• The President’s Desk  — Promising New Technology, Potential Ban on P5P

• Headache Control  — Three Key Nutrients Reduce Intensity and Frequency of a Common Problem

• The Virucidal, Bactericidal and Fungicidal Effects of Glycyrrhizin, Phyllanthus Species and Monolaurin  — 

• Hypercoagulation  — Its Role in Heart Disease, IBS, Migraines, Fibromyalgia and Other Common Disorders

• Lectin Lock™  — Natural Defense Against a Hidden Cause of Digestive Concerns and Weight Gain

• Pet Corner  — Anti-Aging Medicine in Pets

• Nutrition Review  — Latest Research on Multiple Sclerosis, Cardiovascular Health, Vision and More

• Restless Legs
• Postmenopausal College Student
• Vertigo, Hearing Loss
• Psoriasis
• Fibroadenoma
• Cognitive Health
• Immunity, Stress
• Exercise Recovery, Fibromyalgia
• Carpal Tunnel, Neck Tension
• Natto and Vitamin K2
• Epididymal Cysts
• Glabrinex™ and Weight Loss

As we begin the second quarter of 2009 I want to inform you of upcoming changes so that you can plan ahead. We are implementing a state-of-the-art software system to better serve you, our customer. Consequently, May 1 and May 2 we will be closed for processing of orders and shipments. We’ll reopen with new technology on May 4. Whenever a new computer system is introduced, there is a learning curve. So we ask for your patience while we create an enhanced customer experience. Planning for this new system has been an exciting endeavor as we continue to position our employee-owned company for the future.

On another front, we are embarking on an initiative to invest in clinical studies on several of our formulas. As we travel down this path, we will undoubtedly seek input from our loyal customers. While we have tens of thousands of success stories from you, our partners in health, as well as hundreds of research studies to support the use of each of our supplements, the technology has arrived to cost effectively validate the benefits of specific formulas our scientists and doctors have designed. Stay tuned for more on this and other initiatives we plan to pursue in 2009 and beyond.

Finally, last month, I reported that FDA has banned a form of vitamin B6, pyridoxamine dihydrochloride, from being sold as a dietary supplement because pyridoxamine was authorized for investigation as a new drug before it was marketed as a supplement. FDA now has its sights set on another natural and bioavailable form of B6: Pyridoxal-5-Phosphate (P5P). Your right to access P5P is jeopardized due to a proposed FDA petition to ban this form of B6, which is known for supporting healthy homocysteine levels. The ban will make life easier for a pharmaceutical company that manufactures a synthetic form of P5P while making life harder for those individuals who want to consume the natural vitamin. We’ll keep you updated as we hear more about this issue.

Headache is one of the most common problems requiring medical attention. Although the majority of headaches are benign in nature, a small percentage of individuals with significant neurological disease will present with headache as the initial symptom. This occurs for example during different forms of intracranial hemorrhage (when small arteries known as arterioles are injured and prone to hemorrhage as a result of long-standing diabetes or high blood pressure) and after head trauma and the resulting development of benign migraine-like headaches as part of the post-concussive syndrome (headaches, disrupted sleep, poor concentration, altered behavior, and disequilibrium). Thankfully, the above-mentioned causes of headache account for only a fraction of all presentations and can be ruled out by a variety of tests including cat scan (CT), magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), and conventional cerebral angiography.

Although there are many different types of benign headache syndromes, migraine, chronic daily and tension are the three that are most commonly encountered in clinical practice. These three will now be discussed.

Migraines

Migraine headache is a neurological syndrome presenting as throbbing headache often associated with nausea, vomiting, light sensitivity (photophobia), sound sensitivity (sonophobia), flashing lights (photopsia), blurriness or loss of vision, and lightheadedness. The headache can last hours to days and can occur as often as daily or as infrequently as yearly. Other neurological symptoms such as weakness, marching numbness, clumsiness, language problems and confusion may occur in a minority of migraine patients with or without headache. The latter symptoms can often be difficult to differentiate from stroke. In fact, stroke can result from migraine. Migraine headache associated with neurological symptoms is now an accepted stroke risk factor.

The etiology of migraine is still relatively obscure. However, it is thought that there is an abnormality within the brainstem causing abnormal electrical transmission along pain pathways supplying facial and brain blood vessels.¹ This leads to the release of many neurochemicals (e.g. substance P) that cause sterile pain sensitizing swelling (inflammation) of facial and cerebral blood vessels. The latter is what is thought to be responsible for the headache. The migraine associated neurological symptoms have been attributed to spreading depression of electrical activity along the cerebral cortex. This observation may be related to depressed cellular production of energy (ATP) within the brain cell (neuron), abnormal ion transport across neuronal membranes (e.g. voltage-gated calcium channels), or abnormal brainstem inhibition of the cerebral cortex. Vascular diameter changes associated with migraine are now thought to occur in response to cerebral functional changes. However, persistent or even permanent neurological symptoms (e.g. weakness of one side) may be related to persistent spasm of blood vessels and/or excessive adhesiveness of platelets (anti-bleeding cells) resulting in prolonged obstruction of blood flow and possibly stroke.

Two neurochemicals that have been implicated in migraine are serotonin and dopamine. Serotonin, which is thought to be relatively deficient during migraine, has been found to modulate the abnormal electrical transmission within the brainstem as well as the release of neurochemicals at the blood vessel wall. Furthermore, serotonin release within the brainstem causes cerebral arterial vasodilation (expansion of the blood vessels). Dopamine receptor stimulators (agonists) precipitate hypotension and migraine headaches in migraineurs, while dopamine receptor inhibitors (antagonists) abort migraine headaches and prevent the hypotension associated with dopamine receptor stimulation.

Alteration in estrogen and/or progesterone levels also have been implicated in migraine given that many women are susceptible to migraine in and around menses and after being placed on hormonal replacement therapy after menopause.

Chronic Daily Headache

Chronic daily headache describes an entity in which headaches occur daily and throughout most of the day. This can occur de-novo or in patients with existing intermittent migraine headaches which worsen and transform into chronic daily headache. The latter occurs especially in those migraineurs who consume high quantities of over-the-counter painkillers, narcotics, and caffeine-based anti-migraine medications in an attempt to obtain pain relief.

Tension Headaches

Tension headaches present as a squeezing sensation around the temples and forehead. They tend to worsen as the day progresses. Stress is a large contributing factor to this headache type, although stress can affect most major headache types. Techniques such as self-hypnosis, biofeedback, regular exercise and stress reduction can particularly be helpful for this headache type.

Help for Headache Sufferers

The treatment of chronic headaches involves good sleep hygiene, stress reduction, exercise, nutrition, behavioral modification, hormonal manipulation and medication.

Many patients who sleep poorly at night often complain of headaches upon awakening in addition to daytime sleepiness and poor concentration. These symptoms occur most commonly with a condition known as obstructive sleep apnea where patients obstruct their breathing at night usually in conjunction with snoring. This causes a drop in nighttime blood oxygen level and leads to sleep architecture disruption. An overnight sleep study (a polysomnogram) performed at an accredited sleep center can help confirm the condition. Other disorders of sleep such as abnormal leg movements, frequent unexplained awakenings and insomnia can lead to headaches and daytime sleepiness.

Diet and nutrition are well known to influence chronic headaches, especially migraines. Excessive regular caffeine use can result in worsening chronic headaches as well as caffeine withdrawal headaches. A slow taper of caffeine use (e.g. coffee, sodas, teas, chocolate) can result in better long-term headache control. To note, caffeine will often abort an existing migraine headache, but may in the long term aggravate chronic headache control. Orange cheeses containing tyramine (e.g. cheddar cheese), preservatives, monosodium glutamate, peanuts and alcohol are only a few of the many common known precipitants of migraines. A food diary can help determine which of these applies to any given patient. Elimination of a particular food item can drastically improve headache control. A Food Allergy Test (available here) can be an ideal way to determine which foods are to blame.

Medications can be helpful for migraine headaches, but, unfortunately, side effects can limit the utility of these medications in the long term. In clinical studies, nutritional supplementation has recently been evaluated as another means of improving headache control. As mentioned above, a deficit of mitochondrial energy metabolism may play a role in development of migraines. Because riboflavin (vitamin B2) can improve cellular energy production, researchers have studied its actions in people with migraines.

Several studies have found that riboflavin reduced the intensity and frequency of migraine headaches by at least 50 percent in close to 60 percent of patients beginning in the third month of therapy.^2-4

In a 3-month, randomized trial, 55 patients with migraine were given either riboflavin or a placebo. Riboflavin was superior to placebo in reducing attack frequency and headache days. Only 15 percent of the subjects taking a placebo improved, but 59 percent of the riboflavin group experienced at least a 50 percent improvement.³

In another study, after 3 and 6 months, headache frequency was significantly reduced and the use of anti-migraine drugs decreased from 7 units/month to 4.5 units/month.²

Because effect in these studies was not observed until the third month of treatment, compliance and persistence with treatment are necessary. Furthermore, many experts agree that lower doses of riboflavin may be just as helpful as the higher doses used in some of the earlier studies. More recent studies are finding that riboflavin doses as low as 25 mgs per day may be just as effective.⁵ I recommend 100 milligrams per day of riboflavin to start in a supplement combined with magnesium and coenzyme Q10 (CoQ10).

