• The President's Desk  — Health Freedom Victory

• Memory, Mood and the Stress Response  — 

• Test Uncovers a Common Deficiency  — 

• Immunological Memory  — Training the Immune System to Defend Against Viral Invaders

• Lung Health During a Challenging Time of Year  — 

• Pet Corner  — Joint Health in Fall and Winter

• Cognitive Support  — Proactive Strategies Essential to Preserve Brain Function

• Breast Health  — Iodine and Other Nutrients Play a Crucial Role

• B Vitamins Important for Colon Health  — Breaking News
• New Evidence Indicates that Vitamin D is Important for Pregnant Women  — Breaking News
• Omega-3 Fatty Acid Intake Important for Heart Health  — Breaking News
• Natural Supplement Supports Weight Management  — Breaking News
• Potent Antioxidant Studied in Blood Disorders  — Breaking News
• Dietary Supplement May Reduce Inflammation  — Breaking News
• Popular Herb Studied for Bone Health  — Breaking News
• Amino Acid Protects Lung Tissue  — Breaking News
• Important Vitamin and Fatty Acids Studied in Autism  — Breaking News
• Antioxidant Supports Brain Health  — Breaking News

• Venous Insufficiency
• Optic Neuritis
• Toenail Fungus
• Chelation, Bones, Bruising
• Ulcerative Colitis, PSC
• Fibromyalgia
• Emotional Health of 12-Year-Old
• Prostate Health
• Weight Control in Children
• Boosting Immunity
• Digesting Carbs
• Omega-3:6 Ratio

This month, I am pleased to inform you about some very good news that represents a huge step forward in the journey to defend health freedom. I’m referring to a US District Court’s ruling in favor of a nutritional supplements firm and against the Federal Trade Commission (FTC), a landmark case that found FTC’s criticism of the company’s advertising was simply a “difference of opinion.”

The situation began in 2007, when the FTC had filed a motion against the supplement company, claiming it was making unsubstantiated claims. The FTC recommended fining the company $24 million. When it came time for the court to hear the case, the FTC and the supplement company each presented two witnesses, who were physicians, researchers or professors of medicine. The court deemed all the witnesses to be “credible and knowledgeable in their respective fields of expertise.”

After listening to the witnesses, the court’s conclusion was, “In considering the testimony offered by all of the experts the difference between FTC’s experts and the Defendants’ experts came down to a difference of opinion—not necessarily matters of right and wrong.”

Furthermore, neither of FTC’s experts claimed the products in question were ineffective or constituted a health risk to the public. In addition, the court took into account the fact that FTC had provided no evidence that consumers had complained or were harmed by the use of the supplements.

Consequently, Judge Dennis Cavanaugh denied the motion on the grounds that the company had “clearly offered support and substantiation for the claims regarding their products.”

The court’s opinion went on to state, “This is not a case of a company making claims out of thin air.” The court noted that the supplement company presented scientific evidence to back its claims.

This ruling is a huge victory for supplement consumers who have the right to truthful information that is not subject to FTC or FDA censorship.

Psychological stress can have a dramatic effect on various aspects of our health. It can impair memory, reduce mental well-being, wreak havoc on the digestive tract, destroy cardiovascular health and reduce overall lifespan. With the poor economy looming over our heads, there has never been a more stressful time for many of us alive today.

In a three part series in this newsletter, I will discuss the destructive effects of stress on various systems of the body as well as natural stress-reducing supplement regimens. In this first part of the series, I will discuss the ways in which chronic stress can impair memory and how stress is linked to depression.

Chronic Stress and Memory

Stress is known to strongly influence the prefrontal cortex (PFC), a key brain region controlling cognition and emotion. Interestingly, acute, short-term stress can affect corticosteroid stress hormones and the PFC in such a way as to enhance learning and memory. This makes sense due to the fact that when a person is exposed to a dangerous stressor heightened vigilance is essential to survival. However, long-term, chronic stress can have the opposite effect and can damage cognition, emotion and memory.¹

One of the reasons stress is so destructive to memory revolves around the adrenal glands’ production of excessive cortisol, which occurs during chronic stress. High cortisol levels, when maintained for a long time, are known to be linked to poor memory. This has been shown in a number of studies including a recent study where researchers investigated 37 unmedicated, non-delusional patients with major depression and 18 healthy controls. The subjects underwent psychiatric ratings, hourly assessments of cortisol activity over 24 hours, and neuropsychological assessments.

The study authors found that greater cortisol levels in the subjects were related to poorer memory performance. High cortisol levels also were significantly related to impaired verbal memory (paragraph recall).²

Perhaps one of the most graphic illustrations of how stress affects cognition involves Alzheimer’s disease, which is thought to develop as a result of over-production and aggregation of beta-amyloid (Abeta) peptides in the brain. Researchers have found that individuals suffering from chronic stress are at an increased risk for developing Alzheimer’s. Furthermore, in a recent rodent study, researchers induced chronic psychosocial stress in rats then administered Abeta to the animals. The effect of chronic stress on the severity of Abeta-induced spatial learning and memory impairment was tested by three approaches: behavioral testing in a water maze, in vivo electrophysiological recording in anesthetized rats, and analysis to determine protein levels of learning- and memory-related molecules. The results indicated that a marked impairment of learning and memory developed when stress was combined with Abeta, more so than that caused by Abeta alone.

Additionally, there was a significantly greater impairment of early-phase long-term potentiation in chronically stressed/Abeta-treated rats than in either the stressed or Abeta-treated rats.³ Long-term potentiation (LTP) refers to a long-lasting improvement in communication between two neurons that results from stimulating them simultaneously. Neurons use chemical synapses to communicate with each other, and it is thought that memories are encoded by modification of synapses. LTP, therefore, is widely considered to be one of the major cellular mechanisms involved in learning and memory, from the relatively simple learning processes occurring in all animals, to the more complex cognition in humans. Therefore the fact that stress combined with the formation of Abeta proteins impairs LTP indicates that stress plays a destructive role in learning and memory through inhibiting the beneficial effects of LTP.

Stress’s destructive effect on neuronal communication translates into decreased cognitive performance as evidenced by a study of 65 subjects suffering from work-stress-related burnout and 65 demographically matched, healthy reference subjects. Among burnout cases, lower diurnal cortisol variability was related to slower performance in several tests.⁴

Stress also seems to compound the adverse effects on learning and memory that occur after intake of a high-fat diet. Young adult rodents were exposed to chronic psychosocial stress and/or a high-fat diet for 3 months. In a water maze, rats were subjected to 12 learning trials as well as short-term and long-term memory tests. This procedure was applied daily until the animals reached what the researchers called days to criterion (DTC), which is the number of days that the animals took to make zero errors in two consecutive days. Groups were compared based on the number of errors per trial or test as well as on the DTC.

The results indicated that the groups exposed to chronic stress, high-fat diet and both chronic stress and high-fat diet showed impaired learning as indicated by committing significantly more errors than the control group. In memory tests, chronic stress, high-fat diet and chronic stress/high-fat diet groups showed significantly impaired performance compared to the control group. Additionally, the group exposed to both stress and a high-fat diet was the only group that showed significantly impaired performance in memory tests on the fifth training day, suggesting more severe memory impairment in that group. Furthermore, DTC value (the number of days that the animals take to make zero errors in two consecutive days) for all the above groups indicated that chronic stress or high-fat diet alone resulted in a mild impairment of spatial memory, but the combination of chronic stress and high-fat diet resulted in a more severe and long-lasting memory impairment.⁵

Furthermore, humans often have to perform complex social cognitive tasks while under stress (such as during a social conflict). The link between stress and cognitive dysfunction is further cemented by the fact that the brain regions responsible for social cognitive tasks are target regions for stress hormones.⁶

Stress and Depression

Cognitive dysfunction and high cortisol levels often occur side-by-side in depressed individuals. Cortisol’s actions occur via mineralocorticoid and glucocorticoid receptors, which occur in the highest density in the hippocampus, a brain area closely related to cognitive function. Scientists recently examined this connection in 52 medication-free patients with major depression (37 women, 15 men) and 50 healthy control subjects, matched for age, gender, and years of education. The researchers applied several neuropsychological tests and measured salivary cortisol levels four times throughout the same day.

The researchers found that compared with healthy subjects, depressed patients had significantly higher cortisol levels and were impaired in verbal memory, visuospatial memory, working memory, and selective attention. In depressed patients, but not in healthy control subjects, the study authors found that the higher the salivary cortisol levels the greater the impairment of verbal memory and visuospatial memory.⁷ There was also a link between higher cortisol levels in the depressed patients and impaired executive function, a term used by psychologists and neuroscientists to describe brain processes responsible for planning, cognitive flexibility, abstract thinking, rule acquisition, initiating appropriate actions and inhibiting inappropriate actions, and selecting relevant sensory information.

According to the researchers, “Cognitive deficits, especially those closely related to hippocampus function, appear to be related to cortisol secretion in depressed patients. Elevated cortisol may downregulate mineralocorticoid and glucocorticoid receptors in the hippocampus, which could, in part, be responsible for cognitive deficits in depressed patients.”

Cortisol-Controlling Strategies

Three strategies can be employed to reduce the harmful effects of stress on the body. The first step is to take a salivary hormone test (adrenal function panel) in order to measure levels of cortisol in the body and to determine the state of the adrenal glands.

Based on the results of the test, chronically excessive cortisol levels can be lowered using a combination of Relora^® (a proprietary blend of a patented extract from Magnolia officinalis bark and a patent-pending extract from Phellodendron amurense bark) and Sensoril^™ (a patented proprietary extract of roots and leaves from Withania somnifera Dunn, known as Ashwagandha. Both Relora and Sensoril are found in the formula Cortisol Control.

