• The President’s Desk  — Update on FTC Legislation; Health Freedom Victory
• Healthy Aging  — Natural Strategies for Bones and Joints
• A Health-Destroying Toxin No One Can Avoid  — 
• Visceral Fat  — Its Damaging Role in Brain Health
• Sleep Apnea  — The Surprising Culprit Behind a Host of Health Concerns
• Peltier™ Electrolytes  — Rehydrating the Body to Enhance Energy and Endurance

• Lycopene Studied in Lung Health  — Breaking News
• Lutein and Vitamin A Support Visual Function  — Breaking News
• Green Tea Supports Bone Health  — Breaking News
• Antioxidant Protects Neurons from Low-Oxygen Damage  — Breaking News
• Vitamin Linked to Improved Mood and Well Being  — Breaking News
• Vitamin Deficiency Linked to Lymphocyte Neoplasms  — Breaking News
• Mineral Supports Cognitive Function  — Breaking News
• Omega-3 Fatty Acids Studied in Heart Health  — Breaking News

Last month, I informed you about Senate legislation, the Restoring American Financial Stability Act of 2010 (S. 3217), which could interfere with your ability to obtain nutritional supplements. Senators debated including the same amendment in S. 3217 as is contained in the House’s sister bill Wall Street Reform and Consumer Protection Act of 2009 (H.R. 4173). This amendment would allow the FTC an unwarranted amount of control over the supplement industry. The good news is that thanks to you contacting your senators, the amendment was taken out of the senate bill. The bad news? The house and the senate must iron out the differences between the two bills, and the amendment giving FTC expanded powers remains in the House version.

If the House does not remove the amendment, 1) The FTC will be given broad powers to create advertising guidelines inconsistent with what is allowed under DSHEA and the FDA; 2) The FTC will act as a legislative body, creating “rules” in the vitamin supplement industry even though it has no expertise in this area; 3) The FTC will make, approve and police rules with virtually no oversight.

I urge you to contact your senators and your representatives and ask them to oppose the FTC provision in the final bill.

While this sneak attack on supplements is occurring in the legislative branch of government, in the judicial branch, there was a significant victory. Attorney Jonathan Emord successfully argued in front of the United States District Court of the District of Columbia that the FDA smothered free speech when it prohibited cancer-related health claims about the mineral selenium unless the science was completely conclusive or unless disclaimers were added. The judge agreed saying that food and dietary supplement producers have a free speech right to talk about the science behind the product as long as they accurately represent that science. The decision has important ramifications for supplement consumers, who have a right to know about the abundant research that supports the use of nutritional supplements.

The Latest Update

Good news! After we went to press with the July Vitamin Research News, Congress decided to remove the provision in the Wall Street reform bill that would have granted the Federal Trade Commission expanded powers, likely jeopardizing your right to consume affordable nutritional supplements. Thank you to everyone who wrote in to their senators and congresspeople—your efforts paid off.

This is the seventh part in a series addressing the most common health concerns as we age. Previous parts have discussed cardiovascular health, weight loss, blood sugar, cognitive function and gastrointestinal health. In this installment, I will discuss bones and joints and natural strategies to keep them strong.

Pain and discomfort from osteoarthritis can reduce independence and mobility and can prevent us from doing the things we love to do, whether it’s gardening, golf, hiking, skiing or numerous other hobbies. Osteoporosis can be as devastating to the bones as osteoarthritis is to the joints, robbing us of our mobility and quality of life.

Osteoarthritis

Osteoarthritis (OA), the most common type of arthritis, is a degenerative joint disease characterized by the breakdown of the joint’s cartilage. From 1995 to 2005, the latest statistics available from The National Arthritis Data Workgroup show that the prevalence of osteoarthritis in the United States was 26.9 million—an increase of nearly 30 percent over that decade.¹ Pain, the primary symptom of osteoarthritis, can significantly impact patients’ quality of life, not only in regards to physical function but also psychological well-being.¹

Although articular cartilage damage is a major characteristic of OA, the condition is now considered a disease of the entire joint.² In addition to articular cartilage damage, OA is marked by bone spur (osteophyte) formation at the joint margins, muscle atrophy and spasm, and inflammation. The normal anabolic (rebuilding) properties and the catabolic (breaking down) properties within the cartilage become imbalanced, inhibiting the ability of cartilage to repair itself. Inflammatory cytokines (white blood cell proteins that play a role in the inflammatory process) are thought to cause this imbalance.²