Similar to riboflavin, coenzyme Q10 improves mitochondrial energy metabolism and therefore also has produced good results in migraine sufferers. In a double-blind, randomized, placebo-controlled trial, researchers compared CoQ10 and placebo in 42 migraine patients. By the third month of supplementation, CoQ10 was superior to placebo in reducing attack frequency, the number of days subjects had headaches and days-with-nausea in the third treatment month. For migraine attack frequency, the number of subjects experiencing at least a 50 percent improvement was only 14.4 percent for the placebo group and 47.6 percent for the CoQ10 group.⁶

In another study of 32 patients with a history of episodic migraine with or without aura, coenzyme Q10 at a dose of 150 mg per day resulted in a mean reduction in migraine frequency of 55.3 percent by the end of 3 months. The average number of days with migraine prior to the study’s start was 7.34 and this decreased to 2.95 after 3 months of CoQ10, which was a statistically significant response.⁷

Studies have indicated magnesium may be another natural substance useful for migraine prophylaxis.^8-9 A double-blind, randomized, placebo-controlled study compared oral magnesium supplementation in 30 migraine patients without aura to 10 migraine patients taking a placebo. Migraine attack frequency and severity were found to be significantly lower in the magnesium group compared to those in the placebo group.⁸

In another randomized, double blind, placebo-controlled study of children with migraines, researchers found a statistically significant decrease over time in headache frequency in the group taking magnesium but not in the placebo group.⁹

Some researchers have observed a decrease in cerebral intracellular magnesium with migraine.¹⁰

A synergistic combination of riboflavin, CoQ10 and magnesium (NeuroFlavin^™) is now available. I have used this supplement in my clinical practice and found it to be quite effective in supporting the health of migraine patients. I have found that using the supplement together with fish oil and optimizing vitamin D3 status can produce excellent results.

Menstrual Migraines

Fluctuation in estrogen and progesterone levels during menses is thought to be responsible for menstrual migraine. Furthermore, the recurrence or worsening of migraines in women placed on hormonal replacement therapy after menopause lends additional support to estrogen and/or progesterone’s role in migraines. Therefore, conducting a salivary hormone test (which is offered here) to monitor hormone levels in patients with menstrual migraines is warranted. In the appropriate patient, combining the nutrients mentioned above with topical estrogen and progesterone cream may assist with hormonal and migraine regulation.

Conclusion

Chronic migraine headaches are a very common and disabling problem plaguing many individuals. Although most headaches are benign in nature, the lack of headache history, a progressively worsening course, and the presence of associated neurological symptoms should alert an individual to a potentially more serious condition that can mimic migraine and that justifies expeditious medical attention. The prevention of chronic migraine headaches should begin with a thorough evaluation and management of abnormal sleep habits, environmental stressors, dietary triggers and nutrition in general, as well as the institution of a regular exercise program. A medication history is essential given that many medications can worsen headaches (e.g. nitroglycerin agents, narcotics). The institution of the above mentioned recommended supplement protocol (particularly riboflavin, magnesium and coenzyme Q10) for migraine prevention should be considered early on.

It is important to realize that successful management of migraine headache requires a holistic multifaceted approach. Although the process often requires time and patience, the end result is usually quite satisfactory.

References

1. Hamada J. Pathophysiology of migraine—migraine generator. Rinsho Shinkeigaku. 2008 Nov;48(11):857-60.

2. Boehnke C, Reuter U, Flach U, Schuh-Hofer S, Einhäupl KM, Arnold G. High-dose riboflavin treatment is efficacious in migraine prophylaxis: an open study in a tertiary care centre. Eur J Neurol. 2004 Jul;11(7):475-7.

3. Schoenen J, Jacquy J, Lenaerts M. Effectiveness of high-dose riboflavin in migraine prophylaxis. A randomized controlled trial. Neurology. 1998 Feb;50(2):466-70.

4. Schoenen J, Lenaerts M, Bastings E. High-dose riboflavin as a prophylactic treatment of migraine: results of an open pilot study. Cephalalgia. 1994 Oct;14(5):328-9.

5. Maizels M, Blumenfeld A, Burchette R. A combination of riboflavin, magnesium, and feverfew for migraine prophylaxis: a randomized trial. Headache. 2004 Oct;44(9):885-90.

6. Sándor PS, Di Clemente L, Coppola G, Saenger U, Fumal A, Magis D, Seidel L, Agosti RM, Schoenen J. Efficacy of coenzyme Q10 in migraine prophylaxis: a randomized controlled trial. Neurology. 2005 Feb 22;64(4):713-5.

7. Rozen TD, Oshinsky ML, Gebeline CA, Bradley KC, Young WB, Shechter AL, Silberstein SD. Open label trial of coenzyme Q10 as a migraine preventive. Cephalalgia. 2002 Mar;22(2):137-41.

8. Köseoglu E, Talaslioglu A, Gönül AS, Kula M. The effects of magnesium prophylaxis in migraine without aura. Magnes Res. 2008 Jun;21(2):101-8.

9. Wang F, Van Den Eeden SK, Ackerson LM, Salk SE, Reince RH, Elin RJ. Oral magnesium oxide prophylaxis of frequent migrainous headache in children: a randomized, double-blind, placebo-controlled trial. Headache. 2003 Jun;43(6):601-10.

10. Lodi R, Iotti S, Cortelli P, Pierangeli G, Cevoli S, Clementi V, Soriani S, Montagna P, Barbiroli B. Deficient energy metabolism is associated with low free magnesium in the brains of patients with migraine and cluster headache. Brain Res Bull. 2001 Mar 1;54(4):437-41.

Antibiotic, antiviral and antifungal resistance has become a worldwide problem for numerous organisms. The need for safe, effective virucidals, bactericidals and fungicidals not subject to resistance are desperately needed. As microorganisms become resistant to existing drugs, stronger, more toxic drugs are often required to overcome resistance. However, over the course of time these drugs become resistant as well. This review will focus on the promising research that has been conducted on glycyrrhizin, Phyllanthus and monolaurin demonstrating their broad-spectrum activity against a host of microorganisms.

Glycyrrhizin

Glycyrrhizin has been used in Japan for more than 20 years orally and as the intravenous drug Stronger Neo-Minophagen C (SNMC). Oral glycyrrhizin is metabolized in the intestine to glycyrrhetinic acid (GA) and intravenous (IV) glycyrrhizin is metabolized into glycyrrhetinic acid when excreted through the bile into the intestines. Glycyrrhizin and glycyrrhetinic acid exhibit similar properties and have been shown to be effective for Hepatitis A, B, C; HIV; herpes (I, II, zoster (shingles virus), perhaps 6); lichen planus, influenza, CMV (cytomegalovirus) and cancer. Personal experience and reports of effectiveness show it is effective against chronic fatigue immune deficiency syndrome (CFIDS) and the viruses associated with this condition (EBV (Epstein-Barr) virus, CMV), condyloma (genital wart virus) and other "viral" presentations.^1-5

Glycyrrhizin has antiviral activity by inhibiting some RNA transcriptases (e.g. HIV) and an indirect activity by decreasing cell membrane permeability (e.g. hepatocyte injury). It inactivates viruses and inhibits viral proliferation. Glycyrrhizin is a powerful free radical scavenger and it increases gamma interferon, T cells and natural killer cells.

It selectively inhibits an immune system process that leads to inflammatory host cell injury. It may enhance immune adherence responsible for immune phagocytosis (the process by which pathogens "digest" foreign invaders) and regulation of antibody production in protective immunity against invaders. It also inhibits a process in the body known as the arachidonic acid cascade, which is linked to inflammation.^4-5

Glycyrrhizin and Hepatitis

Hepatitis C is occurring at epidemic proportions with an estimated 3.9 million infected in the USA, which is 4 times those infected with HIV, and 170 million worldwide with a reported 8,000-10,000 deaths per year. Mortality is expected to triple by 2010. It increases the risk of death from liver disease 17-fold and increases the risk of death from liver cancer by 6-fold.⁶

Current treatment prognosis with interferon (INF) and antivirals provide less than a 30 percent response rate after 1 year. Of those who exhibit viral clearance, 30-70 percent relapse within the first few months. A sustained response of at least 6 months occurs in 10-15 percent of patients and serious side effects occur such as myalgia, fatigue, fever, headache, nausea, leukopenia, thrombocytopenia, alopecia, irritability, depression, thyroid abnormalities, pulmonary complications and retinal damage. The treatment is often worse than the disease as many patients cannot function or work during treatment. Interferon decreases the risk of progression to hepatocellular carcinoma only in sustained virulogical responders. When ribavirin is used with interferon, reports show a 28-66 percent sustained response in patients although personal communications with infectious disease specialists reveal much poorer response rates. The side effects of combined treatment with ribavirin are significant and serious with an increased risk of hemolytic anemia. Pegylated interferon, in which polyethylene glycol is added to make the interferon last longer in the body, is given with ribavirin and adverse effects and outcome is similar to standard therapy. The treatment is extremely expensive and unaffordable without prescription insurance coverage.^1-7