Studies have shown that these two compounds can alleviate high cortisol’s effects on the body. Fifty stressed people were given 200 mg Relora three times per day for two weeks. Post-trial analysis revealed that 82 percent found Relora effective in controlling stress-induced symptoms, such as depression, anxiety, irritability, emotional ups and downs, concentration difficulties and restlessness. Seventy-eight percent reported increased relaxation, while 74 percent had more restful sleep.⁸

In another trial 12 stressed subjects took Relora for two weeks. Salivary DHEA and cortisol measurements were taken. Morning salivary cortisol levels (when cortisol levels are normally highest) dropped 37 percent, while DHEA levels rose 227 percent. Previously abnormal cortisol/DHEA levels returned to normal in all subjects by the study’s end.⁸

Sensoril, a carefully balanced formulation of the key compounds that provide Ashwagandha’s immunomodulating and anti-stress activity, can work synergistically with Relora. By optimizing the ratio of oligosaccharides to polysaccharides in the Ashwagandha, this formulation protects the withanolides from digestive inactivation and enhances their absorption. Ashwagandha has been used in Ayurvedic medicine for many centuries to promote resistance to stress and has been reported to enhance mental function and memory.

Sensoril’s extracts have been subject to a wide range of tests to measure anti-stress activity. In one experiment, rats were exposed to severe overcrowding conditions or tactile stress (continuous poking), and then given morphine. Seventy percent of the tactile-stressed and 100 percent of the overcrowding-stressed control rats developed convulsions, and 80 percent and 90 percent died, respectively. Yet only 10 percent of the tactile-stressed rats and 10 percent of the overcrowding-stressed rats given morphine plus Sensoril developed convulsions, while 0 percent and 10 percent died.⁹

Severe stress causes adrenal glands to enlarge, and their vitamin C and corticosterone content drops. Another experiment showed that when stress is induced in rats, the rodents given Sensoril had smaller adrenal glands with more corticosterone in them than the unstressed control rats, and almost as much vitamin C.⁹

Adaptogenic Support

Another effective strategy to control stress, thereby improving cognitive function, is to supplement with the adaptogens Eleutherococcus senticosus, Manchurian Thorn Tree (Aralia manchurica), and Schisandra (Schisandra chinensis), all found in AdaptaPhase^® I.

Eleutherococcus has been traditionally used for modulation of stress and fatigue as well as immune-stimulating action. In a single-blind, placebo-controlled crossover study, supplementation with Eleutherococcus was evaluated in regards to maximal working capacity in adolescent males. The results indicated a 23.3 percent increase in total work after Eleutherococcus supplementation.¹⁰ Animal studies measuring forced swimming time show that supplementation with Eleutherococcus inhibits stress-induced cortisol increase and stress-induced immune suppression and improves endurance demonstrated by increased swimming time.¹¹

Schisandra is another adaptogenic traditional Chinese botanical. Evidence suggests that adaptogens such as Schisandra support the stress response both by affecting the sympathetic-adrenal response with short term administration as well as supporting the hypothalamic-pituitary-adrenal axis with longer-term administration.^12-13 Studies using animal models confirm that Schisandra can reduce elevated serum corticosterone levels.¹⁴

Aralia manchurica (Manchurian Thorn Tree) has historically been used in Russia as an adaptogen for fatigue, weakness, headaches, depression, immune support, and stress-overload. One study showed a 90 percent success rate using this herb in individuals with stress overload and weakness.¹⁵Aralia has also been shown to decrease blood glucose levels in animal studies.¹⁶

Conclusion

Chronic stress is an under-recognized factor in the development of cognitive impairment. Furthermore, stress also is linked to depression. Therefore, employing a supplement regimen that combines a cortisol-lowering supplement (Cortisol Control) with adaptogenic support (AdaptaPhase 1) can be an effective strategy to manage stress and preserve memory.

References

1. Yuen EY, Liu W, Karatsoreos IN, Feng J, McEwen BS, Yan Z. Acute stress enhances glutamatergic transmission in prefrontal cortex and facilitates working memory. Proc Natl Acad Sci USA. 2009 Aug 18;106(33):14075-9.

2. Gomez RG, Posener JA, Keller J, DeBattista C, Solvason B, Schatzberg AF. Effects of major depression diagnosis and cortisol levels on indices of neurocognitive function. Psychoneuroendocrinology. 2009 Aug;34(7):1012-8.

3. Srivareerat M, Tran TT, Alzoubi KH, Alkadhi KA. Chronic psychosocial stress exacerbates impairment of cognition and long-term potentiation in beta-amyloid rat model of Alzheimer’s disease. Biol Psychiatry. 2009 Jun 1;65(11):918-26.

4. Osterberg K, Karlson B, Hansen AM. Cognitive performance in patients with burnout, in relation to diurnal salivary cortisol. Stress. 2009;12(1):70-81.

5. Alzoubi KH, Abdul-Razzak KK, Khabour OF, Al-Tuweiq GM, Alzubi MA, Alkadhi KA. Adverse effect of combination of chronic psychosocial stress and high fat diet on hippocampus-dependent memory in rats. Behav Brain Res. 2009 Dec 1;204(1):117-23.

6. Smeets T, Dziobek I, Wolf OT. Horm Behav. Social cognition under stress: Differential effects of stress-induced cortisol elevations in healthy young men and women. 2009 Feb 6. Published Online Ahead of Print.

7. Hinkelmann K, Moritz S, Botzenhardt J, Riedesel K, Wiedemann K, Kellner M, Otte C.Biol Psychiatry. Cognitive Impairment in Major Depression: Association with Salivary Cortisol. 2009 Aug 25. Published Online Ahead of Print.

8. LaValle J and Hawkins, E. Relora—The Natural Breakthrough to Losing Stress-Related Fat and Wrinkles. North Bergen, NJ: Basic Health Publications; 2003:16.

9. Bhattacharya S. et al. Anti-stress activity of sitoindosides VII and VIII, new acylsterylglucosides from Withania somnifera. Phytother Res. 1987;1: 32-37.

10. Kimura Y, Sumiyoshi M. Effects of various Eleutherococcus senticosus cortex on swimming time, natural killer activity and corticosterone level in forced swimming stressed mice. J Ethnopharmacol. 2004 Dec;95(2-3):447-53.

11. Upton R, ed. Schisandra Berry: Analytical, quality control, and therapeutic monograph. Santa Cruz, CA: American Herbal Pharmacopoeia 1999;1-25.

12. Panossian A, Wagner H. Stimulating effect of adaptogens: an overview with particular reference to their efficacy following single dose administration. Phytother Res. 2005 Oct;19(10):819-38.

13. Lee S, Kim DH, Jung JW, et al. Schizandra chinensis and Scutellaria baicalensis counter stress behaviors in mice. Phytother Res. 2007 Dec;21(12):1187-92.

14. Chiu PY, Leung HY, Ko KM. Schisandrin B Enhances Renal Mitochondrial Antioxidant Status, Functional and Structural Integrity, and Protects against Gentamicin-Induced Nephrotoxicity in Rats. Biol Pharm Bull. 2008 Apr;31(4):602-5.

15. Martinez B, Staba EJ. The physiological effects of Aralia, Panax and Eleutherococcus on exercised rats. Jpn J Pharmacol. 1984 Jun;35(2):79-85.

16. Wang L, Tu YC, Lian TW, et al. Distinctive antioxidant and antiinflammatory effects of flavonols. J Agric Food Chem. 2006 Dec 27;54(26):9798-804.

Many people walking around today are likely to be in a developmental stage of some form of preventable disease—albeit a silent stage. It takes “optimal” levels of many nutrients, the amounts of which are unique to each person, to protect the genes and support their proper expression in keeping us ideally “healthy.” Even one mineral deficiency can throw a smooth running train off the tracks because of the cascade of events set into motion. For example, mild to severe deficiency of the mineral zinc is commonplace today and implicated in serious chronic disease processes along with what society considers nuisance conditions such as white spots in the fingernail beds, dandruff, poor quality of handwriting, reduced sense of taste or smell, poor appetite, eating disorders, frequent colds, slow wound healing, benign prostate hypertrophy and acne. The National Health and Nutrition Examination Survey III found that only half of the U.S. population gets even the RDA of zinc.

There are many reasons why Americans are zinc deficient. Soil depletion and conditions, commercial fertilization, food refining, and poor food choices have made dietary zinc less available. Americans eat huge amounts of fast-acting carbohydrates, creating blood glucose that stimulates the release of the hormone insulin from the beta cells of the pancreas. Evidence shows that insulin synthesis, function and secretion is dependent on zinc and that the release of insulin causes a corresponding loss of zinc.^1-2

Zinc deficiency prevents adequate production of insulin, so much so, that an injection of dithiazone, a zinc-chelating agent, produces diabetes in experimental animals.³ Many people avoid foods rich in zinc such as nuts, seeds, seafood, and red meat, due to their belief that these foods are fattening or unhealthful. Furthermore, ongoing (chronic), subacute or recurrent infections can lower zinc status in the marginally sufficient.

Stressors and alcohol consumption also rapidly deplete zinc.⁴ Additionally, many drugs such as cortisone, diuretics, and antacids significantly impair zinc absorption.^5-7 Un-sprouted whole wheat, beans and other grains contain phytates that impair zinc absorption and further contribute to an accumulative zinc deficit.

The essential trace mineral zinc is one of the most heavily researched nutrients. Zinc is found throughout the body and is necessary for growth and development due to its role as a cofactor for more than 300 catalytic and regulatory enzymes and in receptor binding. It is probably most renowned for the role it plays in immunity protecting the thymus, lymphoid tissues, TH-1 immunity and the action of natural killer (NK) cells.^8-10 Dietary deficiencies in zinc can contribute to single- and double-strand DNA breaks and oxidative modifications to DNA that increase risk for cancer development.