The symptoms and signs of knee OA are persistent knee pain, limited morning stiffness, reduced function, crepitus (a crackling sound), restricted movement and bony enlargement.³ The American College of Rheumatology’s criteria for hip OA diagnosis includes the presence of hip pain and at least 2 of the following 3 criteria: evidence of femoral or acetabular (hip joint) bone spurs, joint space narrowing and an increase in erythrocyte sedimentation rate (a test used to measure inflammation, abbreviated Sed Rate often on lab reports), which should be less than 20 mm/hour.⁴

OA can progress in severity relatively quickly. A study published in 2004 followed a group of 32 patients with symptomatic knee OA to evaluate disease progression. These patients were followed for more than 2 years and overall suffered a significant loss in global cartilage volume of 6.1 percent at the end of the study. The loss in cartilage volume occurred as early as 6 months after the study’s start and increased at 18 and 24 months, reflecting a progression in cartilage volume loss over time.⁵

Although once thought of primarily as a disease of the elderly, osteoarthritis is now developing in a large number of people under the age of 60, often due to knee injuries (such as anterior cruciate ligament tears)⁶ or the increased prevalence of obesity.⁷ Until recently, researchers thought that obesity increases knee osteoarthritis risk because the increased weight strains the joints. But new research suggests that the excess levels of the “hunger hormone” leptin secreted by fat cells interacts with the leptin receptors found in normal joint cartilage cells (chondrocytes). The excess leptin causes the cartilage cells to respond in a way that promotes OA.⁷

Osteoporosis

Osteoporosis results in bone mass reduction and consequently an increased risk of fractures. In its initial stages, osteoporosis goes “under the radar” as it causes no symptoms until fractures later develop. The vertebral and hip fractures that occur result in considerable morbidity and mortality^8-10 as well as disability or impairment and a resulting decline in health-related quality of life.^11-13

Vertebral fractures are the most common osteoporotic fractures. Vertebral fractures have a severe long-term impact on health-related quality of life. One recent study showed that from ages 64-82 years, vertebral fractures resulted in more negative impact on quality of life, more severe osteoporosis and a poorer prognosis compared to hip fractures.¹⁴

Although osteoporosis is commonly thought of as a women’s disease, it also can affect men. In the U.S., eight million women and two million men are estimated to have osteoporosis.¹⁵ In men, osteoporosis generally develops approximately 10 years later than in females. Two of the causes of osteoporosis in men are thought to be low vitamin D levels and a decline in testosterone levels.¹⁶

Conventional doctors treating osteoporosis prescribe the bisphosphonate class of drugs, including Fosamax®, Actonel®, Boniva® and Reclast®. However, as ABC News recently reported, these drugs are coming under fire after hundreds of reports of spontaneous fractures in women using them. Studies in various medical journals have indicated that these drugs may have a long-term, bone-destroying effect.¹⁷ One group of researchers stated, “Prescribers should be aware of the possibility of these rare adverse reactions and the prolonged use of bisphosphonates should be reconsidered until long-term robust safety data are available.”¹⁸

Supporting Joint Health

As I describe to my patients looking to support joint health, it is essential to offset current and past wear and tear with equal and greater levels of nutrition to support healthy joints. In my practice, I use a number of natural compounds to support healthy joints including glucosamine sulfate, MSM (methylsulfonylmethane), chondroitin sulfate, Type II Collagen and silica (all found in Nutri-Joint). Researchers recently analyzed randomized controlled studies involving 1,502 patients with knee osteoarthritis and found that even though over the first year glucosamine sulfate did not show a significant effect on joint health, after 3 years, glucosamine sulfate demonstrated a small to moderate protective effect. The same was observed for chondroitin sulfate, which had a small but significant joint protective effect after 2 years.¹⁹

The authors concluded, “This meta-analysis of available data shows that glucosamine and chondroitin sulfate may delay radiological progression of OA of the knee after daily administration for over 2 or 3 years.”

