, I dose strontium at 681mg in one dose prior to bed (each strontium citrate capsule contains 227mg of pure strontium citrate = 3 capsules) on an empty stomach (defined as 2 hours after a meal).

Live and Learn
Lifestyle factors negatively and positively affect bone health. Smoking is toxic to the liver, depletes the body of vitamin C, and decreases blood levels of estrogen. Alcohol inhibits the absorption and increases the excretion of calcium, magnesium, C, zinc, copper, and inhibits B6 functioning. Inactivity is associated with poor bone health. However, regular strength training sessions, three to four times per week, will help increase bone formation. Tension applied to bone by the actions of the muscles during weight lifting stimulates bone regeneration.

Shake, Rattle and Roll
The Beach Boy's weren't the only one’s to sing the praises of “good vibrations”. Researchers reported that having adult ewes stand on a platform with high-frequency vibration for 20 minutes each day for 5 days a week, for over 1 year, increased femoral trabecular bone density by 32%. Bone trabeculae were also shown to have closer spacing, which is consistent with stronger bone. However, there were no changes in cortical bone. This study follows a shorter study involving rats in which similar high frequency, low amplitude vibrations completely blocked the adverse effects on hind limb bone density induced by tail suspension. Could these animal studies be relevant to osteoporosis studies in human beings human beings?

At the recent meeting of the American Society for Bone and Mineral Research, Ward and Colleagues reported results of a small randomized, placebo controlled study among 20 children with cerebral palsy who used a similar vibration platform for 10 minutes per day, 5 days per week for 6 months. The researchers observed a significant increase in tibial, but not lumbar spine density in the treated group. The effects of a non-invasive 'good vibrations' approach, if shown to be generally applicable and comparably effective in human beings, would be of considerable potential benefit. Osteoporosis doesn't have to occur. By eliminating dietary components and lifestyle factors that are detrimental to the skeletal system, and exchanging those with behaviors such as acquiring an optimal intake of all bone-building nutrients from diet and supplements, eradicating deleterious bacterial overgrowth, and partaking in a regular strength-training program, one can enjoy having a strong healthy skeletal system throughout their life.

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