The intravenous drug form of glycyrrhizin, SNMC, is composed of monoammonium glycyrrhizinate (as glycyrrhizin) 4 mg; aminoacetic acid 40 mg; L-cysteine HCL 2 mg; and sodium sulfite 1.6 mg per 2 ml vial. A 20 ml vial provides 40 mg glycyrrhizin, 400 mg glycine and 20 mg L-cysteine. The therapeutic IV dose range is 40-60 ml and as high as 100 ml. The oral therapeutic dose may be as high as 200 mg/day. SNMC has aminoacetic acid and L-cysteine added to prevent pseudoaldosteronism, a condition resulting in sodium retention, potassium depletion and hypertension. However, pseudoaldosteronism is rarely reported at therapeutic doses and can be treated with spironolactone or higher intakes of potassium.^4-5

A comparative study was conducted by dividing at random 100 cases into two groups. Group A received 100 ml SNMC per day for 3 weeks and group B received 40 ml/day for 3 weeks. The patient population consisted of: HBV (hepatitis B virus), HCV (hepatitis C virus) and cirrhosis with 49 percent of patients previously treated with interferon therapy showing no improvement of ALT liver enzyme. ALT reductions (rather than viral load) are the best prognostic predictor with respect to later development of liver cancer. Cases were rated "markedly improved" if ALT levels dropped to less than 1.2 times normal upper limit and "improved" if ALT levels dropped to less than 1.2-1.5 upper limit. After intervention the results revealed that in group A, 23 of 44 cases (52.3 percent) improved and in group B, 12 of 26 cases (26.1 percent) improved. Group A (the higher dose group) showed significant improvement compared to B (the lower dose group).¹

Another study examined collected data on hepatitis C cases treated with SNMC followed for 15 years. Eighty-four patients received 100 ml/day of SNMC for 8 weeks, and thereafter received a maintenance dose of 2-7 times/week for 2-16 years. They were compared to 109 control patients receiving only oral botanical/nutritional supplements. The ALT fell to normal in 35.7 percent of the SNMC group, and 6.4 percent of the control group. After being followed for 15 years the incidence of cirrhosis was 21 percent in the SNMC group compared to 37 percent in the control group. Liver cancer incidence after 15 years was 12 percent in the SNMC group and 25 percent in the control group.²

Fifty-nine patients with chronic hepatitis C, non-responders to interferon or those unlikely to respond to interferon were included in a study where they either received SNMC 3 times per week or 6 times per week for a total of 4 weeks and the results of the two groups were compared to another group receiving a placebo. SNMC was administered either as an IV drip for 15-20 minutes (80, 160, 240 mg glycyrrhizin) or SNMC was given undiluted injected directly into a vein in 3-5 minutes (200 mg glycyrrhizin). The proportion of patients with ALT normalization at the end of treatment was higher in actively treated patients than in placebo; and higher in those receiving SNMC 6 times per week (47 percent) versus 3 times per week (26 percent). Many of the patients asked for prolongation of SNMC therapy rather than interferon because they felt better during glycyrrhizin therapy. Since persistently high ALT greater than 80 IU/L with chronic hepatitis C is associated with more rapid development of liver cancer than persistently low ALT levels less than 80 IU/L, the authors suggest oral glycyrrhizin or glycyrrhetinic acid should be for maintenance therapy.^3-5

A 13-year follow up study with SNMC was conducted with chronic hepatitis C patients. The therapeutic schedule of SNMC was aimed at suppressing ALT levels (below 75 U/L). The patients were administered 40 ml (80 mg glycyrrhizin) of SNMC 5-6 times per week and if ALT was lowered the maintenance therapy was 3 times per week. If this failed to lower ALT levels then SNMC was increased to 100 ml (200 mg glycyrrhizin) 5-6 times per week until patients responded. The maintenance dose was tailored to keep ALT levels low. Liver cirrhosis occurred significantly less frequently in 178 patients on long-term SNMC than in 100 controls (28 percent vs. 48 percent at year 13). Liver cancer developed significantly less frequently in 84 patients on long-term SNMC than in the 109 controls (13 percent vs. 25 percent at year 15). The author notes a relationship between the cumulative ALT score and the increase in the stage of fibrosis, irrespective of the stage of fibrosis found in the first biopsy. To prevent progression of fibrosis the cumulative ALT score needs to be kept increasingly lower as the stage of fibrosis increases. Furthermore, the incidence of liver cancer increases in parallel with the mean ALT score. Oral treatment with glycyrrhizin and IV treatment with SNMC has been shown to significantly improve hepatitis B with marked improvement on indices of liver function and lowering of HbsAg (Hep B surface antigen), the levels of which are often linked to active disease.^4-5

Glycyrrhizin and HIV

AIDS patients with high CD4/CD8 ratios (also known as helper cell/suppressor cell ratios) improved significantly with SNMC (5 mg glycyrrhizin /kg). Almost half the patients improved during treatment. In another study SNMC was given to patients with haemophilia A with HIV infection who were asymptomatic. Glycyrrhizin inhibited viral replication and had interferon-inducing, natural-killer-cell enhancing effects. It was extremely effective in preventing progression to AIDS and improved CD4/CD8. In vitro studies have shown that cell-to-cell infection by HIV1, HIV-2, and T-cell lymphotropic virus type 1 is inhibited by glycyrrhizin. Glycyrrhizin inhibits HIV replication in cultures of cells from HIV-infected patients. In 31 percent of samples, glycyrrhizin inhibited more than 90 percent of HIV replication. Virucidal effects include interference with cell binding, and induction of endogenous interferon gamma. Glycyrrhizin also affects protein kinase II and casein kinase II. Kinases regulate many aspects that control cell growth, movement and cell death.

It also affects transcription factors, groups of proteins that read and interpret the genetic "blueprint" in the DNA, such as activator protein 1, which regulates gene expression in response to bacterial and viral infections, and nuclear factor kappa B, which plays a key role in regulating the immune response to infection.^4-5

SARS and Corona Virus

No treatment for SARS (severe acute respiratory syndrome) has been established. Glycyrrhizin inhibits SARS-associated corona virus replication and inhibits absorption and penetration during the early steps of the replication cycle. Glycyrrhizin is found to be most effective when given both during and after the absorption period.^4-5

Herpes

In vitro studies show glycyrrhizin is effective against varicellea zoster (herpes) inactivating more than 99 percent when incubated with glycyrrhizin for 30 minutes. Glycyrrhizin demonstrates an additive effect when given with acyclovir and beta-interferon. Herpes simplex virus 1 and 2 (HSV-1 and 2), and Epstein Barr virus (EBV) are inactivated in vitro by glycyrrhizin.^4-5

Cytomegalovirus (CMV)

Glycyrrhizin is effective against CMV in vitro and in vivo. Liver dysfunction improved in 4 cases and CMV disappeared after glycyrrhizin was given through IV by the age of 12 months. In 6 infants treated with IV glycyrrhizin (10-20 mg/kg/day), liver dysfunction normalized and CMV disappeared significantly sooner than controls. Six infants received oral glycyrrhizin at a dose of 25 mg/day (2-4 mg/kg) for 12 weeks with similar results demonstrating oral efficacy.^4-5

Upper Respiratory Tract Infections

Patients with upper respiratory tract infections (URTIs) received either glycyrrhizin or placebo in a double-blind, placebo-controlled randomized study. Forty-one patients received 40 mL GL (SNMC) per day and 269 patients received IV placebo. Glycyrrhizin therapy resulted in shorter hospital stay, lower-grade fever and lower cost of therapy.⁷

Summary of GL Effects

Human studies showing efficacy of glycyrrhizin include: hepatitis B, hepatitis C, HIV, upper respiratory tract infections, cytomegalovirus and SARS. In vivo animal studies of glycyrrhizin efficacy include: influenza, herpes, encephalitis and Candida albicans. In vitro studies of glycyrrhizin demonstrate efficacy against hepatitis A, herpes I, II, EBV, zoster, Vaccina virus, Newcastle disease, Vesicular stomatitis, Flaviviruses, respiratory syncytial virus, Kaposi sarcoma-associated herpes virus and H. pylori.