MSM (methylsulfonylmethane), Type II collagen and silica are three other natural substances I like to use in patients concerned about joint health. In a randomized placebo-controlled trial of patients with knee OA, MSM was found to produce significant decreases in pain and physical function impairment.²⁰ Type II collagen has reduced the symptom scores of two standard osteoarthritis indexes by 33 percent and 20 percent in subjects with osteoarthritis of the knee.²¹ According to the researchers, subjects given type II collagen “showed significant enhancement in daily activities suggesting an improvement in their quality of life.” Silica has been shown to increase bone mineral density in calcium deficient animals.²²

Combining the ingredients in Nutri-Joint with Hyaluronic Acid Lozenges can be especially helpful since oral supplementation with HA has showed promising results in subjects aged 40 years and older with knee osteoarthritis.²³ I have discovered over the years that the addition of high molecular weight hyaluronic acid is essential for the creation of a truly comprehensive program, to support optimal joint health and control inflammation.

For patients who are suffering from joint discomfort, I often combine the above substances with turmeric, Boswellia serrata, DL-phenylalanine and nattokinase (all found in EnFlex™). I have found these synergistic substances to improve mobility and quality of life in my patients suffering from stiff joints. DL-phenylalanine acts as a natural analgesic by up-regulating the “endogenous analgesia system” (EAS), a neural pathway that when stimulated suppresses activation of second-order pain-receptive neurons.²⁴ Curcumin, the primary constituent of turmeric, has been shown to inhibit cyclooxygenase (COX), lipoxygenase (LOX) and inducible nitric oxide synthase (iNOS), important enzymes that mediate inflammatory processes.²⁵

Boswellia serrata inhibits the synthesis of pro-inflammatory leukotrienes, reduces swelling and knee pain in patients with knee osteoarthritis and increases knee flexion and walking distance.²⁶ The proteolytic (protein-dissolving) enzyme nattokinase may help control pain through its actions as a fibrinolytic enzyme, which means it breaks down fibrin deposits. The fibrinolytic system is closely linked to control of inflammation.²⁷

Another important component of a joint-support regimen is vitamin D3. Low vitamin D levels are associated with increased incidence of knee OA²⁸ and vitamin D deficient men are twice as likely to have hip OA.²⁹

Supporting Bone Health

Calcium, Vitamin D, Vitamin K and Ipriflavone (ingredients in Osteoflavone Complex) are all essential for promoting strong bones. A meta-analysis reviewing 29 randomized trials concluded that supplementation with calcium and vitamin D3 reduces risk of bone fractures by 24 percent and significantly reduces loss of bone mass.³⁰

High-dose vitamin K supplementation has been shown to improve indices of bone strength in the femoral neck, reduce the incidence of clinical fractures and decrease the subsequent incidence of vertebral fractures in osteoporotic postmenopausal women with a history of at least 5 vertebral fractures.³¹ Ipriflavone, another bone-supporting substance, acts primarily to suppress bone resorption (bone breakdown).³² Close to 500 patients given ipriflavone in double-blind, placebo-controlled studies have noted significant gains of between 0.5 to 7.1 percent in total body, forearm and vertebral bone mineral density.³³

Combining all the above ingredients in Osteoflavone Complex with extra vitamin D3 and vitamin K plus the mineral strontium has produced excellent results in many of my patients. Numerous studies have indicated strontium exerts beneficial effects on bones and produces improved mobility in subjects. Biopsy samples from subjects given strontium carbonate showed a 172 percent increase in the rate of bone formation.³⁴

It is very important to take strontium at least 2 hours away from calcium for maximal impact.

Conclusion

Protecting our joints and bones is an essential step to ensure our independence and mobility aren’t compromised. Consuming Nutri-Joint, HA lozenges and vitamin D3 can help maintain optimal joint health while adding EnFlex™ to this regimen can be helpful for individuals suffering from significant joint discomfort. For bone health, using Osteoflavone Complex together with extra vitamin D3, vitamin K2 and strontium can help us enjoy the activities and hobbies that we love well into our senior years.

References

1. Lawrence RC, Felson DT, Helmick CG, Arnold LM, Choi H, Deyo RA, Gabriel S, Hirsch R, Hochberg MC, Hunder GG, Jordan JM, Katz JN, Kremers HM, Wolfe F (National Arthritis Data Workgroup). Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part II. Arthritis Rheum. 2008 Jan;58(1):26-35.

