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Half of Diabetics in U.S. Have Arthritis, CDC Says
Last Updated: 2008-05-08 13:26:46 -0400 (Reuters Health)
By Julie Steenhuysen

CHICAGO (Reuters Life!) - People with diabetes are twice as likely to have arthritis, putting them in a double bind as the pain in their joints keeps them from getting the exercise they need to keep both diseases at bay, the U.S. Centers for Disease Control and Prevention said on Thursday.

They found that more than half of U.S. adults diagnosed with diabetes also have arthritis. "The prevalence of arthritis in a diabetic population is astoundingly high," said Dr. John Klippel, president of the Arthritis Foundation in a telephone interview. "If in fact you have both conditions, you are quite unlikely to be physically active," he said.

According to the report, nearly 30 percent of diabetics with arthritis are likely to be physically inactive, compared with 21 percent of diabetics who do not have arthritis.

That compares with 17.3 percent of adults with arthritis alone who are inactive, and 10.9 percent of adults with neither condition who are inactive. The CDC said the study suggests the pain of arthritis presents a barrier to physical activity - the very thing that might offer people some relief.

"For people with diabetes, physical activity helps control blood glucose and risk factors for complications. For people with arthritis, physical activity reduces pain and improves function," said Janet Collins, director of the CDC's National Center for Chronic Disease Prevention and Health Promotion.

Klippel thinks two things stand in the way. "Because arthritis affects the joints and is associated with pain, people with arthritis, when they begin to exercise, experience more pain," he said. "The other thing is there is a common misconception that exercise is bad for arthritis and it will damage joints."

He said many forms of exercise are in fact "joint-safe," including walking, swimming and biking. "If people walked 30 minutes a day it would have a profound effect on reducing their pain and improving their symptoms," he said.

Given the scope of the problem, Klippel said the finding will likely affect the way doctors and policymakers go about encouraging their patients to exercise. "Public health programs that are directed at controlling diabetes are going to need to pay a lot more attention to arthritis if they hope to get people to be physically active," he said.

The report is based on data gathered from a random telephone survey in 2005 and 2007. People were asked if they had ever been diagnosed with arthritis or diabetes.

It does not say what type of arthritis people had -- osteoarthritis, rheumatoid arthritis or another form -- or if people had type 2 diabetes, the most common kind that is associated with obesity and lack of exercise. Type 1 diabetes is an autoimmune disease often diagnosed at an early age.

 

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Healthy Teeth and Gums Important During Pregnancy
Last Updated: 2008-05-06 10:41:28 -0400 (Reuters Health)
By Megan Rauscher

NEW YORK (Reuters Health) - The American Dental Association (ADA) is reminding mothers-to-be about the importance of maintaining good oral health during pregnancy.

"There is a lot of research that shows a possible correlation between having untreated gum disease and a higher risk of having a preterm, low birth weight baby," Dr. Sally Cram, ADA consumer advisor noted in a telephone interview with Reuters Health.

In addition, pregnant women with gum disease may be more likely to develop pregnancy-related (i.e., gestational) diabetes. This is a concern, said Cram, a periodontist in Washington, D.C., "because women who develop diabetes during pregnancy often have a lot of problems with the birth; the baby is often overweight and the mother may get high blood pressure, which can be very risky for both mother and fetus." Gestational diabetes often leads to preterm birth. "If you are pregnant or planning a pregnancy, you should schedule a dental checkup to be sure you don't have brewing infection and gum inflammation," Cram advised.

Eating a well-balanced diet, brushing twice a day with fluoride toothpaste and flossing at least once a day is also important, according to Cram. The ADA recommends consumers use dental care products that have earned the ADA Seal of Acceptance. Pregnant women often crave sugary food and beverages, which can lead to cavities.

Don't be surprised if your dentist recommends more frequent cleanings during pregnancy, Cram added. For a woman with a history of gum disease or problems, "your dentist may recommend that you have your teeth cleaned every 2 or 3 months during the pregnancy," she noted.

Rising hormone levels that accompany pregnancy can irritate gums already battling gum disease and make it worse. "When the hormones get really high during pregnancy, some women are more susceptible to what we call pregnancy gingivitis, which is real severe inflammation in their gums. More information about pregnancy and oral health can be found at the American Dental Association's website -- www.ada.org.

 

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U.S. Not Meeting Folate Targets
Last Updated: 2006-10-03 16:01:22 -0400 (Reuters Health)
By Will Boggs, MD

NEW YORK (Reuters Health) - Folate intake in the U.S. is well below targets established by the Food and Drug Administration when it mandated folic acid fortification of enriched grain products in 1998, according to a report in the American Journal of Public Health.

Folate is a B vitamin that is found in food, and folic acid is the synthetic form of folate contained in dietary supplements and added to fortified foods.

"The folic acid fortification program was successful in that it increased the amount of folic acid consumed by women of childbearing age, and neural tube (birth) defects decreased 20 to 32 percent following the policy," Dr. Karen M. Kuntz from Harvard School of Public Health, Boston, told Reuters Health. "However," she said, "the success of the program falls short of the Food and Drug Administration's goal to increase the percent of women of childbearing age consuming a total of at least 400 micrograms per day of folic acid to 50 percent."

Dr. Kuntz and colleagues used data from the National Health and Nutrition Examination Surveys (NHANES III) to estimate folate consumption levels by age, gender, and racial/ethnic subgroups. Average folate intake increased after fortification for all population subgroups, the authors report, with higher average increases for whites than for blacks and Mexican Americans.

In all subgroups, women of reproductive age increased their intake by at least 100 micrograms per day, the results indicate, but persons aged 65 years or older increased their intake by less than 100 micrograms per day. Only 39 percent of white women, 26 percent of black women, and 28 percent of Mexican American women have reached the 400 microgram per day target for folate intake, the researchers note, despite substantial gains since fortification.