Phyllanthus And Hepatitis

Researchers conducted a systematic review of 22 randomized trials for Phyllanthus on chronic hepatitis B (HBV) infections. Combined results showed that Phyllanthus had a positive effect on clearance of HbsAg (Hepatitis B surface antigen). No significant difference of clearing of HBsAg, and HBV DNA was demonstrated between Phyllanthus and interferon. There was also no significant difference between Phyllanthus and interferon in clearing of HBeAg, an antigen of hepatitis B virus sometimes present in the blood during acute infection, usually disappearing afterward but sometimes persisting in chronic disease. Phyllanthus plus interferon showed a better effect of clearance of HBeAg and HBV DNA than interferon alone. Phyllanthus has a significant effect on antiviral activity and was better than interferon for ALT normalization. Phyllanthus amarus and urinaria show positive effects on HBsAg/HBeAg while only urinaria shows a positive effect on HBV DNA.⁸

Twenty-five compounds from Phyllanthus were studied for in vitro effects on hepatitis B. Niranthin, nirtetralin, hinokinin and geraniin suppressed effectively both HBsAG and HBeAG. Niranthin showed the best anti-HBsAG activity; hinokinin, showed the most potent anti-HBeAG activity.⁹

Monolaurin

Lauric acid was discovered as the most active antiviral and antibacterial substance in human breast milk. Monolaurin is the glycerol ester of lauric acid and is more biologically active than lauric acid. Monolaurin has been shown to be active against (in vitro): Influenza virus, Pneumovirus, Paramyxovirus (Newcastle), Morbillivirus (Rubella), Coronavirus (Avian Infectious, Bronchitis virus), herpes simplex I & II, CMV, EBV, HIV, measles, leukemia virus, Simliki forest virus, HPV, Visna virus, Vesicular stomatitits virus, respiratory syncytial virus, Dengue virus (type 1-4), and lymphocytic choriomeningitis. It is effective against Gram Positive Bacteria including: Anthrax, Listeria monocytogenes, Staphylococcus aureus, Groups A, B, F, and G streptococci, Streptococcus agalactiae, Mycobacteria Clostridium perfringens and Gram Negative Bacteria including: Chlamydia pneumonia, Neisseria gonorrhoeae, H. pylori, Mycoplasma pneumonia, and Vibrio parahaemolyticus. It has also been shown to be effective against yeast, fungi and molds including Aspergillus niger, Saccharomyces cerevisiae, Ringworm/Tinea, Malassezia species, Penicillium citrinum, and Candida utilis. A number of protozoa like Giardia lamblia are also inactivated or killed by Monolaurin. Monolaurin acts by disrupting the lipid bylayer of the virus and prevents the attachment to susceptible host cells. Recent evidence has also indicated that it prevents replication and removes all measurable infectivity by directly disintegrating the viral envelope making the virus more susceptible to host defense.¹⁰

Conclusion

There are no known side effects of Phyllanthus or monolaurin and resistance has not been seen with any of these natural compounds including glycyrrhizin. Blood pressure should be monitored and a high potassium diet implemented with patients on glycyrrhizin. There may be a synergy combining these 3 natural compounds (as in the new formula Nutracidin^™) enhancing the virucidal, bactericidal and fungicidal effects. The effective doses may also be lower. Many patients presenting with viral symptoms may be co-infected with bacteria and fungi (and vice versa); therefore the broad spectrum effects of these compounds may optimize patient outcomes.

References

1. Iino S, Tango T, Matsushima T et al. Therapeutic effects of stronger neo-minopahgen C at different doses on chronic hepatitis and liver cirrhosis. Hepatol Res. 2001;19:31-40.

2. Kumada H. Long-term treatment of chronic hepatitis C with glycyrrhizin [Stronger Neo-Minophagen C (SNMC)] for preventing liver cirrhosis and hepatocellular carcinoma. Oncol 2002;62(suppl):94-100.

3. Okuno T, Arai K, Shindo M. Efficacy of interferon combined glycyrrhizin therapy in patients with chronic hepatitis C resistant to interferon therapy. Nippon Rinsho. 2004;52(7): 1823-7.

4. Fiore C, Eisnhut M, Krausse R et al. Antiviral effect of Glycyrrhiza species. Phytother Res 2008;22:141-148.

5. Numazaki K. Glycyrrhizin therapy for viral infections. African J Biotech. 2003;2(10):392-393.

6. Patrick L. Hepatitis C: Epidemiology and review of complementary/alternative medicine treatments. Alt Med Rev. 1999;4(4):220-221.

7. Yanagawa Y, Masatsune O, Fujimoto E et al. Effects and cost of glycyrrhizin in the treatment of upper respiratory tract infections in members of the Japanese maritime self-defense force: preliminary report of a prospective, randomized, double-blind, controlled, parallel-group, alternate day treatment assignment clinical trial. Curr Ther Res. 2004;65(1):26-3.

8. Liu J, Lin H, McIntosh H. Genus Phyllanthus for chronic hepatitis B virus infection: a systematic review. J Viral Hepat. 2001;8:358-366.

9. Huang RL, Huang YL, Chen CC et al. Screening of 25 compounds isolated from Phyllanthus species for anti-human hepatitis B virus in vitro. Phytother Res. 2003;17(5):449-53.

10. Lieberman S, Enig MG, Preuss HG. A review of monolaurin and lauric acid: natural virucidal and bactericidal agents. Alternative & Complementary Therapies 2006;12(6):310-314.

In the minds of many people, blood clots are often thought about in relation to cardiovascular concerns (in a detrimental sense) or in relation to wound healing (in a beneficial sense). However, research is beginning to emphasize an interesting fact—the process causing abnormal blood clotting (known as hypercoagulation) is linked not only to heart disease, stroke and hypertension but also to a wide range of conditions, including inflammatory bowel disease,^1-2 migraines,³ fibromyalgia,⁴ diabetes and diabetic retinopathy,^5-7 varicose veins,^8-9 hemorrhoids,¹⁰ and dementia.¹¹ Some research indicates that hypercoagulation may also be involved in chronic fatigue¹² and Gulf War syndrome.¹² Therefore, the implications of hypercoagulation stretch far beyond heart disease and stroke to also include many of the most common diseases of our time.

Furthermore, research shows that as we age, hypercoagulation increases, and that hypercoagulation becomes even more severe when subjects are under chronic stress.¹³ Many clinicians are reporting a widespread, subclinical chronic coagulation disorder even among patients in their 40s. Consequently, a large group of the population is at risk for not only heart disease, pulmonary embolism, hypertension, strokes and other cardiovascular conditions but also for any of the diseases mentioned above.

This article will describe an ideal way to reduce hypercoagulation and improve blood flow in order to help the body maintain healthy clotting levels. First, however, it will discuss the coagulation process, its role in cardiovascular health and further explain how abnormal coagulation is involved in many chronic disorders.

The Blood-Clotting Cascade

Fibrinogen is a plasma protein that plays a key role in blood clotting. Fibrinogen is converted into the coagulated protein fibrin by the action of thrombin in the presence of calcium, and it is this change that produces coagulation of the blood.¹⁴ When the body is wounded, this process is necessary and essential. However, infection, inflammation, aging and various diseases can trigger excess fibrinogen production. High fibrinogen levels and its conversion into fibrin are responsible for hypercoagulation. The body utilizes many natural methods of breaking down fibrin deposits, but as we age and in various disease states these fibrinolytic processes are often defective.

The Damage is Building in Our Vessels

The blood vessel lining is constantly subjected to free radical attack. Atherosclerosis is accelerated when free radicals cause the blood vessels to become inflamed. The body treats this damage like a wound, covering the damaged area with fibrin deposits and bringing in blood platelets in an attempt to heal the wounded area. Micro-thrombi accumulate on the vessels. At this stage, these micro-thrombi are still reversible. However, over time, with further damage, more fibrin is deposited. Arterial plaques produce chemicals that reduce the body’s ability to break down clots, further compounding the destructive process.

Heart attacks, pulmonary emboli and strokes often occur after a plaque’s cap ruptures. The body, acting as if needs to respond as it would to a wound, deposits fibrin over the rupture and a blood clot forms. This blocks blood flow even more, depriving the heart, lungs or brain of oxygen.

Because the fibrin deposits accumulate over time, the process can begin decades before the actual heart attack or other cardiovascular event occurs, indicating that even people in their forties may already be undergoing the first stages of this process.

Hypercoagulation and the Diseases of Our Time

In addition to cardiovascular disease, an increased state of hypercoagulation and the body’s weakened ability to dismantle abnormal fibrin deposits occurs in the following disorders.

Inflammatory Bowel Disease

Growing evidence recognizes inflammatory bowel disease (IBD) as being characterized by hypercoagulation and an increased tendency toward developing thrombi, blood clots that obstruct a blood vessel or a cavity of the heart. In Crohn’s disease and ulcerative colitis, the two major forms of IBD, patients have abnormalities in coagulation and fibrinolysis, the process by which the body breaks down fibrin. In these patients, abnormal clotting processes were linked to the severity of the Crohn’s Disease Activity Index.¹

Recently, some studies have revealed that the poor mucosal healing, inflammatory ulcerations and damage in the IBD intestine could depend on microvascular dysfunction, resulting in diminished ability for the blood vessels to dilate. IBD also is associated with an increased risk of deep vein thrombosis and pulmonary embolism and these conditions happen at an earlier age in IBD patients compared to non-IBD patients.²

Due to the link between hypercoagulation and IBD, anticoagulants are now often given to these patients.¹⁵

Migraines

The proposal that a primary abnormality of platelet behavior causes migraine was first proposed in 1978. Further studies provide strong additional support for the platelet hypothesis in migraine. Platelets from people with migraines aggregate more readily, their platelet fibrinogen receptors have greater affinity, and their platelet membranes show altered viscosity.³

Fibromyalgia, Chronic Fatigue, Gulf War Syndrome

In chronic fatigue and/or fibromyalgia, patients have demonstrated enhanced platelet activation and fibrinogen and prothrombin activity.⁴

Researchers have also noted activation of the coagulation system in Gulf War Syndrome, which is similar to chronic fatigue syndrome and fibromyalgia.¹² This finding led researchers to conclude, "This evidence of a hypercoagulable state suggests that symptoms may be due to poor blood flow and, therefore, a basis for the potential utility of anticoagulant therapy."¹²