What follows is a partial summary of some of zinc’s functions.

Hormonal Health

Zinc is necessary for hormonal balance. It is a cofactor in thyroid hormone manufacture, conversion of T4 to T3, and thyroid receptor function.^11-12 A study with Down’s syndrome children showed a reduction in thyroid autoantibodies with zinc administration.¹³ It is needed for ovulation and sperm production. Low dietary zinc (even mild deficiencies) also has been associated with hypogonadism,¹⁴ low testosterone¹⁵ and low IGF-1.¹⁶ Zinc’s role in DNA binding proteins also involves the regulation of adrenal hormones (glucocorticoids), vitamin D, vitamin A, cell-cell signaling and bone density.¹⁷

Zinc deficiency reduces circulating luteinizing hormone and testosterone concentrations, alters steroid metabolism in the liver, and modifies sex steroid hormone receptor levels, thereby contributing to the development of male reproductive dysfunction.¹⁸

Strengthening the Gut

Zinc plays a pivotal role in gastrointestinal (GI) health. Mucosal cell differentiation, growth, function, and repair involve zinc. Many individuals with inflammatory bowel disease have zinc deficiencies.^19-22 Zinc improves GI disorders in children, reduces childhood mortality, corrects deficiencies linked to anorexia, hypoguesia (loss of taste), poor growth, alopecia (hair loss), delayed sexual maturation, skin disorders and diarrhea.²³

Antioxidant Abilities

Zinc is a multi-purpose antioxidant and many different biomolecules are protected from oxidation by zinc. In animals, low zinc decreases glutathione, vitamin E, glutathione peroxidase, SOD (superoxide dismutase) and GST (glutathione S-transferase), thus increasing lipid peroxidation. Low zinc intensifies oxidative stress. Zinc induces the synthesis of metallothionein (MT), a potent free radical scavenger. MT proteins normally increase as a protective response to oxidative stress but when zinc is deficient, will actually decrease in response to oxidants. These proteins assist detoxification by binding to toxic metals, particularly mercury and cadmium, transporting them to the liver or kidneys for conjugation and excretion. Zinc is a constituent of the key antioxidant enzyme, copper-zinc SOD. It protects sulfhydral groups on glutathione peroxidase, another vital antioxidant enzyme, prevents copper-induced membrane oxidation and provides a glutamate receptor blockade thereby lessening excitotoxicity.²⁴

Autism and Cognitive Health

Zinc is a mainstay in autism protocols. Autistic children have well-documented low zinc levels, sometimes half the lower limit for age-matched controls. In analyzing over 3,500 autistic children at the Pfeiffer Treatment Center, it was found that high doses of zinc (2-3 mg per kg of body weight per day) are often needed to achieve optimal behavior responses.²⁵ Although long-term supplementation of zinc often requires a balance of supplemental copper, copper excess is evident in autism as higher serum copper and lower ceruloplasmin (unbound copper is considered highly pro-oxidative).^26-27

Many studies show that zinc is also critical for healthy brain function and low levels may contribute to neuro-psychiatric disorders ranging from schizophrenia, dementia, depression, ADD, anorexia and dyslexia to a possible contributor to Alzheimer’s disease.²⁸ Ninety-five percent of seniors (and higher in the hospitalized population) are deficient with many of their problems caused or worsened by low zinc. Within two months of zinc supplementation in the elderly, there was an improvement in resistance to infection along with a greater chance of surviving an infection.²⁹

Vision

A clinical trial sponsored by the National Eye Institute (NEI) and reported in the Archives of Opthamology, found that 80 mg/day of zinc along with vitamin C (500 mg/day), vitamin E (400 IU/day), and beta carotene (15 mg/day), lowered the risk for ARM (age-related macular degeneration) by about 25 percent, possibly slowing the progression of the disease.³⁰

In general, zinc protects the function of essentially all the systems in the body directly or indirectly. It is a very important pre- and post-surgery nutrient. Zinc supplementation has been recently found to protect the endothelial lining of blood vessels, the target of oxidation and inflammation in atherosclerosis.³¹ Zinc deficiency is an etiological agent in periodontal disease resulting in increased permeability of gingival epithelium to bacteria.³² Collective studies also demonstrate that zinc deficient subjects, after taking zinc at the first sign of the common cold, will reduce the duration of the cold.^33-35

Zinc Test

Studies show that gustatory (taste) sensitivity may indicate the availability of zinc. In 1981 Shatzman and Henkin published results of research regarding Gustin, a zinc-dependent salivary (protein) taste bud growth factor, in patients with hypoguesia (loss of taste). Gustin helps discriminate metallic tastes so those who are zinc-deficient cannot perceive the taste. After zinc supplementation there were eventual changes in taste acuity.³⁶

Schauss and Costin noted that zinc deficiency can directly cause a loss of appetite and taste and this was first demonstrated in 1934.³⁷ They additionally found that a percentage of zinc deficient patients are also vitamin B6 and magnesium deficient. If a person is not responding well to zinc therapy it may be due to deficiencies in B6 or magnesium as they are zinc synergists and help with zinc transfer to cells.

The British Medical Association’s British National Formulary, in 1988, was the first peer-reviewed recommendation for the use for the Zinc Taste Test (ZTT) in assessing zinc deficiency.

Information in the Lancet regarding the Zinc Taste Test showed that it was developed because plasma and serum were considered unreliable markers of zinc status (98 percent of total body zinc is intracellular). It was being used in patients with anorexia and depression.^38-39

The Zinc Taste Test, an easy, inexpensive, in-office and in-home testing method to assess zinc need, is now available here as ZincMate^™. It involves swirling approximately 2 tsp. (10 ml) of a solution of zinc sulfate around the mouth for 10 seconds, swallowing or discarding it, and then observing the taste response, which can range from slight to no perceived taste (if deficient) to a strongly observed taste (zinc sufficient). If deficient, which is common, extra supplementation with zinc is recommended along with periodic zinc taste testing until a taste is perceived.

This is a very important deficiency and people have different needs. The optimal supplemental range for zinc is considered to be between 15-75 mg/day. Supplementation at higher levels for extended periods should be monitored and balanced with other trace minerals especially copper and manganese. Due to diet, lifestyle and genetics, it may take some individuals a much longer time to achieve zinc adequacy and restore depleted zinc reserves.

It is interesting to report that popular dental adhesives such as PoliGrip^® and Fixodent^® contain high levels of zinc. A copious use of 2 tubes of adhesive per week would translate to a zinc exposure of 330 mg/day. In four patients the use of dental adhesives eventually depleted copper and led to neurological abnormalities but improved with copper supplementation and adhesive avoidance.⁴⁰

Clinical practitioners should note that with regards to standard blood chemistry panels, if the value of serum alkaline phosphatase (ALP), a zinc metalloprotein enzyme, is below the midline of the reference range, with other subjective indicators as noted throughout the article, consider zinc deficiency⁴¹ and perform a ZTT on the patient (occasionally it may take over a year to see the ALP value change). Excess serum iron may also be contributed to by zinc deficiency (zinc antagonizes iron).

Conclusion

Zinc deficiency is becoming all too common. The consequences of having low levels of this essential mineral include impaired function of the gastrointestinal tract and thyroid gland, decreased immunity, poor skin health, cognition and many other aspects of overall health. A Zinc Taste Test, now being offered here, can help pinpoint whether an individual is deficient and to what extent supplementation is necessary.

References

1. Jansen J, Karges W, Rink L. Zinc and diabetes--clinical links and molecular mechanisms. J Nutr Biochem. 2009 Jun;20(6):399-417.

2. Winterberg B, et al. Zinc in the Treatment of Diabetic Patients. Trace Elements in Medicine. 1989;6(4):173-77.

3. X. Kadota I. Studies on experimental diabetes mellitus as produced by organic reagents; oxine diabetes and dithizonenbsp diabetes. The J of Lab and Clin Med. 1950 Apr;35(4):568-91.

4. Ijuin H. Evaluation of pancreatic exocrine function and zinc absorption in alcoholism. Kurume Med J. 1998;45(1):1-5.

5. Sturniolo GC, etal. Inhibition of Gastric Acid Secretion Reduces Zinc Absorption in Man. J Amer Coll Nutr. 1991;4:372-75.

6. Dietary Supplement Fact Sheet: Zinc. Office of Dietary Supplements of the National Institutes of Health, 7 Nov. 08. Web. 12 Aug. 09. http://ods.od.nih.gov/fact Sheets/Zinc.asp.

7. Peretz A, Neve J, Famaey JP. Effects of chronic and acute corticosteroid therapy on zinc and copper status in rheumatoid arthritis patients. J Trace Elem Electrolytes Health Dis. 1989 Jun;3(2):103-8

8. Prasad AS, Beck FW, Grabowski SM, Kaplan J, Mathog RH. Zinc deficiency: changes in cytokine production and T-cell subpopulations in patients with head and neck cancer and in noncancer subjects. Proceedings of the Association of American Physicians. 1997;109(1):68-77.

9. Prasad AS, Oberleas D. Changes in Activities of Zinc-Dependent Enzymes in Zinc-Deficient Tissues of Rats. J Appl Physiol. 1971;31:842-6.

10. Prasad As. Zinc: Mechanisms of Host Defence. J Nutr. 2007;137:1345-9.

11. Nishiyama S, Futagoishi-Suginohara Y, Matsukura M, et al. Zinc supplementation alters thyroid hormone metabolism in disabled patients with zinc deficiency. J Am Coll Nutr. 1994;13:62-67.

12. Olivieri O, Girelli D, Stanzial AM, et al Selenium, zinc, and thyroid hormones in healthy subjects: low T3/T4 ratio in the elderly is related to impaired selenium status. Biol Trac Elem Res. 1996;51:31-41.