Surprisingly, the investigators say, more than half the subgroups had decreases in folic acid supplementation after the fortification program began. "Talking to patients of all ages (particularly women of childbearing age) about taking a daily multivitamin will move us closer the FDA's goal," Dr. Kuntz said.

SOURCE: American Journal of Public Health, October 2006.

 

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Part I: Cardiovascular Disease. Risk Factors and Fundamental Nutrition
By Decker Weiss, N.D.

For decades, the major cause of death in many industrialized Western countries has been cardiovascular disease (CVD), which includes heart disease and stroke. In the United States, CVD accounts for more deaths than from all cases of cancer, pulmonary disease, pneumonia, influenza, diabetes, and AIDS/HIV combined. It is currently estimated that 60 million Americans suffer from some form of CVD.1

Generally, CVD is the result of multiple genetic, metabolic, behavioral, and environmental influences. These may include elevated stress levels, high blood pressure, physical inactivity, poor diet, and diabetes.1 Fortunately, research suggests that the presence and impact of certain CVD risk factors can be reduced through nutritional support and a healthy lifestyle.

Stress and CVD
Recent studies offer compelling evidence that stress contributes significantly to the development of CVD. For instance, animals who were exposed to varying levels of mental stress demonstrated an increased number of injured cells in the aorta as well as increased atherosclerosisthe buildup of cholesterol-rich plaque in the arteries.2,3 In other mental stress studies, it was shown that stress may cause poor blood circulation and elevated homocysteine in humans.4,5

Stress management, along with nutritional support, can help reduce levels of daily stress and their effects on the body. Studies have shown that the stress on the cardiovascular system may be reduced through group psychotherapy, health education, and behavioral and lifestyle adjustments. In addition, supplementation with antioxidants, magnesium, B vitamins, as well as herbs such as rehmannia root (Rehmannia glutinosa), dong quai root (Angelica sinensis), schisandra fruit (Schisandra chinensis) and codonopsis root (Codonopsis pilosula) may help alleviate and protect against the psychological and physiological effects of stress.6-13

Fundamental Protective Factors
The heart and coronary blood vessels are highly susceptible to oxidative stress caused by the buildup of free radicals, damaging compounds formed by various body functions or taken in from the environment. Nutrients such as vitamin E and coenzyme Q10 have powerful antioxidant capabilities that enable them to prevent the initial free radical damage that contributes to the development of CVD.6

Vitamin E - Over the past few decades, research has continuously shown that vitamin E offers significant protection against CVD. In fact, vitamin E has been shown to reduce the risk of heart attack and atherosclerosis. Since vitamin E is an antioxidant, it plays a significant role is lessening the harmful effects of oxidative stress.6

Coenzyme Q10 (CoQ10) - CoQ10 is found highly concentrated in organs that require a large energy supply, including the heart. However, individuals with cardiac disorders have been identified as having abnormally low levels of CoQ10. Like vitamin E, CoQ10 has antioxidant properties. A study conducted on 40 patients who were treated with 150 mg of CoQ10 for 7 days prior to undergoing elective coronary artery bypass surgery established that the concentrations of oxidative compounds decreased.14

Nutrients for Lowering Blood Pressure and Improving Circulation
High blood pressure may aggravate the build up of plaque (atherosclerosis) on the artery walls, and cause damage to the heart structures. Fortunately, certain nutrients have been shown to naturally lower blood pressure.

Magnesium, Calcium, and Potassium - Epidemiologic data suggests that adequate amounts of these minerals should be consumed to help prevent and treat high blood pressure.15 When 60 patients with high blood pressure were given supplements containing magnesium, blood pressure was significantly reduced after 8 weeks.16

Essential Fatty Acids-Omega-3 and Omega-6 fatty acids act to reduce the production of certain compounds known to negatively affect blood pressure. By reducing the production of these harmful compounds, omega-3 and omega-6 fatty acids support healthy blood flow and thus reduce blood pressure. For instance, in a study of 46 elderly patients, treatment with high doses of omega-3 and omega-6 fatty acids significantly reduced blood pressure in an 8-week period.17

Garlic (Allium sativum) - Garlic has been used since the early part of this century for treatment of elevated blood pressure.18 In an analysis of studies, it was concluded that the overall reduction in blood pressure, as compared to baseline measures, was greater in garlic-treated subjects than in placebo subjects.19 Garlic primarily dilates blood vessels to improve blood flow.

Hawthorn (Crataegus oxyacantha) - The active constituents found in hawthorn may help lower blood pressure, help the heart work more efficiently, and increase ejection fraction - the percentage of blood leaving the heart during each beat.20,21 The higher the ejection fraction, the better the heart's ability to pump oxygen-rich blood throughout the body. These beneficial actions of hawthorn contribute to healthy cardiovascular function.

Horse Chestnut (Aesculus hippocastanum) - Horse chestnut seeds contain a complex mix of flavonols - compounds that increase the tone (strength) of the veins. Increasing vein tone may improve blood flow where restriction may exist due to weak veins.22

Lifestyle and Dietary Factors
While nutritional and herbal support can greatly aid in the prevention of CVD, a healthy lifestyle remains paramount.

Exercise - Regular exercise has been proven to have beneficial effects on a variety of chronic disease conditions, and cardiovascular disease is no exception.1 Sedentary individuals should begin a program that involves aerobic activity that is sustained for a period of 30 minutes at least three times per week.

Diet - Studies show that a diet high in saturated fats, cholesterol, fried foods, sugar, alcohol, caffeine, and animal proteins increases CVD risk. Conversely, the consumption of a diet high in fiber, fruits, and vegetables is recommended.