2. Martel-Pelletier J, Boileau C, Pelletier JP, Roughley PJ. Cartilage in normal and osteoarthritis conditions. Best Pract Res Clin Rheumatol. 2008;22(2):351-384.

3. Zhang W, Doherty M, Peat G, et al. EULAR evidence based recommendations for the diagnosis of knee osteoarthritis. Ann Rheum Dis. 2009 Sep 17. Published online ahead of print.

4. Altman R, Asch E, Bloch D, et al. Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association. Arthritis Rheum. 1986;29(8):1039-1049.

5. .Raynauld JP, Martel-Pelletier J, Berthaiume MJ, et al. Quantitative magnetic resonance imaging evaluation of knee osteoarthritis progression over two years and correlation with clinical symptoms and radiologic changes. Arthritis Rheum. 2004;50(2):476-487.

6. Golightly YM, Marshall SW, Callahan LF, Guskiewicz K. Early-onset arthritis in retired National Football League players. J Phys Act Health. 2009 Sep;6(5):638-43.

7. Griffin TM, Huebner JL, Kraus VB, Guilak F. Extreme obesity due to impaired leptin signaling in mice does not cause knee osteoarthritis. Arthritis Rheum. 2009 Oct;60(10):2935-44.

8. Johnell O, Kanis JA. An estimate of the worldwide prevalence and disability associated with osteoporotic fractures. Osteoporosis International. 2006;V17:1726-1733.

9. Hasserius R, Karlsson MK, Jonsson B, Redlund-Johnell I, Johnell O. Long-term morbidity and mortality after a clinically diagnosed vertebral fracture in the elderly—a 12- and 22-year follow-up of 257 patients. Calcif Tissue Int. 2005;76:235-242.

10. Caliri A, De Filippis L, Bagnato GL, Bagnato GF. Osteoporotic fractures: mortality and quality of life. Panminerva Med. 2007;49:21-27.

11. Lips P, van Schoor NM. Quality of life in patients with osteoporosis. Osteoporosis International. 2005;16:447—455. doi: 10.1007/s00198-004-1762-7.

12. Ettinger B, Black DM, Nevitt MC, Rundle AC, Cauley JA, Cummings SR, Genant HK. Contribution of vertebral deformities to chronic back pain and disability. The Study of Osteoporotic Fractures Research Group. J Bone Miner Res. 1992;7:449-456.

13. Nevitt MC, Ettinger B, Black DM, Stone K, Jamal SA, Ensrud K, Segal M, Genant HK, Cummings SR. The association of radiographically detected vertebral fractures with back pain and function: a prospective study. Ann Intern Med. 1998;128:793-800.

14. Hallberg I, Bachrach-Lindström M, Hammerby S, Toss G, Anna-Christina E. Health-related quality of life after vertebral or hip fracture: a seven-year follow-up study.

BMC Musculoskelet Disord. November 3, 2009; 10: 135. Published online ahead of print.

15. National Osteoporosis Foundation website, www.nof.org, accessed on June 10, 2010.

16. Ducharme N. Clin Geriatr Med. 2010 May;26(2):301-9. Male osteoporosis. Ducharme N.

17. Somford MP, Geurts GF, den Teuling JW, Thomassen BJ, Draijer WF. Long-Term Alendronate Use Not without Consequences? Int J Rheumatol. Published online Jan 27, 2010.

18. Ing-Lorenzini K, Desmeules J, Plachta O, Suva D, Dayer P, Peter R. Low-energy femoral fractures associated with the long-term use of bisphosphonates: a case series from a Swiss university hospital. Drug Saf. 2009;32(9):775-85.

19. Lee YH, Woo JH, Choi SJ, Ji JD, Song GG. Effect of glucosamine or chondroitin sulfate on the osteoarthritis progression: a meta-analysis. Rheumatol Int. 2010 Jan;30(3):357-63.

20. Kim LS, Axelrod LJ, Howard P, Buratovich N, Waters RF. Efficacy of methylsulfonylmethane (MSM) in osteoarthritis pain of the knee: a pilot clinical trial. Osteoarthritis Cartilage. 2006 Mar;14(3):286-94.

21. Crowley DC, Lau FC, Sharma P, Evans M, Guthrie N, Bagchi M, Bagchi D, Dey DK, Raychaudhuri SP. Safety and efficacy of undenatured type II collagen in the treatment of osteoarthritis of the knee: a clinical trial. Int J Med Sci. 2009 Oct 9;6(6):312-21.