Varicose Veins, Venous Insufficiency

Varicose veins, venous insufficiency, venous thrombosis (a blood clot in the veins) and deep vein thrombosis (a blood clot in one or more of the veins in the deep venous system of the upper or lower extremities) are related conditions that involve abnormalities in coagulation and fibrinolysis. Defects in the body’s ability to degrade fibrinogen have been noted in cases where varicose veins progress to venous insufficiency with skin changes and venous ulcers.⁸ In venous thrombosis, researchers have noted hypercoagulability due to local accumulation of activated clotting factors and coagulation activation products.⁹ Hemorrhoids, really varicose veins of the rectum, also are linked to the blood clotting process and studies have found that blood fibrinogen levels are increased in people with hemorrhoids.^{10, 16}

Diabetes

The body naturally destroys clots through the formation of plasmin, a thrombolytic (clot-dissolving) enzyme. Plasmin is made from plasminogen through the action of an enzyme, tissue plasminogen activator (TPA). In obese patients with type 2 diabetes, the ability to break down fibrinogen is impaired by increased plasma concentrations of plasminogen activator inhibitor (PAI)-1.⁵

This impaired ability to break down fibrinogen has been linked to diabetic retinopathy. Hypercoagulation has been detected in the eyes of diabetic subjects along with higher fibrinogen activity.⁶ A state of hypercoagulation and fibrinolytic dysfunction also may contribute to disturbed skin microcirculation and impaired ulcer healing in diabetics.⁷

The high mortality rate in type 2 diabetes is associated with the increased cardiovascular disease risk seen in these patients. One group of researchers suggested that addressing hypercoagulation issues in type 2 diabetic subjects along with high blood pressure and lipid abnormalities may be a more powerful approach to reducing cardiovascular disease risk than addressing high blood sugar levels alone.¹⁷

Nattokinase: A Natural Anti-Coagulant

Nattokinase is an enzyme derived from fermented soy that inhibits fibrin and has fibrinolytic activity. Studies have shown that nattokinase is four times more powerful at dissolving blood clots than plasmin, the human body’s natural defense against clotting activity in the arteries.^18-19 Nattokinase is the safest and most potent natural anti-clotting agent known.^19-20

Nattokinase shows promise in supporting the health of people with thrombosis,^21-22 venous stasis,²² embolism formation,²³ and the devastating blood clotting that arises from cardiovascular disease.²⁴

Nattokinase’s blood clot dissolving ability is well supported by both animal and human studies. In one study, a control and a nattokinase-fed group of rodents were used to test the formation of blood clots near the site of artery damage. In the nattokinase-fed group, the great majority of the blood clots around the site of arterial injury detached from the surface of the vessel and dissolved.²⁵

In a human study, researchers tested nattokinase on passengers undergoing a long plane flight, who are often at increased risk of deep vein thrombosis (artery blood clots) in the legs. The trial involved 204 passengers on 7- to 8-hour flights. The researchers measured edema (swelling of the legs) and superficial and deep vein thrombosis in persons considered at high risk for developing these conditions.²⁶ An exercise program was used in both the control and the nattokinase-supplemented group.

In the group not given nattokinase, 5.4 percent developed deep vein thrombosis and 7.6 percent developed superficial thromboses. Twelve percent experienced swelling of the legs. In the nattokinase group, no deep vein thromboses developed. The control group had a total of 18 thrombotic events (19.6 percent) compared to only 7 percent (all superficial thromboses) in the nattokinase group. All "events were asymptomatic," not leading to further complications.²⁶ Furthermore, leg swelling increased 12 percent in the untreated group and was reduced 15 percent in the nattokinase group. The authors concluded that nattokinase was "effective in reducing thrombotic events and in controlling edema in high risk subjects in long flights."²⁶

Blood Pressure Support

Nattokinase’s effects on the blood vessels also helps maintain healthy blood pressure levels as shown in a trial involving 86 participants previously diagnosed with pre-hypertension or stage I hypertension. These previously untreated people had systolic blood pressure between 130 to 159 mm./Hg.²⁷ The active treatment group was given 2,000 FU (fibrinolytic units) of nattokinase per capsule, versus a placebo in the control group. After eight weeks, systolic blood pressure dropped -5.5 mmHg and diastolic blood pressure declined -2.84 mmHg in the nattokinase group. The study authors concluded, "These findings suggest that increased intake of nattokinase may play an important role in preventing and treating hypertension."²⁷

Furthermore, nattokinase stopped artery (intimal) thickening in 2 animal studies where it was administered orally. Artery intimal thickening causes blood pressure to rise because of a loss of flexibility of the artery.^{19, 25}

Nattokinase and Cognitive Health

Amyloid deposits are particles of oxidized protein that build up inside all non-dividing, or post mitotic cells, such as the brain, heart and other key cells.^28-29 Amyloid buildup slowly shuts down the ability of the cell to function properly and acts as an irritant, increasing free radical generation. Brain cells are especially vulnerable to amyloid buildup during disease processes.²⁸ Amyloid proteins occur in much greater abundance in Alzheimer’s disease and maturity onset diabetes than in the normal aging cells.^28-29

Over the past 40 years, only a few compounds have been reported to dissolve amyloid protein. In 2009, however, researchers discovered that nattokinase could cleave amyloid and enhance amyloid clearance.²⁰ The researchers discovered that nattokinase, but not trypsin or plasmin, has the ability to degrade amyloid.²⁰

Other Clinical Uses

Health care practitioners find that nattokinase is helpful in supporting the health of individuals with a number of other disorders. Clinicians, for example, have noted that nattokinase is useful in Lyme disease patients possibly because Borrelia burgdorferi, the organism responsible for Lyme disease, uses a critical receptor involved in blood clot formation and impaired circulation (hemostasis) to infect blood platelets.³⁰

Clinicians also have used nattokinase in patients with dysmenorrhea (painful menstruation).

Conclusion

Hypercoagulation is linked to heart disease, strokes, hypertension, pulmonary embolism, venous insufficiency, inflammatory bowel disease, fibromyalgia, chronic fatigue syndrome, diabetes and migraines. Nattokinase has impressive blood clot dissolving or thrombolytic activity matched by no other enzyme. Consequently, nattokinase is an ideal natural approach to stop excessive coagulation, improve heart health, and reduce factors involved in a host of disorders.

References

1. Shen J, Ran ZH, Zhang Y, Cai Q, Yin HM, Zhou XT, Xiao SD. Biomarkers of altered coagulation and fibrinolysis as measures of disease activity in active inflammatory bowel disease: A gender-stratified, cohort analysis. Thromb Res. 2009;123(4):604-11.

2. Yoshida H, Granger DN. Inflammatory bowel disease: A paradigm for the link between coagulation and inflammation. Inflamm Bowel Dis. 2009 Feb 27. Published Online Ahead of Print.

3. Hanington E. Migraine: the platelet hypothesis after 10 years. Biomed Pharmacother. 1989;43(10):719-26.

4. Berg D, Berg LH, Couvaras J, Harrison H. Chronic fatigue syndrome and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis. Blood Coagul Fibrinolysis. 1999 Oct;10(7):435-8.

 5. Aso Y, Matsumoto S, Fujiwara Y, Tayama K, Inukai T, Takemura Y. Impaired fibrinolytic compensation for hypercoagulability in obese patients with type 2 diabetes: association with increased plasminogen activator inhibitor-1. Metabolism. 2002 Apr;51(4):471-6.

6. Evgrafov VIu, Markova OA, Grishin VL, Efimov VS. [Changes in general hemostasis in patients with diabetic retinopathy] [Article in Russian] Vestn Oftalmol. 2004 May-Jun;120(3):29-31.

7. Kalani M, Silveira A, Blombäck M, Apelqvist J, Eliasson B, Eriksson JW, Fagrell B, Torffvit O, Hamsten A, Jörneskog G. Beneficial effects of dalteparin on haemostatic function and local tissue oxygenation in patients with diabetes, severe vascular disease and foot ulcers. Thromb Res. 2007;120(5):653-61.

8. Blomgren L, Johansson G, Siegbahn A, Bergqvist D. Coagulation and fibrinolysis in chronic venous insufficiency. Vasa. 2001 Jul;30(3):184-7.

9. Decousus H, Epinat M, Guillot K, Quenet S, Boissier C, Tardy B. Superficial vein thrombosis: risk factors, diagnosis, and treatment. Curr Opin Pulm Med. 2003 Sep;9(5):393-7.

10. Denis J, Garrigues JM, Trochet JP, Gerentes I, Taccoen A. [Rheological parameters in hemorrhoid pathology] [Article in French]. Ann Gastroenterol Hepatol (Paris). 1994 Sep;30(4):181-4.

11. Hsu RL, Lee KT, Wang JH, Lee LY, Chen, RP. Amyloid-degrading ability of nattokinase from Bacillus subtilis natto. J Agric Food Chem. 2009 Jan 28; 57 (2):503-8.

12. Hannan KL, Berg DE, Baumzweiger W, Harrison HH, Berg LH, Ramirez R, Nichols D. Activation of the coagulation system in Gulf War Illness: a potential pathophysiologic link with chronic fatigue syndrome. A laboratory approach to diagnosis. Blood Coagul Fibrinolysis. 2000 Oct;11(7):673-8.