Diabetes - Up to 70% of deaths in persons with diabetes are from coronary artery disease and congestive heart failure.23-25 A reduction of carbohydrates and the addition of nutritional factors such as chromium, vanadium, fenugreek, and B vitamins can help stabilize blood glucose and increase insulin sensitivity, and thus are important in preventing CVD.26-29

Conclusion
Researchers are beginning to realize that while clinical care is sometimes necessary and important, it often falls short in the realm of prevention. A great deal of examination conducted over the last few decades has identified select nutrients and herbs that have a profound positive effect on the cardiovascular system. It is now understood that the sooner preventive measures are taken, the more likely CVD can be prevented.1

References
1. Cardiovascular Disease. Centers for Disease Control and Prevention. (n.d.). Retrieved July 14, 1999, from http://www.cdc.gov/nccdphp/cardiov.htm
2. Watson SL, Shively, CA, Kaplan JR, et al. Effects of chronic social separation on cardiovascular disease risk factors in female cynomolgus monkeys. Atherosclerosis 1998;137(2):259-66.
3. Skantze HB, Kaplan J, Pettersson K, et al. Psychosocial stress causes endothelial injury in cynomolgus monkeys via beta1-adrenoceptor activation. Atherosclerosis 1998;136(1):153-61.
4. Stone PH, Krantz DS, McMahon RP, et al. Relationship among mental stress-induced ischemia and ischemia during daily life and during exercise: the psychophysiologic investigations of myocardial ischemia (PIMI) study. J Am Coll Cardiol 1999;33(6):1476-84.
5. Stoney CM. Plasma homocysteine levels increase in women during psychological stress. Life Sci 1999;64(25):2359-65.
6. Sinatra ST, DeMarco J. Free radicals, oxidative stress, oxidized low density lipoprotein (LDL), and the heart: antioxidants and other strategies to limit cardiovascular damage. Conn Med 1995;59(10):579-88.
7. Guyton AC. Textbook of Medical Physiology. 8th ed. Philadelphia: W.B. Saunders; 1991.
8. Galland L. Magnesium, stress and neuropsychiatric disorders. Magnes Trace Elem 1991;10:287-301.
9. Seelig MS. Consequences of magnesium deficiency on the enhancement of stress reactions; preventive and therapeutic implications (a review).
10. J Amer Coll Nutr 1994;13(5):429-46.
11. Santhosh-Kumar CR, Hassell KL, Deutsch JC, et al. Are neuropsychiatric manifestations of folate, cobalamin and pyridoxine deficiency mediated through imbalances in excitatory sulfur amino acids - Med Hypotheses 1994;43:239-44.
12. Baldewicz T, Goodkin K, Feaster DJ, et al. Plama pyridoxine deficiency is related to increased psychological distress in recently bereaved homosexual men. Psychosom Med 1998;60(3):297-308.
13. Bown D. Encyclopedia of Herbs & Their Uses. New York: Dorling Kindersley; 1995.
14. Bensky D, Gamble A. Chinese Herbal Medicine: Materia Medica. Seattle: Eastland Pr; 1993.
15. Chello M, Mastroroberto P, Romano R, et al. Protection by coenzyme Q10 from myocardial reperfusion injury during coronary artery bypass grafting. Ann Thorac Surg 1994;58(5):1427-32.
16. Kendler BS. Recent nutritional approaches to the prevention and therapy of cardiovascular disease. Prog Cardio Nursing 1997;12(3):3-23.
17. Kawano Y, Matsuoka H, Takishita S, et al. Effects of magnesium supplementation in hypertensive patients: assessment by office, home, and ambulatory blood pressures. Hypertension 1998;32(2):260-65.
18. Margolin G et al. Blood pressure lowering in elderly subjects: a double-blind crossover study of omega-3 and omega-6 fatty acids. Am J Clin Nutr 1991;53:562-72.
19. Koch HP, Lawson LD, eds. Garlic: The Science and Therapeutic Application of Allium sativum L. and Related Species. 2nd ed. Baltimore: Williams & Wilkins; 1996.
20. Silagy CA, Neil HA. A meta-analysis of the effect of garlic on blood pressure. J Hypertens 1994;12(4):463-68.
21. Busse W. Standardized Crataegus extract clinical monograph. Quar Rev Natl Med 1996(Fall):189-97.
22. Leuchtgens H. Crataegus special extract WS 1442 in NYHA II heart failure. A placebo controlled randomized double-blind study. Fortschr Med 1993;111(20-21):352-54.
23. Tyler VE. Herbs of Choice: The Therapeutic Use of Phytochemicals. New York: Pharmaceutical Products Press; 1994.
24. Liu S, Stampfer MJ, Manson JE, et al. A prospective study of glycaemic load and risk of myocardial infarction in women. FASEB J 1998;12:A260.
25. Wolever TM. The glycemic index. World Rev Nutr Diet 1990;62:120-85.
26. Frost G, Leeds AA, Dore CJ, et al. Glycaemic index as a determinant of serum HDL-cholesterol concentration. Lancet 1993;353:1045-48.
27. Sharma RD, Raghuram TC, Rao NS. Effect of fenugreek seeds on blood glucose and serum lipids in type I diabetes. Eur J Clin Nutr 1990;44:301-06.
28. Whitney EN, Rolfes SR. Understanding Nutrition. New York: West Publishing; 1993.
29. Boden G, Chen X, Ruiz J, et al. Effects of vanadyl sulfate on carbohydrate and lipid metabolism in patients with non-insulin-dependent diabetes mellitus. Metabolism 1996;45(9):1130-35.
30. Anderson R, Polansky MM, Bryden NA, et al. Supplemental-chromium effects on glucose, insulin, glucagon, and urinary chromium losses in subjects consuming controlled low-chromium diets. Am J Clin Nutr 1991;54:909-16.