13. Licastro F, Mocchegiani E, Zannoti M, et al. Zinc affects the metabolism of thyroid hormones in children with Down’s syndrome: normalization of TSH and of reverse T3 plasmic levels of dietary zinc supplementation. Int J Neurosci. 1992;65:259-68.

14. Mahan LK, Escott-Stump S. Krause’s Food, Nutrition and Diet Therapy.11th ed. Philadelphia: W.B. Saunders; 2004.

15. Prasad AS, Montzoros CS, Beck FW, et al. Zinc status and healthy testosterone levels of healthy adults. Nutrition. 1996;12(5):344-348.

16. Ninh NX, Thissen JP, Collette L, et al. Zinc supplementation increases growth and circulating insulin-like growth factor I (IGF-I) in growth-retarded Vietnamese children. Am J Clin Nutr. 1996;63(4):514-519.

17. Mutlu M, Argun M, Kilic E, Saraymen R, Yazar S. Magnesium, zinc and copper status in osteoporotic, osteopenic and normal post-menopausal women. J Int Med Res. 2007;35:692-5.

18. Om AS, Chung KW. Dietary zinc deficiency alters 5 alpha-reduction and aromatization of testosterone and androgen and estrogen receptors in rat liver. J Nutr. 1996 Apr;126(4):842-8.

19. Ojuawo A, Keith L. The serum concentrations of zinc, copper and selenium in children with inflammatory bowel disease. Cent Afr J Med. 2002;49(9-10):116-19.

20. Geering BJ, Badart-Smook A, Stockbrugger RW, Brummer RJ. Comprehensive nutritional status in recently diagnosed patients with inflammatory bowel disease compared with population controls. Eur J Clin Nutr. 2000;54(6):514-21.

21. Fleming CR, Huizenga KA, McCall JT, et al. Zinc nutrition in Crohn’s disease. Dig Dis Sci. 1981;26(10):865-70.

22. Hendricks KM, Walker WA. Zinc deficiency in inflammatory bowel disease. Nutr Rev. 1988;46(12):401-8.

23. Quinn, Sheila. Textbook of Functional Medicine. Ed. David S. Jones. 1st ed. Vol. 1. Gig Harbor: The Institute for Functional Medicine, 2005;26:374.

24. Quinn, Sheila. Textbook of Functional Medicine. Ed. David S. Jones. 1st ed. Vol. 1. Gig Harbor: The Institute for Functional Medicine, 2005;30:520-21.

25. Walsh WJ, Usman A, Tarpey J, et al. Metallothionein and Autism, 2nd edition, Monograph. Health Research Institute. Naperville, Illinois. 2002

26. Walsh W. Metallothionein deficiency in autism spectrum disorders. National Conference of the Autism Society of America. Seattle, Washington. July 7-10,2004. p. 342-349.

27. Chauhan A, Chauhan VP, Brown WT, et al. Oxidative stress in autism: Increased lipid peroxidation and reduced serum levels of ceruloplasmin and transferrin-the antioxidant proteins. Life Sci. 2004;75:2539-49.

28. Zinc Deficiency Tied to Neurofibrillary Tangles in Alzheimer’s. Family Practice News. October 15-31, 1990;20(20):7.

29. Mocchegiani E, et al. Zinc and immunoresistance to infection in aging: new biological tools. Trends Pharmacol Sci 2000 Jun;21(6):205-8.

30. Mares Perlman JA, Klein R, Klein BE, Greger JL, Brady WE, Palta M, Ritter LL. Association of zinc and antioxidant nutrients with age-related maculopathy. Arch Ophthalmol. 1996 Aug; 114:8:991-7.

31. Meerarani P, et al. Zinc protects against apoptosis of endothelial cells induced by linoleic acid and tumor necrosis factor alpha. Am J Clin Nutr 2000 Jan;71(1):81-7.

32. Polenik, P. Zinc in Etiology of Periodontal Disease. Medical Hypotheses. 1993;40:182-185.

33. Prasad AS, Fitzgerald JT, Bao B, Beck FWJ, Chandrasekar PH. Duration of symptoms and plasma cytokine levels in patients with the common cold. A randomized, double blind, placebo-controlled trial. Annals of Int Med. 2000 Aug;133:245-252.

34. Novick SG. How does zinc modify the common cold? Clinical observations and implications regarding mechanisms of action. Med Hypothesis 1996 Mar;46(3):295-302.

35. Godfrey JC, Godfrey NJ, Novick SG. Zinc for treating the common cold: review of all clinical trials since 1984. Alter Ther Health Med. 1996 Nov;2(6):63-72.

36. Shatzman AR, Henkin RI. Gustin concentration changes relative to salivary zinc and taste in humans. Proc Natl Acad Sci. 1981 June;78(6):3867-387.

37. Schauss A, Costin C. Zinc as a nutrient in the treatment of eating disorders. Am J Nat Med. 1997 Dec;4:8-10.

38. Bryce-Smith D, Simpson RI. Case of anorexia nervosa responding to zinc sulphate. Lancet. 1984 Aug11; 2(8398):350.

39. Bryce-Smith D, Simpson RID, Southon S, Johnson IT, Gee JM. Anorexia, depression, and zinc deficiency. Lancet. 1984 Nov17; 2(8412):1162-3.

40. Nations SP, Boyer PJ, Love LA, Burritt MF, Butz JA, Wolfe GI, Hynan LS, Reisch J, Trivedi JR. Denture Cream–An unusual source of excess zinc leading to hypocupremia and neurological disease. Neurology. 2008;71:639-643.

41. Weismann K, Hoyer H. Serum alkaline phosphatase and serum zinc levels in the diagnosis and exclusion of zinc deficiency in man. Am J Clin Nutr. 1985;41:1214-1219.

The immune system has an amazing ability to not only survey the body and remove any foreign invaders, but also to remember previous pathogens. The immune system has two main components: innate and acquired immunity. Innate immunity includes the non-specific components of the immune system that are present at birth such as skin, mucous membranes, cough reflex, low pH of the stomach, enzymes in saliva, and many types of white blood cells.

The acquired component of the immune system, on the other hand, is highly specialized and functions to recognize and remember foreign agents. This immunological memory allows for faster and stronger immune responses each time a particular pathogen is encountered. Initial contact with an agent (antigen) activates white blood cells known as lymphocytes, which produce proteins specific to that foreign agent. An antigen is any substance, usually a protein or large sugar molecule, which causes your immune system to produce antibodies to it or elicit an immune response.

Acquired immunity is divided into two major categories known as humoral and cell-mediated responses.

Humoral responses are mediated by antibodies, also known as immunoglobulins. Immunoglobulins are proteins made by B lymphocytes (white blood cells that mature in the bone marrow), which function to identify and neutralize foreign agents, such as bacteria and viruses. Humans produce an estimated 10 billion different antibodies, each capable of binding a distinct epitope, a unique area on an antigen that is recognized by the antibody.¹

The cell-mediated immune response involves white blood cells called T-lymphocytes (T-cells). T-cells are processed in the thymus to recognize and respond to a specific antigen. There are several types of T-cells including helper T-cells, killer T-cells (also called cytotoxic T-cells), memory T-cells, and suppressor (or regulatory) T-cells. It is the memory T-cells that are most important in forming immunological memory as they are long-living cells programmed to recognize and respond to a pathogen once it has invaded. The memory T-cells allows for a faster and stronger immune response at a later encounter with the invader compared to the initial response. The memory T-cells can quickly proliferate to large numbers of helper T-cells upon re-exposure to the antigen, thus providing the immune system with a type of memory against past infections.

Lymphocytes have antigen-specific receptors on their membranes. Antigens bind to these receptors on the lymphocytes, which activates the cell resulting in the release of chemical messengers known as lymphokines or cytokines. These chemical messengers then induce activity by other white blood cells. T-cells also have molecules on their membranes that interact with antigen-presenting cells, which are cells that present antigens to the T-cells. Once a T-helper cell recognizes an antigen, the lymphocyte migrates to lymphoid tissues and divides into both memory T-cells and killer T-cells.

Supporting the body’s immunological memory can help the immune system ward off infections such as the flu. Influenza is a respiratory illness caused by influenza viruses. The severity of the illness varies with increased risk of complications in young children, the elderly, and in those individuals with chronic conditions such as lung or heart disease. Each year in the United States, approximately 5-20 percent of the population gets the flu; with flu-related complications resulting in more than 200,000 people hospitalized and 36,000 deaths.² Many health officials state that the flu season for this year may be worse than previous years due to the first influenza pandemic in more than 40 years. Children are more susceptible to complications caused by the flu, including the 2009 H1N1 flu strain, as they have less developed immune systems, making strengthening their immunological memory even more important. The H1N1 flu strain seems to differ from the other flu strains in that children and younger adults seem to have a predisposition towards it whereas older individuals are more protected due to immunological memory. This underlies the importance of strengthening immunological memory in all ages to keep the body’s defenses strong.