13. Wirtz PH, Redwine LS, Baertschi C, Spillmann M, Ehlert U, von Känel R. Coagulation activity before and after acute psychosocial stress increases with age. Psychosom Med. 2008 May;70(4):476-81.

14. Stedman’s Medical Dictionary, 21st edition, The Williams and Wilkens Company, Baltimore, 1966.

15. Papa A, Scaldaferri F, Danese S, Guglielmo S, Roberto I, Bonizzi M, Mocci G, Felice C, Ricci C, Andrisani G, Fedeli G, Gasbarrini G, Gasbarrini A. Vascular involvement in inflammatory bowel disease: pathogenesis and clinical aspects. Dig Dis. 2008;26(2):149-55.

16. Gaj F, Trecca A, Suppa M, Sposato M, Coppola A, De Paola G, Aguglia F. [Hemorrhoidal thrombosis. A clinical and therapeutical study on 22 consecutive patients] [Article in Italian] Chir Ital. 2006 Mar-Apr;58(2):219-23.

17. Simon K, Dobó E, Nádasy T, Retih I, Rácz I. [What is the most effective approach to the reduction of cardiovascular risk in type-2 diabetes mellitus?] [Article in Hungarian]. Orv Hetil. 2006 Aug 6;147(31):1443-6.

18. Sumi H, Hamada H, Tsushima H, Mihara H, Muraki H. A novel fibrinolytic enzyme (nattokinase) in the vegetable cheese Natto; a typical and popular soybean food in the Japanese diet. Experientia. 1987 Oct 15; 43(10): 1110-1.

19. Suzuki Y, Kondo K, Matsumoto Y, Zhao BQ, Otsuguro K, et al. Dietary supplementation of fermented soybean, natto, suppresses intimal thickening and modulates the lysis of mural thrombi after endothelial injury in rat femoral artery. Life Sci. 2003 Jul 25; 73(10):1289-98.

20. Hsu RL, Lee KT, Wang JH, Lee LY, Chen RP. Amyloid-degrading ability of nattokinase from Bacillus subtilis natto. J Agric Food Chem. 2009 Jan 28; 57(2):503-8.

21. Tai MW, Sweet BV.  Nattokinase for prevention of thrombosis. Am J Health Syst Pharm. 2006 Jun 15; 63 (12); 1121-3.

22. Cesarone MR, Belcaro G, Nickolaides AN, Ricci A, Geroulaklos G., et al. Angiogiology. 2003 Sep-Oct; 54(5); 531-9.

23. Evgrafov VIu, Markova OA, Grishin VL, Efimov VS. [Changes in general hemostasis in patients with diabetic retinopathy] [Article in Russian] Vestn Oftalmol. 2004 May-Jun;120(3):29-31.

24. Pais E, Alexy T, Holsworth RE Jr, Meismelman HJ. Effects of nattokinase, a pro-fibrinolytic enzyme, on red blood cell aggregation and whole blood viscosity. Clin Hemorheol Microcirc. 2006; 35 (1-2):139-42.

25. Suzuki Y, Kondo K, Ichise H, Tsukamato Y, Urano T, Umemura K. Dietary supplementation with fermented soybeans suppresses intimal thickening. Nutrition. 2003 Mar: 19(3): 261-4.

26. Cesarone MR, Belcaro G, Nickolaides AN, Ricci A, Geroulakos G, Ippolito E, Brandoloni R. Prevention of venous thrombosis in long haul flights: the LONFLIT-FLITE randomized, controlled trial. Angiology. 2003 Sep-Oct; 54(5):531-9.

27. Kim JY, Gum SN, Paik JK, Lim HH, Kim KC, Ogasawara K., et al. Effects of nattokinase on blood pressure: a randomized, controlled trial. Hypertens Res. 2008 Aug; 31(8):1583-8.

28. Reddy PH. Mitochondrial dysfunction in aging and Alzheimer’s disease: strategies to protect neurons. Antioxid Redox Signal. 2007 Oct; 9 (10): 1647-58.

29. Pepys MB. Pathogenesis, diagnosis and treatment of systemic amyloidosis. Philos Trans R Soc Lond B Biol Sci. 2001 Feb 28; 356 (1406): 203-10.

30. Coburn J, Leong JM, Erban JK. Integrin alpha IIb beta 3 mediates binding of the Lyme disease agent Borrelia burgdorferi to human platelets. Proc Natl Acad Sci U S A. 1993 Aug 1;90(15):7059-63.

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 due to lifestyle, etc., but lectins give us a reason for poor digestion that is perhaps not so obvious. This article will answer the question, "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 article "Lectins: Their Damaging Role in Intestinal Health, Rheumatoid Arthritis and Weight Loss."

• 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 (Table 1).

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 "Lectins: Their Damaging Role in Intestinal Health, Rheumatoid Arthritis and Weight Loss" 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 NAG’s 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 fucoidin’s 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 can’t 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. D’Adamo, 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.

6. Zapopozhets TS, Besednova NN, Loenko luN. Antibacterial and immunomodulating activity of fucoidin. Antibiot Khimioter. 1995; 40: 9-13. [Article in Russian]

7. Baba M, Snoeck R, Pauwels R, de Clereq E. Sulfated polysaccharides are potent and selective inhibitors of various enveloped viruses, including herpes simplex virus, cytomegalovirus, vesicular stomatitis virus, and human immunodeficiency virus. Antimicrob Agents Chemother. 1988; 32: 1742-1745.

8. Criado MT, Ferreiros CM. Selective interaction of a Fucus vesiculosus lectin-like mucopolysaccharide with several Candida species. Ann Microbiol (Paris). 1983; 134A: 149-154.

9. Criado MT, Ferreiros CM. Toxicity of an algal mucopolysaccharide for Escherichia coli and Neisseria meningitides strains. Rev Esp. Fisiol. 1984; 40: 227-230.

10. Lynch G, Low L, Li S, et al. Sulfated polyanions prevent HIV infection of lymphocytes by disruption of the CD-4gp120 interaction, but do not inhibit monocyte infection. J Leukoc Biol. 1994; 56: 266-272.

11. Beress A, Wassermann O, Tahhan S, et al. A new procedure for the isolation of anti-HIV compounds (polysaccharides and polyphenols) from the marine alga Fucus vesiculosus. J Nat Products. 1993; 56: 478-488. [published erratum appears in J Nat Prod. 1996 May; 59(5): 552.]

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. D’Adamo 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.

19. Mandel KG, Daggy BP, Brodie DA, Jacoby HI. Review article: alginate-raft formulations in the treatment of heartburn and acid reflux. Aliment Pharmacol Ther. 2000; 14: 669-690.

20. Anderson DM, Brydon WG, Eastwood MA, Sedgwick DM. Dietary effects of  sodium alginate in humans. Food Addit Contam. 1991; 8: 237-248.

When I first started in practice in the early ’70s, it was unusual to see a dog live longer than 12 to 14 years of age. Over the 30 plus years, that has changed to where I see quite a number of dogs living to 14 to 18 years of age. It seems that the increase in years of the dogs and cats mirrors what has been happening in the human model.

The first action that makes a difference in helping our pet friends live longer, healthier lives is keeping them fit. By that, I mean they need to have a waist between the chest and the hips when standing. If there is no waist, they are already overweight. There have been many studies showing that restricted calories lead to a longer life. Research on fruit flies, mice, rats and monkeys showed an increase in longevity and decrease in age-related problems such as Alzheimer’s disease. While this research is not 100 percent definitive, keeping your pet at a healthy weight is proven to delay the onset of osteoarthritis and likely extend life in comparison to overweight pets we see so often.

A 40-pound dog that has an extra 10 pounds of unneeded weight is 20 percent overweight. This is the same as a 150-pound person weighing in at 180 pounds. For the person, that is like carrying around a large bag of dog food all the time. Remember, an oatmeal cookie given to a 20-pound dog is equivalent to a hamburger for an adult.

For maximum longevity in our pets, we therefore need to pay attention to what we are feeding them. Dogs living longer isn’t the only thing that has changed over the years. What used to be $7 to $10 for a 30- to 50-pound bag of dog food is now $20 to $30 for a 30-pound bag. This will provide minimum nutrition and keep the body going for a similar amount of time but there are many premium foods and super premium foods available. The premium and super premium dog foods provide more micronutrients and specific supplements incorporated into the food. Besides these foods, there are supplements for dogs that support other factors, just as there are for humans.

Resveratrol is thought to provide help with longevity in mice and rats and may be helpful in humans. Something to think about is the fact that grapes and raisins are toxic to dogs and when given in a quantity such as a box of raisins to an average dog, can cause death. Resveratrol is found in small quantities in red wine and the skin of grapes. However, I cannot find any source that shows resveratrol to be toxic and the toxin in the grapes/raisins is unknown. The primary source of resveratrol used in supplementation is the Giant Knotweed as it is much more concentrated in that plant than in grapes. The research done, in mouse and rat models, shows no signs of toxicity and I cannot find any source that shows resveratrol to be toxic in dogs, nor have I seen any problems with dogs taking resveratrol.