Advanced Nutrition Publications 2002



 

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Part II: Cardiovascular Disease. Nutritional Management of Clinical Markers
By Decker Weiss, N.D.

The battle to reduce the incidence of cardiovascular disease (CVD) has led researchers to the identification of several independent clinical markers that may play an even greater role in the development of CVD than well-known risk factors such as stress, hypertension, and diet.

These clinical markers include elevated levels of blood lipids, homocysteine, lipoprotein(a), and C-reactive protein as well as increased fibrinogen formation and platelet aggregation.1 Information gathered from these various clinical markers is of great value in identifying those at risk for CVD, including those who may not exhibit conventional risk factors. Through individual lifestyle changes along with combined vitamins, minerals, herbs, and antioxidant nutrients, independent clinical markers can be addressed and the risk of CVD may be reduced.

Blood Lipid Levels and CVD
The link between elevated blood lipid levels and CVD is well-documented.2-5 "Blood lipids" typically refers to triglycerides and the various forms of cholesterol. To find effective natural therapies for lowering blood lipid levels, numerous scientific studies have been conducted.6-10

Nutrients for Lowering Blood Lipid Levels
Inositol Hexanicotinate (IHN) - While niacin is a well-established CVD therapy due to its lipid lowering activity, it has many side effects. IHN is a natural, slowly metabolized form of niacin that is relatively free of adverse side effects as compared to regular niacin.11 A recent study showed that IHN is useful in decreasing levels of harmful cholesterol (LDL) while simultaneously increasing levels of beneficial cholesterol (HDL).12

Guggulipid - Guggulipid is derived from the mukul myrrh tree, Commiphora mukul. Human and animal research has shown that guggulipid is effective in lowering total cholesterol and triglycerides, while increasing HDLthe beneficial cholesterol.13-15 In a 12-week trial, 205 patients received 500 mg of guggulipid 3 times daily. A significant lowering of serum cholesterol (23.6%) and serum triglycerides (22.6%) was observed in 70% to 80% of the patients on the guggulipid. Of those who responded to therapy, 60% also had increased HDL cholesterol.8

Arjuna Bark (Terminalia arjuna) & Pushkarmoola Root (Inula racemosa) - Arjuna bark has historically been used to support cardiac function in Indian medicine (Ayurveda).9 More recently, it has been shown to lower blood lipid levels and improve the signs and symptoms of heart failure.16 Pushkarmoola root is another herb that promotes healthy lipid levels. A recent study demonstrated significant reductions in triglycerides and cholesterol after patients were given 1000 mg per day of pushkarmoola powder for 4 weeks.17

Garlic (Allium sativum) - Garlic exhibits a variety of useful effects in reducing risk factors of CVD. In a recent study, patients with coronary artery disease were given 4 g per day of garlic for 3 months. At the end of this study, LDL cholesterol levels decreased by 12.8%, triglycerides decreased by 15.2%, and HDL cholesterol levels increased by 22.3%.7 In addition, garlic's antioxidant activity provides protection against atherosclerosis (the build-up of cholesterol-rich plaque in the arteries).

Essential Fatty Acids - Various omega-3 fatty acids, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have received considerable attention for their lipid-lowering potential.10 In addition, omega-3 fatty acids help regulate blood pressure, heart rate, and blood clotting.18

Nutrients for Lowering Lipoprotein(a)
Lipoprotein(a), or Lp(a), is another blood lipid that, independent of cholesterol or triglycerides, indicates CVD risk. Reductions in Lp(a) of 31% and 36.4% have been observed in patients taking coenzyme Q10 (CoQ10) and IHN, respectively.19,20

Nutrients for Controlling Homocysteine Levels
Research has established that high levels of the amino acid homocysteine are a significant risk factor for CVD.21-24 The following nutrients help prevent a harmful excess of homocysteine:

Folate, Vitamin B6, Vitamin B12 - Low levels of these nutrients have been associated with an increased risk of CVD.21 Furthermore, the incidence of CVD is lowest among individuals with the highest intake of these nutrients. These vitamins play an important role in controlling homocysteine formation. In one recent study, men treated with a daily dose of 0.65 mg of folic acid, 0.4 mg of vitamin B12, and 10 mg of vitamin B6 for 6 weeks had a 49.8% reduction in homocysteine.25


Trimethylglycine (TMG) and Choline - TMG and choline are important factors in maintaining healthy homocysteine levels. TMG also assists the body in utilizing vitamins B6 and B12 and folate, which further supports the reduction of homocysteine.

Nutrients for Controlling Fibrinogen Levels and Platelet Aggregation
Elevated fibrinogen levels are a primary risk factor for CVD. Fibrinogen is converted to fibrin, a thread-like substance that can trap blood cells, platelets, and plasma to form a blood clot. Fibrin can also bind cholesterol, causing plaque development in the arteries.1,26 These processes compromise cardiovascular circulation. The following nutrients can help prevent this process:

Essential Fatty Acids - Essential fatty acids help prevent the lumping together of platelets, termed "platelet aggregation." One study showed a 60% to 65% decrease in platelet adhesion to fibrinogen after participants consumed high doses of the omega-3 fatty acid, EPA.27

Vitamin E - One of vitamin E's many beneficial effects on cardiovascular health include its ability to inhibit platelet aggregation.28,29 The cardiovascular-friendly actions of vitamin E make it a truly important preventive tool in CVD.