Supporting Immunological Memory

A special formulation of mushrooms combined with the green tea polyphenol epigallocatechin 3-gallate (known as ImmuneAssist^® 24/7) has been shown to help promote the acquired immune response. A significant amount of research suggests that Lentinula edodes (Shitake) impacts both innate and acquired immunity. Shitake promotes the innate immunity by significantly increasing the ability of macrophages, a type of white blood cell, to engulf foreign particles and pathogens.³ The beta-glucan constituent in shitake also induces the activation of antigen-specific cytotoxic T-cells and macrophages, helper T-cells and natural killer (NK) cells, promotes T-cell differentiation and inhibits suppressor T-cell activity.^4-6 Suppressor T-cells inhibit the production of cytotoxic T-cells. Similarly, the mushroom Agaricus blazei enhances the induction of antigen-specific cytotoxic T-cells and significantly increases populations of helper T-cells.^7-8

The mushrooms Ganoderma lucidum (Reishi) and Grifola frondosa (Maitake) also affect the immune response. The major immunomodulating effects of the Reishi constituents are activation of immune effector cells such as T-cells, macrophages, and NK cells.^9-10 Reishi constituents are potent stimulators of macrophages and have been shown to increase the expression of surface molecules on antigen-presenting macrophages.¹¹ Reishi was also shown to augment the toxicity of cytotoxic T-cells by as much as 100 percent when administered at a concentration of 200 µg/ml.¹² Research indicates that maitake beta-glucan enhances the activities of NK cells, macrophages, the antibody response, and cytotoxic T-cells.^13-14

Cordyceps sinensis and Coriolus versicolor are additional medicinal mushrooms that have been shown to directly impact the acquired immune response by enhancing the production of T-cells.^15-16Cordyceps has been shown to significantly increase the number of helper T-cells and increase the ratio of T-helper to T-suppressor cells.¹⁷Coriolus contains several immune modulating constituents including multiple beta-glucans, PSK, and polysaccharide peptide (PSP),¹⁸ which have been shown to increase suppressed killer T-cell activity.¹⁹

ImmuneAssist 24/7 combines the above mushrooms hybridized to bring out the most potent aspects of their immune enhancement properties. This allows the mushrooms to possess greater potential than any other mushrooms grown elsewhere today, including wild crafted varieties.

Green tea contains the polyphenol epigallocatechin 3-gallate (EGCG). This green tea constituent has significant immune modulating activity. Green tea supplementation has been shown to increase gamma-delta T-cell proliferation and function as well as increased secretion of the cytokine interferon-gamma in response to gamma-delta T-cell antigens. Gamma-delta T-cells play a complex role in the development of immunological memory. This same study also showed that green tea supplementation decreased the number of subjects with cold and flu symptoms and the duration of symptoms compared to subjects receiving the placebo.²⁰ In addition, green tea constituents have been shown to directly inhibit influenza virus replication.²¹

A purified form of EGCG is used within the formula ImmuneAssist 24/7. The EGCG is suspended in a time-released matrix so that it doesn’t break down in stomach acid, allowing much more of this virus-blocking compound into the blood stream than can be obtained by drinking green tea.

Conclusion

Supporting the body’s natural defenses is always important. With this year’s flu season expected to be more severe than ever, it is essential to optimize health. Supporting the ability of the immune system to recognize and remember pathogens by consuming a powerful blend of mushrooms and ECGC is an important way in which the body can be strengthened throughout the coming months and beyond.

References

1. Fanning LJ, Connor AM, Wu GE. Development of the immunoglobulin repertoire. Clin Immunol Immunopathol. 1996 Apr;79(1):1-14.

2. Centers for Disease Control and Prevention. Seasonal Influenza: The Disease. Available at: http://www.cdc.gov/flu/about/disease/. Accessed on: 9-12-09.

3. Zheng R, Jie S, Hanchuan D, et al. Characterization and immunomodulating activities of polysaccharide from Lentinus edodes. Int Immunopharmacol. 2005 May;5(5):811-20.

4. Bohn JA., BeMiller JN. (1-3)Beta-D-Glucans as biological response modifiers: a review of structure-functional activity relationships. Carbohydrate Polymers. 1995;28: 3-14.

5. Chihara G. Immunopharmacology of Lentinan, a polysaccharide isolated from Lentinus edodes: its applications as a host defence potentiator. International Journal of OrientalMedicine. 1992;17:57-77.

6. Aoki T. Lentinan. In Immune Modulation Agents and Their Mechanisms. Femchel RL, Chirgis MA (editors). Immunology Studies. 1984;25:62-77.

7. Takimoto H, Wakita D, Kawaguchi K, et al. Potentiation of cytotoxic activity in naive and tumor-bearing mice by oral administration of hot-water extracts from Agaricus brazei fruiting bodies. Biol Pharm Bull. 2004 Mar;27(3):404-6.

8. Mizuno M, Morimoto M, Minato K, et al. Polysaccharides from Agaricus blazei stimulate lymphocyte T-cell subsets in mice. Biosci Biotechnol Biochem. 1998 Mar;62(3):434-7.

9. Gao Y, Zhou S. The Immunomodulating Effects of Ganoderma lucidum (Curt.: Fr.) P. Karst. (Ling Zhi, Reishi Mushroom) (Aphyllophoromycetideae). Internation Journal of Medicinal Mushrooms. 2002; 4(1).

10. Gao Y, Zhou S, Jiang W, et al. Effects of ganopoly (a Ganoderma lucidum polysaccharide extract) on the immune functions in advanced-stage cancer patients. Immunol Invest. 2003 Aug;32(3):201-15.

11. Oh JY, Cho KJ, Chung SH. Activation of macrophages by GLB, a protein-polysaccharide of the growing tips of Ganoderma lucidum. Yakhak Hoeji. 1998; 42: 302-6.

12. Lei LS, Lin ZB. Effect of Ganoderma polysaccharides on T cell subpopulations and production of interleukin-2 in mixed lymphocyte response. Yao Hsueh Huseh Pao – Acta Pharmaceutica Sinica. 1992; 27:335-9.

13. Suzuki I, Hashimoto K, Oikawa S, et al. Antitumor and immunomodulating activities of a beta-glucan obtained from liquid-cultured Grifola frondosa. Chem Pharm Bull. 1989;37:410-413.

14. Ross GD, Vetvicka V, Yan J, et al. Therapeutic intervention with complement and beta-glucan in cancer. Immunopharmacology. 1999;42:61–74.

15. Cheng Q. Effect of cordyceps sinensis on cellular immunity in rats with chronic renal insufficiency. Zhonghua Yi Xue Za Zhi. 1992 Jan;72(1):27-9, 63.

16. Tsukagoshi S, Hashimoto Y, Fujii G, et al. Krestin (PSK). Cancer Treat Rev. 1984 Jun;11(2):131-55.

17. Chen GZ, Chen GL, Sun T, et al. Effects of Cordyceps sinensis on murine T lymphocyte subsets. Chin Med J. 1991;104:4–8.

18. Dong Y, Yang MM, Kwan CY. In vitro inhibition of proliferation of HL-60 cells by tetrandrine and Coriolus versicolor peptide derived from Chinese medicinal herbs. Life Sci. 1997;60:PL135–140.

19. Ng TB. A review of research on the protein-bound polysaccharide (polysaccharopeptide, PSP) from the mushroom Coriolus versicolor (Basidiomycetes: Polyporaceae). Gen Pharmacol. 1998;30:1–4.

20. Rowe CA, Nantz MP, Bukowski JF, et al. Specific formulation of Camellia sinensis prevents cold and flu symptoms and enhances gamma,delta T cell function: a randomized, double-blind, placebo-controlled study. J Am Coll Nutr. 2007 Oct;26(5):445-52.

21. Song JM, Lee KH, Seong BL. Antiviral effect of catechins in green tea on influenza virus. Antiviral Res. 2005 Nov;68(2):66-74.

Optimal lung health is imperative for combating influenza as this infection primarily affects the nose, throat, and lungs. Influenza complications are more likely in individuals with chronic lung conditions such as asthma, chronic bronchitis, emphysema, and cystic fibrosis. Symptoms of influenza, particularly lung symptoms, are made much worse by the immune system responding in an exaggerated way to the virus, rather than by the virus itself. During influenza infection, the prolonged response of the immune system can cause the lungs to become inflamed resulting in airway blockage and difficulty breathing. Generally, this occurs between day 2 and day 4 of the illness, in which the systemic symptoms begin to subside and respiratory symptoms begin to increase.

Supplements to optimize lung health such as N-acetyl-cysteine (NAC) may help decrease these exaggerated lung symptoms and complications during an influenza infection. NAC is a derivative of the amino acid L-cysteine and can increase the level of the potent antioxidant glutathione. NAC is used in the treatment of numerous lung conditions due to its antioxidant and anti-inflammatory properties and expectorant and mucous thinning activity.

Reactive oxygen species (ROS) and cytokines in the lungs, in addition to the superoxide-generating xanthine oxidase enzyme in lung tissue, have been implicated in the pathogenesis of influenza. Animal models have shown that supplementation with NAC significantly decreased the mortality in mice infected with influenza by modulating the ROS.¹ The enzyme NADPH oxidase may also be a major source of influenza-evoked oxidative stress in lung epithelial cells contributing to the over-exuberant lung inflammation and lethality in influenza infections. The ability of NAC to diminish oxidative stress such as the ROS induced by NADP oxidase may be one of the mechanisms in which NAC protects lung tissue during an influenza infection.² In addition, glutathione can bind to nitric oxide (NO), which is elevated in severe respiratory diseases such as asthma, emphysema, and cystic fibrosis, which results in reduced inflammatory effects of NO.³

Additionally, NAC acts directly on the immune system to stimulate the immune response by enhancing T-cell proliferation.⁴ Research also indicates that glutathione levels are decreased in many diseases including viral infections and immune dysfunctions and glutathione and NAC has been shown to inhibit vital replication. Additionally, evidence suggests that glutathione levels within the antigen-presenting cells influences the cytokine response pattern as sufficient glutathione levels are required for T-cell differentiation and activation of macrophages, NK cells, and T-cells and promotes cytokine activity that predominates during a viral infection.⁵

References

1. Ungheri D, Pisani C, Sanson G, et al. Protective effect of n-acetylcysteine in a model of influenza infection in mice. Int J Immunopathol Pharmacol. 2000 Sep-Dec;13(3):123-8.