22. Kim MH, Bae YJ, Choi MK, Chung YS. Silicon supplementation improves the bone mineral density of calcium-deficient ovariectomized rats by reducing bone resorption. Biol Trace Elem Res. 2009 Jun;128(3):239-47.

23. Kalman DS, Heimer M, Valdeon A, Schwartz H, Sheldon E. Effect of a natural extract of chicken combs with a high content of hyaluronic acid (Hyal-Joint) on pain relief and quality of life in subjects with knee osteoarthritis: a pilot randomized double-blind placebo-controlled trial. Nutr J. 2008 Jan 21;7:3.

24. Russell AL, McCarty MF. DL-phenylalanine markedly potentiates opiate analgesia - an example of nutrient/pharmaceutical up-regulation of the endogenous analgesia system. Med Hypotheses. 2000 Oct;55(4):283-8.

25. Menon VP, Sudheer AR. Antioxidant and anti-inflammatory properties of curcumin. Adv Exp Med Biol. 2007;595:105-125.

26. Kimmatkar N, Thawani V, Hingorani L, et al. Efficacy and tolerability of Boswellia serrata extract in treatment of osteoarthritis of knee—a randomized double blind placebo controlled trial. Phytomedicine. 2003 Jan;10(1):3-7.

27. Urano T, Ihara H, Umemura K, et al. The profibrinolytic enzyme subtilisin NAT purified from Bacillus subtilis Cleaves and inactivates plasminogen activator inhibitor type 1. J Biol Chem. 2001 Jul 6;276(27):24690-24696.

28. Bergink AP, Uitterlinden AG, Van Leeuwen JP, Buurman CJ, Hofman A, Verhaar JA, Pols HA. Vitamin D status, bone mineral density, and the development of radiographic osteoarthritis of the knee: The Rotterdam Study. J Clin Rheumatol. 2009 Aug;15(5):230-7.

29. Chaganti RK, Parimi N, Cawthon P, Dam TL, Nevitt MC, Lane NE. Association of 25-hydroxyvitamin D with prevalent osteoarthritis of the hip in elderly men: the osteoporotic fractures in men study. Arthritis Rheum. 2010 Feb;62(2):511-4.

30. Stránský M, Rysavá L. Nutrition as prevention and treatment of osteoporosis. Physiol Res. 2009;58 Suppl 1:S7-S11.

31. Iwamoto J. [Anti-fracture efficacy of vitamin K] [Article in Japanese]. Clin Calcium. 2009 Dec;19(12):1805-14.

32. Miyauchi A, et al. Novel ipriflavone receptors coupled to calcium influx regulate osteoclast differentiation and function. Endocrinology. 1996; 13: 3544-50.

33. Agnusdei D, Bufalino L. Efficacy of ipriflavone in established osteoporosis and long-term safety. Calcif Tissue Int. 1997;61 Suppl 1:S23-7.

34. Marie PJ, Skoryna SC, Pivon RJ, Chabot G, Glorieux FH, Stara JF. Histomorphometry of bone changes in stable strontium therapy. In: Trace substances in environmental health XIX, edited by D.D. Hemphill, University of Missouri, Columbia, Missouri, 1985, 193-208.

Summer may bring increased exposure to more than just the sun. Summer gives us longer days, BBQs, pool parties, campfires, more alcohol and sweet beverages, road trips with the car windows and top down and home improvements. Harmless as they seem, these factors and more increase our exposure to multiple environmental toxins. One particular toxin that affects millions in the population is acetaldehyde.

Acetaldehyde belongs to the larger chemical family of aldehydes, which are pervasive environmental toxins. The human body possesses enzymes that convert it to a less-harmful substance and therefore is protected from small exposures. However, acetaldehyde at toxic levels can make its way into the brain from sources such as alcohol consumption, Candida sp. (yeast) overgrowth, breathing air contaminated with acetaldehyde from cigarette and other smoke, smog, vehicle and factory exhaust, synthetic fragrances and many commercially manufactured materials. Acetaldehyde and its close relative formaldehyde are used in the synthesis of chemicals such as plastics, dyes, fabrics, adhesives, fuels, plywood, particleboard, insulating foam, fragrances, preservatives and more. Besides being an occupational hazard, these materials are found throughout the home especially in new carpets, furniture and floors and can out-gas aldehydes into the air for years, creating continuous exposure. Aldehydes are among the top chemicals released into the environment daily.