Select Herbs - Garlic reduces platelet aggregation by inhibiting fibrinogen. In addition, herbs such as Ginkgo biloba, ginger (Zingiber officinale), boswellia (Boswellia serrata), curcumin, a major component of turmeric (Curcuma longa), and coleus (Coleus forskohlii) have also been shown to reduce platelet aggregation through various modes of action.30-32

C-Reactive Protein
The level of C-reactive protein has been recognized as a long-term marker of CVD risk.1 Due to the link between platelet aggregation and levels of C-reactive protein, the nutrients discussed in relation to controlling fibrinogen levels and platelet aggregation offer suitable nutritional support.

Conclusion
Abundant scientific literature and clinical studies indicate that nutritional measures can have a significant positive impact on the progression of CVD. Thus, the importance of implementing measures to prevent its occurrence cannot be overstated.33 Through the combination of lifestyle changes and supplementation with specific nutrients and herbs, the risk of CVD may be greatly reduced.

References
1. Oparil S, Oberman A. Nontraditional cardiovascular risk factors. Am J Med Sci 1999;317(3):193-207.
2. Criqui MH, Heiss G, Cohn R, et al. Plasma triglyceride level and mortality from coronary heart disease. N Engl J Med 1993;328:1220-25.
3. Havranek EP. Primary prevention of CHD: nine ways to reduce risk. Am Fam Phys 1999;59(6):1455-63.
4. Sinatra ST, DeMarco J. Free radicals, oxidative stress, oxidized low density lipoprotein (LDL), and the heart: antioxidants and other strategies to limit cardiovascular damage. Conn Med 1995;59(10):579-88.
5. Yu-Poth S, Zhao G, Etherton T, et al. Effects of the National Cholesterol Education Program's Step I and Step II dietary intervention programs on cardiovascular disease risk factors: a meta-analysis. Am J Clin Nutr 1999;69:632-46.
6. Figge HL, Figge J, Souney P, et al. Nicotinic acid: a review of its clinical use in the treatment of lipid disorders. Pharmacother 1988;8(5):287-94.
7. Bordia A, Verma SK, Srivastava KC. Effect of garlic (Allium sativum) on blood lipids, blood sugar, fibrinogen and fibrinolytic activity in patients with coronary artery disease. Prost Leuks Ess Fatty Acids 1998;58(4):257-63.
8. Nityanand S, Srivastava JS, Asthana OP. Clinical trials with gugulipid. A new hypolipedemic agent. J Assoc Physicians India 1989;37(5):323-28.
9. Ram A, Lauria P, Gupta R, et al. Hypocholesterolaemic effects of Terminalia arjuna tree bark. J Ethnopharmacol 1997;55:165-69.
10. Levy E, Thibault L, Turgeon J,et al. Beneficial effects of fish-oil supplements on lipids, lipoproteins, and lipoprotein lipase in patients with glycogen storage disease type I. Am J Clin Nutr 1993;57:922-29.
11. Head KA. Inositol hexanicotinate: a safer alternative to niacin. Alt Med Rev 1996;1(3):176-84.
12. Goldberg AC. Clinical trial experience with extended-release niacin (Niaspan): dose-escalation study. Am J Cardiol 1998;82(12A):35U-38U.
13. Verma SK, Bordia A. Effect of Commiphora mukul (gum guggulu) in patients of hyperlipidemia with special reference to HDL-cholesterol. Indian J Med Res 1998;87:356-60.
14. Kapor LD. Handbook of Ayurvedic Medicinal Plants. CRC Press: Boca Raton, FL; 1990.
15. Satyavati GV. Guggulipid: A promising hypolipidaemic agent from gum guggul (Commiphora wightii). In: Economic and Medicinal Plant Research Vol 5. Plants and Traditional Medicine. New York: Academic Pr; 1991.
16. Bharani A, Ganguly A, Bhargava KD. Salutary effect of Terminalia arjuna in patients with severe refractory heart failure. Int J Cardiol 1995;49:191-99.
17. Bajpai HS, Ojha JK, Sharma PV. Inula racemosa as a hypolipidemic agent. Diabetes 1978;27(2):467.
18. Mahan LK, Escott-Stump S. Food, Nutrition, and Diet Therapy. 9th ed. Philadelphia: W.B. Saunders; 1996.
19. Seed M, O'Conner B, Perombelon N, et al. The effect of nicotinc acid and acipimox on lipoprotein(a) concentration and turnover. Atherosclerosis 1993;101(1):61-68.
20. Singh RB, Niaz MA. Serum concentration of lipoprotein(a) decreases on treatment with hydrosoluble coenzyme Q10 in patients with coronary artery disease: discovery of a new role. Int J Cardiol 1999;68:23-29.
21. Rimm EB, Willett WC, Hu FB, et al. Folate and vitamin B6 from diet and supplements in relation to risk of coronary heart disease among women. JAMA 1998;279(5):359-64.
22. Nygard O, Nordrehaug JE, Refsum H, et al. Plasma homocysteine levels and mortality in patients with coronary artery disease. N Engl J Med 1997;337:230-36. Selhub J, Jacques PF, Bostom AG, et al. Relationship between plasma homocysteine, vitamin status and extracranial carotid-artery stenosis in the Framingham Study population. J Nutr 1996;126:1258S-65S.
23. Abby SL, Harris IM, Harris KM. Homocysteine and cardiovascular disease. J Am Board Fam Prac 1998;11(5):391-98.
24. Ubbink JB, Vermaak WJH, van der Merwe A, et al. Vitamin requirements for the treatment of hyperhomocysteinemia in humans. J Nutr 1994;124:1927-33.
25. Ma J, Hennekens CH, Ridker PM, et al. A prospective study of fibrinogen and risk of myocardial infarction in the Physicians' Health Study. J Am Coll Cardiol 1999;33:1347-52.
26. Li X, Steiner M. Fish oil: a potent inhibitor of platelet adhesiveness. Blood 1009;76(5):938-45.
27. Chan AC. Vitamin E and atherosclerosis. J Nutr 1998; 128:1593-96.
28. Devaraj S, Jialal I. The effects of alpha-tocopherol on critical cells in atherogenesis. Curr Opin Lipidol 1998;9:11-15.
29. Srivastava KC. Isolation and effects of some ginger components on platelet aggregation and eicosanoid biosynthesis. Prost Leuks Med 1986;25:187-98.
30. Ammon HPT, Safayhi H, Mack T, et al. Mechanism of antiinflammatory actions of curcumine and boswellic acid. J Ethnopharmacol 1993;38:113-19.
31. Srivastava KC, Bordia A, Verma SK. Curcumin, a major component of food spice turmeric (Curcuma longa) inhibits aggregation and alters eicosanoid metabolism in human blood platelets. Prost Leuks Essent Fatty Acids 1995;52:223-27.
32. Cardiovascular Disease. Centers for Disease Control and Prevention. (n.d.). Retrieved July 14, 1999, from http://www.cdc.gov/nccdphp/cardiov.htm