2. McCarty MF, Barroso-Aranda J, Contreras F. Practical strategies for targeting NF-kappaB and NADPH oxidase may improve survival during lethal influenza epidemics. Med Hypotheses. 2009 Jun 30. Published Online Ahead of Print.

3. Bengtsson A, Lundberg M, Avila-Carino J, et al. Thiols decrease cytokine levels and down-regulate the expression of CD30 on human attergen-specific T helper (Th) 0 and Th2 cells. Clin Exp Immunol.  2001 Mar; 123(3):350-60.

4. Hadzic T, Li L, Cheng N, et al. The role of low molecular weight thiols in T lymphocyte proliferation and IL-2 secretion. J Immunol. 2005 Dec 15;175(12):7965-72.

5. Fraternale A, Paoletti MF, Casabianca A, et al. Antiviral and immunomodulatory properties of new pro-glutathione (GSH) molecules. Curr Med Chem. 2006;13(15):1749-55.

As fall approaches, osteoarthritis (OA) becomes more of a factor again. During the warm days of summer, dogs and cats with OA get along better with and without supplements or medications. As the nights and days become cooler, both people and pets with OA notice that they are feeling a little stiffer when first getting up and around. With motion, the discomfort that causes the stiffness usually goes away or moves to the back of the consciousness.

Our pets rely on us to help them through the discomfort. We can give them aspirin at a dose of 10 mg per kilogram of body weight twice daily. There is a risk of stomach irritation, ulceration and bleeding if too much is given. Acetaminophen can be given at the same dose, 10 mg per kilogram twice daily; however, I am personally much less comfortable with it because the drug is so hard on the liver.

The following is a list of prescription non-steroidal anti-inflammatory drugs that have been developed for dogs: Rimadyl^®, Deramaxx^®, Previcox^®, Metacam^® and Zubrin^®. These are prescribed only by veterinarians who will address the possible side effects of the one they prefer. The good part about that is the side effects are rare in the NSAIDs that are made for pets when used as directed. That is not true if one is using NSAIDs made for humans. Most of the human NSAIDs do not have a safe dose listed for use in animals and an overdose may lead to the death of your pet.

Other drugs, which come from your veterinarian, may be used to control the discomfort including tramadol, gabapentin, amantadine and opoids.

On the natural side, glucosamine, chondroitin, and MSM are ingredients that have been used since the late 1970s. I found a product made for animals about three years after having a deranged knee repaired in the mid ’70s. I took it for about a year and decided it would be good for the pets that I was helping. In fact, this proved to be true, and I turned out to be a good test subject.

If you look at the research, some of the papers say it makes little if any difference when you give glucosamine or chondroitin to an osteoarthritic dog or cat, and some of the papers, on the other hand, show a definite difference. Speaking from experience, I have found the glucosamine and chondroitin to be very effective and would not give up my supplement without a scuffle.

A study by University of Maryland School of Pharmacy investigated 50 some retail products of glucosamine/chondroitin and found that close to 40 percent of the products had little of the ingredient in the tablet/capsule/powder that was listed on the label. Therefore, consider that if you purchased a product and gave it according to the directions for 6 to 8 weeks and saw no change, you may have one of those products.

Consequently, you might want to try another source if you have been giving your pet a product and had no apparent results. Always look for a company that you know has high ethics and integrity, such as Vitamin Research Products, which offers Nutri-Joint for Pets. It has a dose of glucosamine and chondroitin that I would give at ¼ teaspoon per 10 to 20 pounds for 6 to 8 weeks then reduce to 2/3 to ½ the original dose and continue to give to your pet. The other advantage of this product is that it has some other ingredients that are very helpful in controlling discomfort. Often times a combination of pain meds, NSAIDs and natural supplements can give your pet a new leash on life.

Although I don’t believe Nutri-Joint can actually create new cartilage when the cartilage has been destroyed, I do believe it may help with cartilage turnover, making the amount that is left better. It may also help make the joint fluid thicker and more slippery. It can make a real difference in your pet’s ability to function, which leads to a higher quality of life.

Mild cognitive impairment is a diagnosis given to individuals who have cognitive impairments beyond that expected for their age and education, but that do not interfere significantly with their daily activities. Mild cognitive impairment may or may not lead to Alzheimer’s disease. Researchers are becoming increasingly more interested in this type of cognitive impairment because in individuals at high-risk for dementia, protective strategies at this early stage may very well be more effective than those implemented after the disease process is fully underway.

In the course of researching Alzheimer’s disease after symptoms appear, scientists are now increasingly focusing their efforts on identifying diagnostic techniques and identification of proteins that appear in predementia and mild cognitive impairment as a predictor of who will go on to develop Alzheimer’s.¹ Researchers are taking note that most of the damage in Alzheimer’s and other dementias occur decades before the typical hallmarks of disease appear, indicating that proactive strategies prior to the actual onset of symptoms may prove to be the most effective way to enhance cognitive health. The identification of pre-disease biomarkers in predementia, mild cognitive impairment and Alzheimer’s has already pointed to ways in which proactive steps can be taken to enhance brain health long before irreversible signs of dementia occur.^2-5

Amyloid Accumulation

Traditional observations of neuro-anatomic abnormalities in the brains of people with Alzheimer’s disease were first described by Alois Alzheimer in 1911, in brain tissue that he had obtained during autopsies and then mounted and stained on microscope slides; his microscopic observations showed two structural changes common to all Alzheimer’s diseased brains—the presence of amyloid plaques and neurofibrillary tangles. Dr. Alzheimer’s original slides were retrieved and re-examined in 1999, and again clearly confirmed the two hallmarks of AD—neuorofibrillary tangles and amyloid plaque.⁶

An important component of amyloid plaque is the protein known as beta amyloid, made from a larger protein called beta amyloid precursor protein. One well-excepted theory is that Alzheimer’s disease is caused by an accumulation of the breakdown products of beta amyloid precursor protein, which slowly clumps together to form amyloid plaque. Enzymes can dissolve a few pieces of the clumped precursor protein, but greater accumulations of beta amyloid cannot be dissolved and the deposition of beta amyloid continues to grow into larger and larger amyloid plaques in the brain.⁶

This phenomenon is known as the amyloid cascade hypothesis and it is based on observations that the genetic status of certain Alzheimer’s patients causes them to either overproduce beta amyloid precursor protein or degrade it faster, producing very toxic smaller proteins. Amyloid plaque is found around and in between nerve cells, predominantly in the brain. The mere presence of amyloid plaque generates free radicals and is highly irritating to nerve cells.

Other, smaller proteins, called tau proteins, make amyloid plaque even more deadly to nerve cells. Both tau protein and beta amyloid are found in the brain and the cerebrospinal fluid of people with Alzheimer’s disease. Measurements of the quantities and disposition of these proteins make excellent diagnostic tools to measure the extent of the progression of Alzheimer’s disease in an individual; these measurements also are used to estimate the chances of whether a person with mild cognitive impairment will progress towards Alzheimer’s disease.⁶

Neurofibrillary tangles, the other hallmark of AD, are protein deposits found inside the neurons. They are made of tau proteins that become tangled or aggregated into an insoluble form similar to amyloid plaque. It is still controversial whether these tangles play a causative role in AD, but they are not associated with the earliest symptoms of AD. However, the number of neurofibrillary tangles correlates with the severity of dementia.⁶

Once the amyloid plaques begin to form it is much harder to reverse the damage that has already been done. Evidence indicates that brain changes leading to later cognitive impairment can begin very early in life and it is at earlier stages that taking protective measures can have a huge impact. By 2009, 603 autopsies in a small community in Finland showed a close association with amyloid plaque and neurofibrillary tangles in humans who carried the gene expressing apolipoprotein E (APOE), which is responsible for converting the less harmful amyloid beta protein into the toxic and insoluble fibrous amyloid plaque. Brain changes consisting of the typical amyloid plaque and neurofibrillary tangles due to the presence of ApoE genes began to show up at 30 years of age and reached an occurrence of 100 percent in the oldest people. The most obvious brain change differences occurred between the ages of 50 through 59, the most common age diagnosis of early cognitive impairment.⁷

Sooner Rather Than Later

Magnetic resonance imaging (MRI) has created enormous breakthroughs in diagnosing and predicting Alzheimer’s disease and dementias many years before family members and physicians can detect symptoms.

New diagnostic tests are painting an even clearer picture about when and how Alzheimer’s disease develops. It is believed by most experts in the field that the development of full-blown cognitive disorders such as mild cognitive impairment and Alzheimer’s disease takes place over approximately 20 years, from initiation to full progression.^8-9 Therefore, cognitive-supporting strategies such as dietary supplements, growth factors and antioxidants are likely to be the most efficacious method of maintaining brain health before significant brain neurodegenerative symptoms appear.

As a global approach to maintaining brain health, an ongoing cognitive enhancing nutritional supplement regimen that starts as early as possible can be an effective strategy.