Ribonucleic acid (RNA) is another product that appears to make a difference in our pets. Supplemental ribonucleic acid (RNA) may help boost our immune systems, increase energy levels, neutralize toxins, repair cell damage and improve skin elasticity. Older dogs seem to be able to function better in all facets of their life when they are taking RNA supplements. RNA can be given by itself or can be found in the product RejuvaPet, which has several other ingredients that may help pets function at a higher level than what is expected at their age.

In conclusion, I believe both products, in conjunction with proper weight maintenance, will help your pets live a longer, healthier life.

Vitamins Studied for Their Role in Managing Celiac Disease

A group of three important vitamins may support the health of people with celiac disease, a new study found.

Celiac disease is caused by an intolerance to gluten in wheat. It is reported to affect up to 1 percent of children and 1.2 percent of adults, according to a study in the Gut journal. Many clinicians also believe that subclinical celiac disease is prevalent in a far greater percentage of the population.

Celiac disease is a malabsorption syndrome, and therefore, sufferers are at increased risk of various nutrient deficiencies, including folate and vitamin B12. Low levels of each of these vitamins have been linked to higher levels of homocysteine, an amino acid implicated in heart disease, and celiac disease sufferers have a greater incidence of high homocysteine levels compared to healthy controls. The consequences of higher homocysteine levels in celiac disease may include an increased tendency to develop occlusive venous and arterial disease.

Because of the connection between high homocysteine levels and celiac disease, researchers decided to study the effect of vitamin B6, folate, and vitamin B12 on fasting plasma homocysteine levels. The study authors measured homocysteine levels in 51 consecutive adults 18 to 63 years old who had celiac disease and compared them to 50 healthy control individuals. Twenty-five of the subjects already used B vitamin supplements. Twenty-six of the subjects suffered from villus atrophy as a result of the celiac disease. Atrophy of the villus may affect the way celiac patients absorb nutrients since the villus, the multiple, minute projections of the intestinal mucosa into the lumen of the small intestines, increase the surface area for absorption of water and nutrients.

Patients with celiac disease who were using vitamin supplements (including the patients who had villus atrophy) had higher serum vitamin B6, folate, and vitamin B12 levels compared to patients who did not use the supplements or healthy controls. Lower plasma homocysteine levels were found in celiac patients using B vitamin supplements than in patients who did not use the supplements or healthy controls. Vitamin B6 and folate (although not vitamin B12) were significantly and independently associated with homocysteine levels.

The study authors concluded, "The regular use of B-vitamin supplements is effective in reduction of homocysteine levels in patients with celiac disease and should be considered in disease management."

Reference:

Hadithi M, Mulder CJ, Stam F, Azizi J, Crusius JB, Pena AS, Stehouwer CD, Smulders YM. Effect of B vitamin supplementation on plasma homocysteine levels in celiac disease. World J Gastroenterol. 2009 Feb 28;15(8):955-960.

Folic acid, vitamin B6 and vitamin B12 are found in Extension B-Plex. Another formula, Advanced Methyl Caps, also contains folic acid, vitamin B6 and vitamin B12 as well as betaine, another nutrient known to lower homocysteine levels.

Vitamin K2 Supports Heart Health

Vitamin K2 may decrease the risk of developing coronary heart disease in postmenopausal women, a new study has found.

Researchers evaluated data from 16,057 postmenopausal women, aged between 49 and 70. None of the women had cardiovascular disease at the start of the study. Dietary intakes were determined using a food frequency questionnaire.

After more than eight years of follow up, researchers observed an association between a higher consumption of natural vitamin K2, particularly menaquinone-7, -8, and -9, and a significantly reduced prevalence of coronary heart disease. For every 10-microgram increase in the amount of vitamin K2 consumed, there was a 9 percent reduction in the risk of developing coronary heart disease (CHD).

In this study, consumption of vitamin K1 had no effect on heart health. The researchers believe that the differences between vitamin K2 and K1 may be due to the different distribution of each in the body. K1 is primarily taken-up by the liver and then removed from circulation, while K2 is transported also to extra-hepatic tissues, such as vessel wall and bones-tissue. Therefore, K2 is cleared more slowly from the liver, making it available for a longer time.

The researchers concluded, "A high intake of menoquinones, especially MK-7, MK-8 and MK-9, could protect against CHD. However, more research is necessary to define optimal intake levels of vitamin K intake for the prevention of CHD."

Reference:

Gast GC, de Roos NM, Sluijs I, Bots ML, Beulens JW, Geleijnse JM, Witteman JC, Grobbee DE, Peeters PH, van der Schouw YT. A high menaquinone reduces the incidence of coronary heart disease in women. Nutr Metab Cardiovasc Dis. 2009 Jan 27. Published Online Ahead of Print.

Vitamin D May Reduce Multiple Sclerosis Risk

Scientists have released the results of a new study, which investigated whether vitamin D supplementation could influence a gene linked to an increased risk of developing multiple sclerosis.

Past epidemiological studies have found strong evidence implicating reduced exposure to sunlight and an increased risk of MS. Vitamin D is produced in the skin after it is exposed to sunlight. One previous study in 257 US military personnel with multiple sclerosis found that higher levels of vitamin D in the body may reduce the risk of developing MS by as much as 62 percent.

Following up on this past evidence, the authors of the current study investigated whether a gene that triples the risk of developing multiple sclerosis (the HLA-DRB1 gene) was sensitive to vitamin D. In 322 subjects (some with and some without MS), the gene was indeed influenced by vitamin D compared to in 168 controls.

The researchers wrote, "Given that a high frequency of vitamin D insufficiency in the general population has been observed, our data support the case for supplementation during critical time periods to reduce the prevalence of this devastating disease."

Reference:

Ramagopalan SV, Maugeri NJ, Handunnetthi L, Lincoln MR, Orton SM, Dyment DA, Deluca GC, Herrera BM, Chao MJ, Sadovnick AD, Ebers GC, Knight JC. Expression of the multiple sclerosis-associated MHC class II Allele HLA-DRB1*1501 is regulated by vitamin D. PLoS Genet. 2009 Feb;5(2):e1000369. Published Online Ahead of Print.

Important Nutrients May Have the Ability to Improve Hearing

Scientists investigated a group of four nutrients to determine whether they could play a role in preventing temporary and permanent hearing loss.

In one study, researchers gave guinea pigs beta-carotene, vitamins C and E and magnesium one day before the animals were exposed to four-hours of 110 decibel (dB) noise, which is similar to the level reached at a loud concert. Another group of control animals received saline injections once per day. The researchers found that the animals given the antioxidants and magnesium did not experience the temporary hearing loss that occurred in the control animals immediately after exposure to the noise as well as 24 hours later. Animals treated with the nutrients had better hearing outcomes at the final test time.

In a second study, scientists investigated whether the same supplements could prevent the permanent hearing loss caused by exposure to a single loud sound in mice. Twenty-eight days prior to noise exposure, they added two different doses of the dietary supplements to the animals’ diets. Control animals were fed an otherwise identical, nutritionally complete diet with none of the supplemental nutrients.

The results indicated that mice receiving the higher doses of the supplements had significantly less permanent hearing loss than control animals. Decreasing the amount of vitamin content in the enhanced diet also produced a reduction in protection against permanent hearing loss. Oral treatment with this combination of antioxidants and magnesium before exposure of the animals to the loud noise also protected a variety of cells in the inner ear, specifically in the lateral wall, an inner ear structure linked to age-related hearing loss.

The study authors wrote, "These data support the potential for translation of these agents to human populations given the well-established safety profile for high-level supplementation of these micronutrients, as shown in multiple long-term human studies."

References:

LePrell C, Schmitt J, Dolan DF, Boxer P, Prieskorn D, Deremer S, Goodson M.  Prevention of Temporary Noise-Induced Threshold Deficits Using Dietary Agents. Abstract #827.  Presented at the 32nd Annual Midwinter Research Meeting of the Association for Research in Otolaryngology, Baltimore, Maryland, February 18, 2009.

LePrell C, Ohlemiller KK, Gagnon PM, Bennett DC. Reduction in Permanent Noise-Induced Threshold Deficits in Mice Fed a Combination of Dietary Agents. Abstract #826.  Presented at the 32nd Annual Midwinter Research Meeting of the Association for Research in Otolaryngology, Baltimore, Maryland, February 18, 2009.

A multivitamin such as Extend Plus provides an easy way to obtain vitamins C and E, magnesium and beta-carotene along with other important nutrients.

Nattokinase May Support Memory and Inhibit a Protein Implicated in Mad Cow Disease

An enzyme extracted from fermented soy known as Nattokinase, well documented with evidence of its ability to dissolve clots and thus play a role in cardiovascular health, is now being studied for another set of abilities.

When beta-amyloid plaque accumulates in the brain there is an increase in brain cell damage and death from oxidative stress. This results in cognitive dysfunction and an increased risk of Alzheimer’s disease. Amyloid fibrils contribute to the formation of amyloid plaque and also are involved in prion diseases, such as bovine spongiform encephalopathy (mad cow disease).

In one of the first investigations to explore nattokinase’s effect on amyloid plaque, researchers studied the enzyme’s action against three types of amyloid fibrils: A-beta-40 fibrils, linked to Alzheimer’s; insulin fibrils, linked to diabetic complications; and prion peptide fibrils, responsible for prion diseases. The researchers reported that nattokinase was able to degrade all three different amyloid fibrils.