Advanced Nutrition Publications 2002

 

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The Anti-Inflammatory Effects of Proteolytic Enzymes, Flavonoids, and Vitamin C in Comparison to NSAIDs

The term "proteolytic" refers to the group of enzymes that break down proteins. In the body, proteolytic enzymes - including trypsin, chymotrypsin, bromelain, and pancreatin - are produced in the pancreas. Because numerous studies have revealed their wide ranging benefits, these enzymes are available in supplemental form. According to Dr. J.P. Tarayre and Dr. H. Lauressergues in Drug Research, "The proteolytic enzymes, trypsin and chymotrypsin in particular, possess anti-inflammatory properties which have been known for some years now." Additional research has demonstrated the ability of proteolytic enzymes to accelerate recovery after minor injury and reduce the pain and stiffness that often accompany rheumatoid arthritis.

To further confirm these findings, researchers compared the anti-inflammatory effects of trypsin and chymotrypsin to seven well known non-steroidal anti-inflammatory drugs (NSAIDs). The proteolytic enzymes were combined with flavonoids and vitamin C - other substances known to reduce inflammation.

Researchers injected carrageenan - a seaweed extract that has been shown to induce inflammation and edema - in the hind paw of experimental rats. After determining the degree of inflammation and swelling in each animal, researchers examined the anti-inflammatory effects of trypsin and chymotrypsin combined with flavonoids and vitamin C.

Researchers concluded that "The combination studied...shows a more [profound] action than that of the non-steroidal anti-inflammatory substances [without] any side effects."

Drug Research 1977;27(6):1144-49.
Advanced Nutrition Publications 2002

 

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A Natural Defense Against the Hidden Causes of Food Intolerance

 

Lectin LockTM
Natural Defense Against a Hidden Cause of Digestive Concerns and Weight Gain

By Carolyn Pierini, CLS (ASCP), CNC

Last months article on lectins and their damaging potential to our health was a technical introduction to their chemistry. For many it was the first exposure to an extensive and emerging science that has far reaching applications. The fact that lectins interact with us on a day-to-day basis makes it an important topic to become familiar with even though our understanding of lectin effects is a complex one to grasp. It is generally accepted that real health begins with proper digestion demanding an intact and blissfully functioning digestive system. But it would appear from the amount of complaints related to digestion that physicians encounter daily that this first stage of health is being seriously compromised and in need of investigation. There are the probable reasons for faulty digestion like poor food quality, unhealthful eating habits around lifestyle, etc., but lectins give us a reason for poor digestion that is perhaps not so obvious.

While the first article was a technical glimpse into the world of lectins, this article will answer the question begged from the last article, So if lectins are in my foods and many are potentially harmful to me then what can I do to minimize my exposure to them? As part of the answer to this question, here is a very simplified recap of what lectins are, including their digestive impact and effects on our systemic health.1 Lectins are a class of proteins that are found in common foods especially grains, seeds, beans, nuts, some fruits and vegetables, and seafood. They act as a sort of an immune system for plants by sticking themselves to the structural carbohydrates (sugars) of invaders. When we eat foods containing these proteins we risk lectin attachments to the structural carbohydrates (sugars) antigens found in the gut and immune system. Our unique genetic make-up and the state of health will determine the lectins we are sensitive to and how we will react to them. It is important to note that many people will report that they do not feel any digestive disturbances but that does not mean that lectins are not affecting them. Lectin damage may be cumulative and show up as pathology years later. Lectin attacks in the gut initiate inflammation that may be expressed in other parts of the body. The fact that as humans we possess these cell surface sugars, such as n-acetylglucosamine, fucose, and mannose, and more, means that certain lectins that bind to those sugars will affect us all (but to different degrees). Also there are other genes that directly and indirectly affect how we deal with lectins.

Lectins from the diet damage the delicate intestinal lining (the microvilli) and negatively influence gut permeability (leaky gut) and protein digestion.

Lectins are capable of being actively endocytosed (transported) across the intestinal membranes into the general circulation where they may attach to other tissues (connective, nervous, bladder) causing immune dysfunction and systemic inflammation.

Lectins contribute to food sensitivities (or food intolerances) and may provoke the immune system to make antibodies against them.

Lectins are chemical messengers potent enough to initiate and aggravate existing inflammatory conditions including autoimmune diseases ( e.g. thyroiditis, lupus, rheumatoid arthritis, scleroderma, fibromyalgia, and pemphigus).