Protecting the brain against oxidative stress and cross-linking as well as nourishing the health of neurons are some of the most important steps we can take to maintain cognitive health. Preventing cross-linking is important because protein cross-linking promotes beta-amyloid plaque formation. Glycated proteins are known to accumulate in the cerebrospinal fluid (CSF) of Alzheimer’s disease patients. At the same time, levels of carnosine, which prevents the glycation of proteins, dramatically decline with age in the CSF of humans.¹⁰

Carnosine and histidine (found in AGEBlock^®) are potent cross-linking inhibitors. Carnosine prevents oxidation and glycation, both of which contribute to the cross-linking of proteins.¹¹ The amino acid constituent of carnosine known as histidine is thought to be responsible for its anti-cross-linking actions.¹¹In vitro studies also have shown that carnosine protects against Amyloid beta₄₂ peptide-induced neurotoxicity.¹²

Antioxidants such as (R)-Lipoic Acid and N-acetyl cysteine (NAC), which is also found in AGEBlock, can help protect the brain against oxidative stress and related free radical-induced injury, that is involved in the amyloid formation process. Furthermore, the deposition of amyloid protein is known to cause excessive free radical damage in the brain leading to progressive inflammation that may play a significant role in the neurotoxicity of Alzheimer’s disease.^13-14

Combining an anti-cross-linking, antioxidant supplement AGEBlock with nutritional support for neuronal health can further help to maintain or improve the functions of neurons in the brain. Acetyl L-carnitine, acetyl L-carnitine arginate, Gotu kola, Ginkgo biloba, and uridine (all found in Neuron Growth Factors-NGF^™) can help provide a strong foundation for brain health. Acetyl carnitine has been shown to increase brain cell levels of glutathione, a key endogenous antioxidant that declines with age. Pretreatment with acetyl carnitine also protects neurons against the neurotoxicity induced by Amyloid beta₄₂ peptide and lowers protein oxidation; in addition, it prevents the death of neurons in a dose-dependent manner.¹⁵

Supplements such as acetyl carnitine, which stimulate nerve growth factor, are important because studies show that increased nerve growth factor (NGF) levels indicate early reductions in predementia and dementia brains. Further, NGF reductions lead to further accumulation of beta amyloid precursor protein (Abeta), contributing to the continuation of a vicious cycle. Increasing the production of nerve growth factor, on the other hand, shifts the balance toward (proper) processing of beta amyloid precursor protein and, therefore, a reduction in brain-damaging amyloid proteins. Acetyl carnitine supplementation showed reductions in Amyloid beta₄₂ by 26 percent and Amyloid beta₄₀ by 46 percent in treated brain cells compared to untreated, control cells.¹⁶

Acetyl carnitine arginate protects brain cells in a variety of ways—it increases nerve growth factor levels synergistically when used with acetyl carnitine. During in vitro studies, it also protected against a very toxic beta amyloid fragment, Amyloid beta_25-35 and completely blocked the formation of amyloid precursor protein.^17-18

When brain cells are exposed for 8 days to the amyloid beta_25-35 peptide there is often considerable cell death, depending on the study cited. Acetyl carnitine arginate completely reversed the toxicity of amyloid beta_25-35, which is caused by disruption of calcium2+ balance or alterations in divalent cation “homeostasis.”¹⁸

Neurites and dendrites, the long fibrous outgrowths of neurons that are the communications network that allow brain cells to cross-talk and communicate, are severely disrupted in dementias. Natural compounds such as acetyl L-carnitine arginate and uridine have been shown to regrow and replace the neurite and dendrite neural communications network in the brain. These compounds disrupt the formation of amyloid precursor protein, strongly believed to be the primary cause of beta amyloid plaque formation in the brain.^19-22

Gotu kola (Centella asiatica) also impacted the amyloid cascade in brain cells by decreasing Amyloid beta_{42 and 40} when fed orally for eight months to mice that had genetic predispositions that cause them to overproduce these proteins. Lowering Amyloid beta₄₂ disrupts amyloid precursor protein production. Gotu kola also scavenges free radicals, reduces cell membrane damage caused by lipid peroxidation and decreases DNA damage.^23-26

Another important neuroprotective nutrient is Ginkgo biloba. In one recent genetically engineered mouse model of Alzheimer’s disease, Ginkgo biloba administered orally for 16 months lowered amyloid precursor protein by 50 percent in the brain cortex compared to controls not given Ginkgo.²⁷ The authors of the study concluded that “potential neuroprotective properties of Ginkgo may be, at least partly, related to its APP [amyloid precursor protein] lowering activity.”

Another group of natural substances can work synergistically with those found in Neuron Growth Factors to help strengthen the brain. Huperzine A, choline, DMAE, pyroglutamic acid, L-Phenylalanine, and vinpocetine—all found in Extension IQ^™ along with Ginkgo—can be part of a proactive regimen to support brain health.

A 2007 cell culture study showed Huperzine A regulates amyloid precursor protein by directing amyloid precursor protein to a non-amyloid producing pathway. Huperzine A also blocked A-beta₄₂ production through its well-known acetylcholinesterase (ACH) inhibiting properties.²⁸ Acetylcholine is a key brain neurotransmitter which declines with normal aging, but levels are severely disrupted in dementias.¹⁹ Choline is an essential dietary precursor source of acetylcholine from lecithin and DMAE is a supplemental source, which is rapidly converted in one step to acetylcholine.

The natural plant product vinpocetine has been widely used in dementias, particularly those involving blood flow to the brain. A human trial tested the blood flow in stroke patients and subjects with mild cognitive impairment. The subjects were given vinpocetine for 12 weeks, then the researchers measured changes using the standard Clinical Global Impression scale (CGI). The authors found a significant improvement in cognitive functions using psychometric tests. Patients with mild cognitive impairment judged their improvements higher than the investigators’ opinions, who also rated good improvements. The final conclusion of the trial was that the authors recommend the use of vinpocetine for patients with mild cognitive impairment.²⁹

Conclusion

Research indicates that dementia develops long before overt signs appear, with changes in the brain beginning as early as age 30. Therefore, beginning a proactive, cognitive-enhancing supplement regimen using Neuron Growth Factors and Extension IQ plus AGEBlock, can protect vital brain functioning and maintain optimal cognitive capacity.

References

1. Cummings, JL, Doody, R, Clark, C. Disease-modifying therapies for Alzheimer disease: challenges to early intervention. Neurology. 2007 Oct 16; 69: 1622-34.

2. Diniz, BS, Pinto-Junior, JA, Forlenza, OV. Do CSF, total tau, phosphorylated tau, and beta- amyloid 42 help to predict progression of mild cognitive impairment to Alzheimer’s disease? A systematic review and meta-analysis of the literature. World J Biol Psychiatry. 2008; 9 (3): 172-82.

3. Esposito, E, Rotillo, D, Di Matteo, V, Di Giulio, C, Cacchio, M, Algeri, S. A review of specific dietary antioxidants and the effects on biochemical mechanisms related to neurodegenerative processes. Neurobiol Aging. 2002 Sep-Oct; 23 (5): 719-35.

4. Schott, JM, Kennedy, J, Fox, NC. New developments in mild cognitive impairment and Alzheimer’s disease. Curr Opin Neurol. 2006 Dec; 19 (6): 552-8.

5. Mattay, VS, Goldberg, TE, Sambataro, F, Weinberger, DR. Neurobiology of cognitive aging: insights from imaging genetics. Biol Psychol. 2008 Sep; 79 (1): 9-22.

6. Pacifico, A, Schubb, H, Ugolini, V. Structural changes characteristic of Alzheimer’s disease. Texas Arrhytmia Institute. 2008.

7. Kok, E, Haikonen, S, Luota, T, Huhtala, H, Goebeler, S, Haapasalo, H, Karhunen, PJ. Apolipoprotein E-dependent accumulation of Alzheimer disease-related lesions begins in middle age. Ann. Neurol. 2009 Jun; 65 (6): 650-7.

8. Kastenholz, B, Garfin, DE. Medicinal plants: a natural chaperones source for treating neurological disorders. Protein Pept Lett. 2009; 16 (2): 116-20.

9. Birch, CS, Brasch, NE, McCaddon, A, Williams, JH. A novel role for vitamin B(12): Cobalamins are intracellular antioxidants in vitro. Free Rad Biol Med. 2009 Jul 15; 47 (2): 184-8.

10. Hipkiss AR. Could carnosine or related structures suppress Alzheimer’s disease? J Alzheimers Dis. 2007 May;11(2):229-40.

11. Hobart LJ, Seibel I, Yeargans GS, Seidler N. Anti-crosslinking properties of carnosine: significance of histidine. Life Sci. 2004 Jul 30;75(11):1379-89.

12. Fu Q, Dai H, Hu W, Fan Y, Shen Y, Zhang W, Chen Z. Carnosine protects against Abeta42-induced neurotoxicity in differentiated rat PC12 cells. Cell Mol Neurobiol. 2008 Feb;28(2):307-16.

13. Nakamura M, Ando Y. [Amyloidosis and oxidative stress]. Rinsho Byori. 2003 Feb;51(2):140-5.

14. Jesudason EP, Masilamoni JG, Ashok BS, Baben B, Arul V, Jesudoss KS, Jebaraj WC, Dhandayuthapani S, Vignesh S, Jayakumar R. Inhibitory effects of short-term administration of DL-alpha-lipoic acid on oxidative vulnerability induced by Abeta amyloid fibrils (25-35) in mice. Mol Cell Biochem. 2008 Apr;311(1-2):145-56.

15. Abdul. HM, Calabrese, V, Calvani, M, Butterfield, DA. Acetyl-L-carnitine-induced up-regulation of heat shock proteins protects cortical neurons against amyloid-beta peptide 1-42-mediated oxidative stress and neurotoxicity: implications for Alzheimer’s disease. J Neurosci Res. 2006 Aug 1: 84 (2): 398-408.

16. Chauhan, NB, Siegel, GJ. Effect of PPF and ALCAR on the induction of NGF-and p75-mRNA and on APP processing in Tg576 brain. Neurochem Int. 2003 Aug; 43 (3): 225-33.

17. Westlund, KN, Lu, Y., Werrbach-Perez, K., Hulsebosch, CE, Morgan, B., et al. Effects of nerve growth factor and acetyl-L-carnitine arginyl amide on the human neuronal line HCN-1A. Int J Dev Neurosci. 1992 Oct; 10(5):361-73.

18. Scorziello, A., Meucci, O., Calvani, M., Schettini, G. Acetyl-L-carnitine arginine amide prevents beta 25-35-induced neurotoxicity in cerebellar granule cells. Neurochem Res. 1997 Mar; 22 (3); 257-65.