According to the scientists, "Since natto has been ingested by humans for a long time, it would be worthwhile to carry out an epidemiological study on the rate of occurrence of various amyloid-related diseases in a population regularly consuming natto."

Reference:

Hsu RL, Lee KT, Wang JH, Lee LY, Chen RP. Amyloid-degrading ability of nattokinase from Bacillus subtilis natto. J Agric Food Chem. 2009 Jan 28;57(2):503-8.

Cranberry Extract May Have Effects Beyond Urinary Tract Health

Cranberry extract, long recognized for its role in stopping E. Coli bacteria from adhering to the urinary tract, is now being studied for another interesting property.

Scientists investigated whether cranberry extract or quercetin (one of the fruit’s major flavonoid compounds) would have an effect on colon health. During the in vitro study, the researchers exposed a human colon cancer cell line to different doses of cranberry extract or quercetin. The study authors then measured the expression of cyclooxygenase-2 (COX-2), an enzyme linked to inflammation.

The researchers found that both the cranberry extract and quercetin decreased COX-2 expression. Furthermore, when the cells were stimulated with a tumor-promoting compound, a decrease of COX-2 expression occurred.

The researchers concluded that the study demonstrates the mechanism behind the link between inflammation and cancer and that "the anti-inflammatory properties of crude cranberry extract or quercetin can be used to modulate this pathway."

According to the researchers, "The results suggest that a possible mechanism involved in the anti-cancer activity of cranberry and quercetin is partly mediated through its anti-inflammatory action. These findings indicate that cranberry and quercetin may reduce the risk of colon cancer possibly by suppressing inflammatory responses."

Reference:

Narayansingh R, Hurta RAR. Cranberry extract and quercetin modulate the expression of cyclooxygenase-2 (COX-2) and IB in human colon cancer cells. Journal of the Science of Food and Agriculture. February 2009. 89(3);542 – 547.

Cranberry Concentrate is found as a stand alone supplement and in D-Mannose. Quercetin is found with other synergistic ingredients in QuerCelain^®, Bioflavonoid Complex with Quercetin and in Extension Resveratrol.

Combination of Three Vitamins Found to be Important for Eye Health

Age-related macular degeneration (AMD) is a retinal disease that causes central vision loss and leaves only peripheral vision. It is a common disease that affects 25 to 30 million people worldwide.  Previously, studies have found that dietary nutrients such as lutein may play a protective role against AMD.

Past epidemiological studies found a direct association between blood concentrations of the amino acid homocysteine and the risk of age-related macular degeneration. However, unambiguous data from randomized clinical trials designed to examine the effect of therapy to lower homocysteine levels in AMD has been, until now, lacking.

In a new randomized, double-blind, placebo-controlled trial, scientists studied the effects of three nutrients known to lower homocysteine levels—vitamins B6, B12 and folic acid—in 5,442 female health care professionals 40 years or older with preexisting cardiovascular disease or 3 or more cardiovascular disease risk factors. A total of 5,205 of these women did not have a diagnosis of AMD at baseline and were included in the study. Participants were randomly assigned to receive a combination of folic acid (2.5 mg/day), pyridoxine hydrochloride (50 mg/day), and vitamin B12 (1 mg/day) or placebo.

After an average of 7.3 years of treatment and follow-up, there were 55 cases of AMD in the B vitamin group and 82 in the placebo group. For visually significant AMD, there were 26 cases in the group given the B vitamins and 44 in the placebo group.

The researchers believe the results suggest that in women with a high risk of cardiovascular disease, daily supplementation with folic acid, pyridoxine and vitamin B12 may reduce the risk of AMD.

Reference:

Christen WG, Glynn RJ, Chew EY, Albert CM, Manson JE. Folic acid, pyridoxine, and cyanocobalamin combination treatment and age-related macular degeneration in women: the Women’s Antioxidant and Folic Acid Cardiovascular Study. Arch Intern Med. 2009 Feb 23;169(4):335-41.

Folic acid, pyridoxine hydrochloride and vitamin B12 are found in Extension B-Plex. Another formula, Advanced Methyl Caps, also contains folic acid, vitamin B6 (as pyridoxal-5-phosphate) and vitamin B12 as well as betaine, another nutrient known to lower homocysteine levels.

Botanical May Reduce Risk of Strokes

A new analysis of the medical literature indicates that a popular botanical may reduce the risk of strokes.

Experimental models of stroke provide consistent evidence of smaller stroke occurrences in animals ingesting tea components or tea extracts. In the new analysis, researchers assessed whether there is a similar reduction in stroke risk in humans who drink green or black tea. The researchers sought to identify and summarize all human clinical and observational data on green and black tea and stroke. The study authors pooled data from 9 studies involving 4,378 strokes among 194,965 individuals.

The results indicated that regardless of their country of origin, individuals consuming 3 or more cups of green or black tea per day had a 21 percent lower risk of stroke than those consuming less than 1 cup per day.

Although the scientists aren’t certain which compounds in tea produce these effects, they theorize that a component of green tea known as L-theanine, which is nearly 100 percent absorbed and travels across the blood-brain barrier, may be responsible.

According to the researchers, "Although a randomized clinical trial would be necessary to confirm the effect, this meta-analysis suggests that daily consumption of either green or black tea equaling 3 cups per day could prevent the onset of ischemic stroke."

Reference:

Arab L, Liu W, Elashoff D. Green and Black Tea Consumption and Risk of Stroke. A Meta-Analysis. Stroke. 2009 Feb 19. Published Online Ahead of Print.

Individuals who do not want to consume large amounts of green or black tea as a beverage can take green tea extract capsules. The green tea extract available here is very low in caffeine. L-theanine capsules also are available here.

Two Nutrients Found to Improve Prostate Health

In a first-of-its-kind study, researchers have discovered that two nutrients may be involved in stopping a process linked to prostate cancer by altering the expression of certain prostate genes that are linked to the development of tumors.

In the new study, scientists from the University of Texas MD Anderson Cancer Center in Houston gave 39 prostate cancer patients vitamin E (400 IU alpha-tocopherol) or selenium (200 micrograms), and either both supplements or a placebo for three to six weeks prior to removing the subjects’ prostates. The researchers then took prostate biopsy samples from surgically removed prostates in order to investigate if the vitamin supplements affected gene expression.

The results indicated that the expression of certain genes did differ between groups receiving the supplements and placebo. Specifically, the expression of several pathways associated with cancer was altered in a way unfavorable to cancer development in the supplement groups compared with the placebo group. The study authors reported a change in the expression of the TP53 gene, which codes for p53, an important protein that acts as a tumor suppressor and is involved in the functioning of a normal cell cycle. In the group given both vitamin E and selenium, the gene acted in a similar way to that observed in people with no prostate cancer. Thus, these two supplements induced gene expression patterns in the malignant prostate glands that were similar to those found in healthy prostates.

Reference:

Tsavachidou D, McDonnell TJ, Wen S, Wang X, Vakar-Lopez F, Pisters LL, Pettaway CA, Wood CG, Do KA, Thall PF, Stephens C, Efstathiou E, Taylor R, Menter DG, Troncoso P, Lippman SM, Logothetis CJ, Kim J. Selenium and Vitamin E: Cell Type- and Intervention-Specific Tissue Effects in Prostate Cancer. J Natl Cancer Inst. 2009 Feb 24. Published Online Ahead of Print.

Lutein May Stop Damage Resulting From Modern-Day Problem

The carotenoid lutein, long studied for its possible role in protecting against age-related macular degeneration, may have another role to play in eye health, researchers have found.

In modern society people often spend many hours in front of a computer, a practice that strains the eyes. Lutein is a nutrient known to support eye health. Therefore, scientists examined the effect of different doses of lutein supplementation on visual function in subjects with long-term computer display light exposure. Thirty-seven healthy subjects who ranged in age from 22 to 30 years and who were regular computer users were randomly assigned to one of three groups. One group received 6 mg of lutein per day, another group received 12 mg lutein per day and a third group received a placebo.

At the study’s start and on week 12, the scientists measured levels of serum lutein and visual performance indices such as visual acuity, contrast sensitivity and glare sensitivity in the subjects.

After 12 weeks of lutein supplementation, there was an increase in serum lutein concentrations in the groups given 6 mg per day and 12 mg per day. In the group taking 12 mg lutein per day there was a trend toward increase in visual acuity. Both lutein groups experienced improvements in regards to sensitivity to contrast on a computer screen, said the researchers, with the improvements reaching statistical significance in the high-dose group.

According to the researchers, "Visual function in healthy subjects who received the lutein supplement improved, especially in contrast sensitivity, suggesting that a higher intake of lutein may have beneficial effects on visual performance."

Reference:

Maa L, Lina X-M, Zoua Z-Y, Xua X-R, Lia Y, Xua R. A 12-week lutein supplementation improves visual function in Chinese people with long-term computer display light exposure. British Journal of Nutrition. 2009 February 19. Published Online Ahead of Print.

In addition to being offered as a stand-alone product, lutein also is found in Extension Vision along with other synergistic ingredients.