Lectins affect metabolism by mimicking hormones like insulin and blocking digestive hormones like cholecystokinin (CCK), contributing to significant weight gain. Weight gain is not as easy as calories in-calories out. All of the hormonal influences on metabolism are affected by insulin. How your body metabolizes calories is controlled by insulin. Refer to the January article for more detail here.

Lectins stimulate polyamines in the gut, which decreases the natural killer cell population and contribute to halitosis (bad-breath). Polyamines are endogenous growth factors that can stimulate growth in the digestive organs. According to animal studies, increases in the size of the intestines, pancreas and liver occurred when test animals were fed dietary lectins.

Symptoms of Lectin Sensitivities
Many of the common health problems that people complain of from day-to-day are related to the foods they consume. They do not often make the connection between how they feel and what they ate because often the reaction to food is not immediate and may appear over the course of several days. Lectin reactions are food intolerances and may cause true food allergies (see table below).

Symptoms of Lectin-Related Food Intolerances
Headaches, brain fog, lack of concentration
Skin problems such as acne, eczema, itchy skin
Water retention (edema) and puffiness in face, extremities, under the eyes
Bloating - a very common reaction
Easy weight gain and stubborn weight loss
Post-meal fatigue and chronic fatigue in general
Excess mucous, chronic clearing of the throat
Respiratory problems (asthma, chronic, non-infectious coughing)
Joint stiffness and pain (especially in the morning)
Urinary weaknesses, chronic urinary tract infection or cystitus
Abdominal pain and gas with meals, excessive belching (lectins have also been shown to reduce HCL levels)
Gastric reflux and stomach upset
IBS, spastic colon, other intestinal irritation
Hyperactivity, especially in children
Sinus problems, itchy nose (hayfever-like reactions), congestion and post-nasal drip
Insulin shifts in blood sugar control

Genetic individuality determines our recognition of food as friend or foe and it is not based on the nutritional value of a food. For example, tomatoes contain lycopene, an important antioxidant, but tomatoes also contain a panhemagglutinin lectin (Lycopersicon esculentum agglutinin) that is not harmless. It lowers mucin, binds to blood cells, nerve tissue, and interferes with gastrin in the stomach creating problems in susceptible people. (Consider watermelon, guava and red grapefruit or a supplement to consume adequate amounts of lycopene.) The same is true of many foods. Foods like corn, dairy, chicken, peas, bananas, beans and legumes, soy, potatoes, pomegranate, nuts, cantaloupe, seafood, wheat, millet, and many more, although they contain a variety of very healthful nutrients, contain potentially dangerous lectins that can be a problem for some people.


A Natural Shield Against Lectins
Since lectins are so prevalent in the diet it was suggested in the first article that a supplement regimen be considered to reduce lectin interactions. Lectins have the ability to bind to sugar residues of polysaccharides and amino sugars in the gut and on the intestinal cell surfaces. By consuming an array of these friendly sugar structures, which are part of our digestive makeup, then a type of decoy system is implemented in which sacrificial molecules are present to bind lectins and keep them from sticking to our cells and causing damage. The application of a lectin-locking device exists in a new product called Lectin Lock. Supplementing with these decoy sugars at the start of a meal allows for the binding of potentially harmful lectins and their elimination through the gut. Besides the all-important lectin binding, the product supports health in numerous other ways.

Mucins, which have been called digestive gatekeepers, are a family of heavily glycosylated proteins that protectively line the digestive tract. Saliva contains mucin, which moistens and lubricates the food we eat. According to Wikipedia, the dense sugar-coating of mucins makes them resistant to protein breakdown, which may be important in maintaining mucosal barriers in the gut. Mucins protect against yeast, bacteria and food sensitivities. Mucin has lectin-binding capacity. It contains the sugars that lectins like to stick to including sialic acids.

N-acetylglucosamine (NAG), the very specific form of glucosamine that binds the disruptive wheat lectin called wheat germ agglutinin (WGA), is another important nutrient. NAG is a glycoprotein contributing to the total glycosylation of the human body, which plays an important role in body structure and biological functions like immune regulation, inflammation, and cell signaling. This particular form of glucosamine is the most effective for lectin-binding. One of NAGs most interesting abilities is its tendency to suppress the anti-secretin effects of the lectin WGA. Secretin is a digestive hormone, which stimulates the pancreas to secrete pancreatic juice. The lectin WGA has been shown to inhibit secretin production by about 57 percent. However, administration of N-acetyglucosamine completely suppressed this effect.2 Binding or locking lectins that interfere with secretin may be particularly important in the management of autism. One abstract on secretin reported a study of three children with autism and GI problems who were given an infusion of secretin and became more social and communicative.3

Another lectin-blocking substance is Bladderwrack (Fucus vesiculosus). This nutritious seaweed component makes several contributions. The particular fucose sugars found in Bladderwrack, called fucoidins, are capable of binding to lectins and also microorganisms such as viruses, bacteria and yeast. Fucose is a favorite sugar attachment site on the surface of cells for Helicobacter pylori (the bacteria responsible for ulcers and gastritis) and Candida albicans. Microbes like these must be able to attach and anchor themselves to cells in order to become a problem. Therefore, L-fucose becomes an anti-attachment type of therapy. The fucose in Bladderwrack can bind not only to problem lectins but also to these two opportunistic pathogens, preventing their attachments and locking them up for elimination from the body. Supplementing with Bladderwrack reduces H. pylori, C. albicans, and harmful lectins, providing an example of selective therapy that doesn't disrupt other balances in the GI tract.