19. Sarter, M, Bruno, JP. Developmental origins of the age-related decline in cortical cholinergic function and associated cognitive abilities. Neurobiol Aging. 2004 Oct; 25(9):1127-39.

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Of all the cancers women develop, 29 percent are breast cancer. By age 25, 1 in 19,608 women will develop breast cancer. By age 50, this number changes to a shocking 1 in 50 and by age 75 an even more dismal statistic: 1 in 11. In a total lifetime, one woman in 8 will develop breast cancer.

In January 2005, cancer became the leading cause of death in the United States. Each year about 211,000 cases of breast cancer are diagnosed in the USA. The number of new breast cancer cases increased from 82 per 100,000 women in 1973 to 195 per 100,000 women in 2000. The main cause of death prior to that was heart disease. The estimated death rate from breast cancer is 40,600: 40,200 females and 400 males.

Much is said in the public media about a genetic link with this cancer. Yet, genetics play only a small role in the development of breast cancer—less than 7 percent. In the September 8, 2006 issue of USA TODAY one of the lead articles was on Killer Cancer Genes ID’d. It mentioned that 122 breast cancer-causing genes have been identified. The scientist quoted in the article mentioned that we may not be able to tackle all the genes in a tumor but that we may have to work on silencing the cancer-causing genes. Doctors in the future may find that silencing even one of these genes could be enough to keep a tumor in check or kill it. They mention in the article that treatments could be a decade or more to develop.

Yet, the technology for tomorrow is here today in the supplements we have at our disposal. For example, methylation of DNA and gene silencing are affected by nutrition. Many articles exist on silencing genes and how the use of methyl-folic acid, methyl-vitamin B12, selenium, trimethylglycine powder and zinc help to methylate the DNA.

Breast Cancer Risk Factors

Many breast cancer risk factors have been identified such as a high-fat diet, low-fiber diet, tobacco use, and alcohol use. These risk factors can be modified by an individual. There are other factors that are mostly out of a woman’s control. The longer a woman is exposed to estrogen in her body, for example, the higher her risk. This would include early age at menarche, late age at menopause, long-term use of birth control pills and nulliparity (never having given birth). There seems to be a group of women whose use of birth control pills for more that 4 years puts them at higher risk before age 45. Women who take thyroid hormone are also at higher risk for developing breast cancer.1 Conversely, a lower risk for breast cancer is seen in women who are late in age at menarche, early age at menopause, and early age at first pregnancy.

Fibrocystic Breasts

In the New England Journal of Medicine, July 22, 2005 issue, there was a lead article showing that benign breast changes in women are associated with breast cancer. Benign breast changes is a new term for what we have called fibrocystic breast disease (FBD) in the past. FBD is currently affecting about 84 percent of the female population in North America.2 FBD is a misnomer because the medical problem is not a disease in the strictest sense. It is more a problem of cyclic breast pain that is associated with the menstrual cycle. In some patients the breast pain is seen daily, regardless of their menstrual cycle. Tissue biopsy for these benign breast changes that do grow larger are called proliferative lesions and if they do not grow they are called non-proliferative lesions.

Non-proliferative lesions (non-growers) can include cyst of the breast, radial scars, apocrine cells which generally make up sweat glands—the breasts are classified as a modified sweat gland—fibroadenoma, and hyperplastic cells that are normal in appearance under the microscope but are more numerous than usual. Proliferative lesions with normal cells are called sclerosing adenosis, which have a slightly increased risk (1.5 to 2 times). There are proliferative lesions with abnormal or atypical cells that are called hyperplasia—high degree with a moderate increased risk of breast cancer of (4 to 5 times), lobular neoplasia and intraductal papilloma. As a rule in medicine, the more abnormal cells look under the microscope, i.e., the more atypical the cells look, the higher the risk of cancer being present.

Iodine’s Supportive Role

Back in the early 1990s it was noted that patients who had iodine deficiency had associated benign breast changes. By giving these patient’s iodine the breast changes that were present would regress.2 It had been noticed a few years earlier that in animal studies, where the animal had been denied access to iodine, the animals developed benign breast changes like humans.3-5 In animal studies, researchers have been able to produce breast cancer in animals by depriving them of iodine.4

In my own personal medical practice I have literally seen the regression of cysts, nodules, scar tissue, and painful breast with the use of 50 mg of Iodoral® per day for 2-3 years. The breast pain goes away in just a few weeks, but the cyst/cysts, scar tissue and breast nodules take up to 2 to 3 years to resolve. On mammograms I have seen a 50 to 80 percent reduction in the scar tissue present in the breast. Studies are needed to show via biopsy that the many different types of FBD will regress with iodine supplementation.

Before starting on iodine therapy, a patient should have their thyroid hormone values investigated. A doctor should check the size of the thyroid for enlargement and or nodules. An iodine-loading test should also be done prior to starting iodine therapy to establish the need for iodine therapy. In this test the patient is given 50 mg of iodine and a 24-hour urine test is then collected. The iodine level in the urine is measured. The more saturated the body is with iodine the higher the level of iodine excreted. The more saturated the body is, the less breast abnormalities have been seen. The test is repeated at 3 months to document increasing saturation. If saturation is not occurring then further investigation is called for to find out why saturation isn’t happening.

Additional Support

Several other nutrients/hormones are also important to breast health and can be used in conjunction with Iodoral. DIM (diindolylmethane), the nutrient derived from cruciferous vegetables, for example, is influential in helping the body metabolize estrogen. DIM has been shown to change the way estrogen is metabolized. Metabolism of the natural estrogen estradiol occurs via one of two pathways. The tumor enhancer metabolic pathway, 16 alpha-hydroxylation, is elevated in patients with breast and endometrial cancer and in those at increased risk of such cancers. This increased 16 alpha-hydroxylation activity has been shown to precede clinical evidence of cancer, and it represents a significant risk factor for developing estrogen-dependent tumors.

Conversely, when estrogen veers away from the 16-alpha pathway and takes another route out of the body, the incidence of cancer decreases. This alternate route, which acts as a tumor suppressor metabolic pathway, is called 2-hydroxylation, a process that transforms estrogen into 2-hydroxyestrone (20HEI), an antiestrogen. Healthy individuals not at risk for breast or endometrial cancer bypass the 16-alpha route and instead metabolize estrogen through this preferable pathway. DIM signals the body to metabolize estrogen via the tumor suppressor 2-hydroxylation pathway.

In addition to this more well known estrogen-related mechanism of action of DIM, recent research also indicates that DIM can prevent angiogenesis, the process by which new blood vessels develop. Cancer cells use the development of new blood vessels to spread throughout the body. In mice, DIM inhibited angiogenesis by up to 76 percent.6 In addition, in mice implanted with human breast cancer cells, tumor growth was inhibited by 64 percent in animals treated with DIM.6

Another means of supporting breast health is by using natural progesterone cream. A syndrome known as Estrogen Dominance is prevalent in women, especially postmenopausal women. According to progesterone researcher Dr. John Lee, estrogen unopposed by progesterone results in a number of adverse effects including painful breasts, fibrocystic breast disease, and breast cancer.

Estrogen dominance usually occurs at menopause, when progesterone production falls to approximately 1 percent of its pre-menopausal level. At this time, the production of estrogen falls to about 50 percent of its pre-menopausal levels. This dramatically alters the estrogen: progesterone ratio, causing estrogen to become toxic without progesterone to oppose it. As a result, the risks for breast and uterine cancer and fibrocystic breast disease increase.7 Therefore, progesterone also has a crucial role to play in maintaining breast health.

Vitamin D is another breast-supportive nutrient. Women who have mutations in their vitamin D receptor gene are nearly twice as likely to develop breast cancer compared to women who do not have the mutation. The vitamin D receptor gene controls the action of vitamin D in the body. Scientists have found that Caucasian women with certain versions of this gene not only have an increased risk of breast cancer but also may suffer from a more aggressive form of the disease if it spreads. The results suggest that vitamin D does indeed play a part in protecting the body against breast cancer, as past studies indicate.

Five to ten percent of breast cancer cases are due to already established gene mutations such as BRCA1. However, the underlying cause of breast cancer in women who do not have this gene and have no family history of the disease has remained a mystery. The study suggests that the mutation in the Vitamin D receptor gene may have a role to play in disease development in women who would not ordinarily be expected to develop the disease.8

References

1. Kapdi CC, Wolfe JN. Breast Cancer. Relationship to Thyroid Supplements for Hypothyroidism. JAMA. 1976 Sep 6;236(10):1124-7.

2. Ghent WR, Eskin BA, Low DA, et al. Iodine Replacement in Fibrocystic Disease of the Breast. Can J Surg. 1993; 36:453-460.

3. Eskin BA, Bartuska DG, Dunn MRea. Mammary Gland Dysplasia in Iodine Deficiency. JAMA. 1967; 200:115-119.

4. Eskin BA. Iodine Metabolism and Breast Cancer. Trans New York Acad of Sciences. 1970; 32:911-947.

5. Eskin BA. Iodine and Mammary Cancer. Adv Exp Med Biol. 1977; 91:293-304.

6. Chang X, Tou JC, Hong C, Kim HA, Riby JE, Firestone GL, Bjeldanes LF. 3,3’-Diindolylmethane inhibits angiogenesis and the growth of transplantable human breast carcinoma in athymic mice. Carcinogenesis. 2005 Apr;26(4):771-8.

7. Lee, John R., What Your Doctor May Not Tell You About Menopause. Warner Books, May, 1996.

8. Guy M, Lowe LC, Bretherton-Watt D, Mansi JL, Peckitt C, Bliss J, Wilson RG, Thomas V, Colston KW. Vitamin D receptor gene polymorphisms and breast cancer risk. Clin Cancer Res. 2004 Aug 15;10(16):5472-81.