The following article provides an overview of acetaldehyde and the danger it poses.

Acetaldehyde Exposure

Alcohol

One of the main significant acetaldehyde exposure routes is through alcohol (ethanol) consumption. Ethanol metabolism starts with the conversion of alcohol to acetaldehyde, which is at least 30 times more toxic than alcohol. Ideally, acetaldehyde is then oxidized to acetic acid and ultimately into Acetyl-CoA, which will be used for cellular energy. Unfortunately, in many if not most people, this conversion is slow and not always efficient due to genetic variations of the enzymes that perform this step, insufficient nutrient cofactors or exposure to related chemicals utilizing the same metabolic enzymes and nutrients. The result may be high acetaldehyde levels, which can cause significant damage to the liver where the bulk of alcohol metabolism occurs.¹ Other alcohol metabolism sites that expose tissue to acetaldehyde’s damaging effects are the pancreas, gastrointestinal tract and in particular, the brain.^2-3 Alcohol may result in “drunkenness”—the central nervous system effects of relaxation, loss of coordination and inhibition of judgment—but acetaldehyde is responsible for the “hangover,” the toxic side effects that can eventually damage the brain.

Candida

Another important exposure route to toxic acetaldehyde levels is through its production by the opportunistic yeast, Candida albicans. In small numbers, this yeast may be kept in check in the gut by the immune system and friendly bacteria such as Lactobacillus sp. and Bifidobacterium sp. But in many people, increasing carbohydrates, especially sweets, will cause chronic Candidiasis. Candida produces acetaldehyde in the GI tract by sugar fermentation. The typical American diet along with drug and antibiotic therapies, hypochlorhydria (low stomach acid), chronic stress, environmental toxins, etc. have altered gut integrity and immunity and predisposed millions of people to yeast overgrowth or the “Candida Syndrome.”⁴ A person with this condition who also drinks beer, wine or liqueurs not only produces acetaldehyde from the alcohol but also delivers more sugar for yeast production of acetaldehyde, creating a double-barreled dose. Acetaldehyde produced in the gut can eventually reach more parts of the body, flooding the system and increasing the risk for damage.⁵

Pollution

Through the burning of tobacco, petroleum fuels, natural gas, wood and trash, aldehydes, including acetaldehyde, are present in the air we breathe. Vehicle and factory exhaust can create a chronic but significant exposure source to those who live near heavily trafficked areas or who spend hours commuting on freeways. Acetaldehyde contributes to photochemical “smog” formation when it reacts with other volatile substances in the air. Open car windows increase exposure, as does breathing in acetaldehyde-containing fumes near gas pumps. Cigarette smokers and others around them are exposed through inhaling smoke. According to the Environmental Protection Agency (EPA), wood smoke from campfires, wood-burning stoves and residential fireplaces is more toxic than cigarette smoke. But the acetaldehyde level released from burning items such as plastics, styrofoam and batteries is even higher.⁶ While acetaldehyde exposure from auto exhaust and cigarettes may be less than that from alcohol, research shows that low dose chronic exposure may still be sufficient to gradually damage proteins, enzymes and other cellular structures in the brain and other organs.⁷

Furthermore, most fragrances today are made from synthetic chemicals, many of which are toxic. Air fresheners, scented candles, cleaning products, cologne or perfume and more can create a source of chronic exposure to many toxic chemicals including acetaldehyde. Children and babies are particularly susceptible. Additionally, the Environmental Working Group (EWG) lists acetaldehyde as one of the contaminants released from polyethylene plastic bottles.⁸

Detrimental Effects

Acetaldehyde is classified as a probable human carcinogen linked to nose and throat irritation and cancer as well as a toxicant to the neurological (neurotoxin), respiratory, endocrine and immune systems. Animal research also shows that this chemical crosses the placental barrier causing skeletal deformities, reduced birth weights and infant death.⁹