Studies also have shown fucoidins antimicrobial effects against herpes simplex virus, human cytomegalovirus, human immunodeficiency virus (HIV), certain strains of E. coli and all strains tested of Neisseria meningitides. Research and in vitro studies have provided evidence that fucose sugars have been found to prevent the initial HIV viral attachment to cells necessary for HIV infection. The same concept was used in studies of malarial spread through the red blood cells with the same conclusion. Thus fucose sugars inhibit the spread of these infections through selectively binding to the organisms so they cant bind to the cells of the body. As a possible addition to conventional treatment, fucoidins offer an adjunctive support that may improve clinical outcomes. Fucose sugars also support the immune system through enhancing phagocytosis (engulfing and destroying pathogens by white blood cells) and controlling inflammation. Bladderwrack has been shown to support thyroid function in boosting metabolism contributing to weight loss. 4-17

Okra is a vegetable and a rich source of lectin-binding protective mucilage. It helps protect the digestive tract from lectins and harmful microorganisms. Like the other ingredients discussed in this article, it also helps remove existing lectins that are already attached to cells. It is a rich source of bioavailable calcium. Okra in combination with the proteolytic enzyme pepsin may help to clear away excess mucous formed as a result of food intolerance or food allergy in the digestive tract thus allowing for better absorption of nutrients. Okra is often beneficial for ulcers, colitis, malabsorption, and other intestinal problems. It essentially helps to clean the intestine.

D-mannose is also a common binding sugar for lectins. It is capable of binding with the lectins in grains and other foods and also microorganisms as discussed in the January article on lectins. Sodium alginate is a soluble fiber derived from seaweed and is resistant to digestion. It is fermented in part by the colonic bacteria to highly beneficial short-chain fatty acids including butyrate, which is a favorite food for the colonic epithelial cells that use these fatty acids for energy. Sodium alginate may have cholesterol-binding (lowering) and blood-sugar regulating properties. It is also used for detoxification. Sodium alginate is used in the treatment of GERD as it reacts with gastric acids to form a viscous gel called the alginate raft. This alginate raft floats on top of gastric contents and acts as a barrier to acid and food reflux.18-20

In addition, the sugars in Lectin Lock encourage healthy bowel flora and enhance joint and synovial health. Supplementing your diet with these sugars also is a key component in achieving weight loss goals. As a general rule, lectins that bind D-mannose or N-acetylglucosamine increase the ability to store fat and decrease fat burning, while lectins that bind with fucose tend to reduce fat burning.

New Lectin-Blocking Supplement
The natural substances mentioned above, all contained in the novel new supplement Lectin Lock, help to protect against adverse reactions caused by lectins. Obviously, if you know that a particular food is a definite problem, using the natural agents contained in the supplement is not an invitation to indulge freely on that food. However, Lectin Lock can help support the occasional cheating on the menu. Taken as 2 or more capsules at the start of a meal this product may be a valuable aid in:

1. Promoting weight loss through improved metabolism and energy
2. Restoring proper water balance
3. Achieving healthy joints, muscles, and organs
4. Reducing inflammation (that lies at the core of chronic disease) and improving immune function
5. Repairing the digestive tract and keeping it healthy
6. Facilitating healthy detoxification in the liver and the gut
7. Support with any meal but especially when eating out, when consuming junk food or fast food diets, and when highly processed and refined, prepared foods are eaten (many gums found in commercially processed foods can intensify the effects of dietary lectins, i.e., carrageenan, acacia, guar, xanthan, arabic).

Larch AG is a complementary product to Lectin Lock when gut repair and maintenance is the focus.

References
1. Pierini, Carolyn M. Lectins: Their Damaging Role in Intestinal Health, Rheumatoid Arthritis and Weight Loss. Vitamin Research News. 2007;21(1): 1-4
2. Mikkat U, Damm I, Schroder G, Schmidt K, Wirth C, Weber H, Jones L. Effect of the Lectin Wheat Germ Agglutinin (WGA) and Ulex europaeus Agglutinin (UEA-1) on the alpha-amylase secretion of rat pancreas in vitro and in vivo. Pancreas 1998 May; 16(4): 529-38.
3. Horvath K, et al. Improved social and language skills after secretin administration in patients with autistic spectrum disorders. Journal of the Association for Academic Minority Physicians 1998; 9(1): 9-15.
4. DAdamo, Peter J. Live Right for Your Type. 1st ed. New York: Penguin Putman Inc. 2001. 163.
5. Nishino T, Nishioka C, Ura H, Nagumo T. Isolation and partial characterization of a novel amino sugar-containing fucan sulfate from commercial Fucus vesiculosus fucoidin. Carbohdr Res. 1994; 255: 213-224.
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12. Pearce-Pratt R, Phillips DM. Sulfated polysaccharides inhibit lymphocyte-to-epithelial transmission of human immunodeficiency virus-1. Biol Reprod. 1996; 54: 173-182.
13. DAdamo P. Eat Right for Your Type. Putnam: 1997.
14. Boren T, Falk P, Roth KA, et al. Attachment of Helicobacter pylori to human gastric epithelium mediated by blood group antigens. Science. 1993; 262:1892-1895. 15. Rowe A, Berendt AR, Marsh K, Newbold CL. Plasmodium falciparum: a family of sulphated glycoconjugates disrupts erythrocyte rosettes. Exp Parasitol. 1994; 79: 506-516.
16. Clark DL, Su S, Davidson EA. Saccharide anions as inhibitors of the malarial parasite. Glycoconj J. 1997; 14: 473-479.
17. Angstwurm K, Weber JR, Segert A, et al. Fucoidin, a polysaccharide inhibiting leukocyte rolling, attenuates inflammatory responses in experimental pneumococcal meningitis in rats. Neurosci Lett. 1995; 191: 1-4.
18. Kimura Y, Watanabe K, Okuda H. Effects of soluble sodium alginate on cholesterol excretion and glucose tolerance in rats. J Ethnopharmacol. 1996; 54: 47-54.
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