Acetaldehyde significantly compromises brain function. It is considered to be the substance that directly contributes to the toxic effects and the chemical dependency to alcohol and cigarettes. Addictive, opiate-like biochemicals are formed in the brain when acetaldehyde combines with the key neurotransmitters, dopamine and serotonin. In acetaldehyde’s presence, dopamine is converted into salsolinol and serotonin into beta-carboline, both of which are very addictive tetrahydroisoquinolines (TIQs).^10-11 Moreover, metabolites of salsolinol are neurotoxic to dopaminergic neurons inducing cell death and eliciting symptoms nearly identical to idiopathic Parkinson’s disease.^12-13

Acetaldehyde damages the membranes of red blood cells (RBC) making them less flexible in passing through tiny capillaries, and it can alter hemoglobin, the oxygen transporter in the RBC.¹⁴ These two effects reduce available oxygen to the cells, especially in the brain.

Acetaldehyde disables the protein tubulin from assembling into microtubules in the brain.¹⁵ Microtubules structurally and nutritionally support the dendrites, the feathery-looking extensions from the nerve cells’ main body, which connect many nerve cells to each other. Without the microtubules, the dendrites atrophy and die. This can be seen in chronic alcoholism and Alzheimer’s disease.

Acetaldehyde and Nutrient Deficiencies

In addition to its toxic effects, acetaldehyde induces deficiencies of nutrients used for its detoxification. As an example, vitamin B1 (thiamine) is depleted through alcohol and acetaldehyde detoxification.¹⁶ B1 is essential in carbohydrate metabolism for energy production, of which the brain uses 20 percent. Acetaldehyde-induced B1 depletions exacerbate the already low B1 levels common in the population due to diuretics and other drugs, over-consumption of simple carbohydrates (dysglycemia) and adrenal stress. In addition to its many functions, thiamine, the “nerve vitamin,” is critical to nerves and neurotransmitters. Even mild, chronic B1 deficiency can produce brain-related symptoms such as emotional instability, confusion, depression, fatigue, irritability, headaches, sensitivity to noise, insomnia, decreased short-term memory, brain-fog and a feeling of impending doom.^17-18

Relevant to this time of year, B1­deficiency-related lactic acidosis can make people more vulnerable to bug bites, since many insects, particularly mosquitoes, are attracted to mild acids.¹⁹

Furthermore, people with chemical sensitivities to aldehydes may also be sensitive to seemingly unrelated substances like sulfites (preservatives) from wines and foods, and the smell of chlorine from pools and bleach.

The under appreciated essential trace mineral molybdenum is also involved with acetaldehyde metabolism. A molybdenum deficiency not only affects this process but also other enzymes in the body that require molybdenum as a cofactor—for example, sulfite oxidase, responsible for converting irritating sulfites into harmless sulfates for use in liver detoxification and cartilage. Sulfur-containing amino acids, as important free radical scavengers, also use this molybdenum-dependent pathway. Molybdenum has been shown to reduce sulfite sensitivity by increasing sulfite oxidase activity.²⁰ Sulfites also destroy vitamin B1’s biological activity, contributing to a deficiency. Nutrient depletion leads to sensitivity to other chemicals that use these same pathways. This has been demonstrated in patients with Candidiasis as the excess stress put on the enzyme systems to detoxify acetaldehyde often leave them with sensitivities to multiple chemicals especially fragrances. Supplementing with the appropriate cofactors may improve an individual’s ability to handle Candida-generated acetaldehyde.²¹

Acetaldehyde Relief

Acetaldehyde toxicity can be acute or chronic. In order to stop this toxicity, levels of key nutrients that metabolize and clear acetaldehyde must be adequate. Some of these nutrients are cofactors to the enzymes that metabolize acetaldehyde and others, such as sulfur-containing compounds, are necessary to scavenge or “mop up” any stray un-metabolized acetaldehyde. Supplementation with specific nutrients offers an important level of prevention and protection from toxicity. In one animal study, pretreatment of the animals with B1, vitamin C and the sulfur-containing amino acid cysteine completely blocked the LD-90 dose of acetaldehyde (the dose that would normally kill 90 percent of the animals).²² In another study, cysteine lowered in the digestive tract the amount of acetaldehyde produced by smoking and alcohol consumption. Both of these risk factors are considered the main causes of upper digestive tract cancer in 75 percent of developed countries with acetaldehyde as the probable cause.²³

A new product helps neutralize acetaldehyde, stopping the damaging effects of this widely present compound that is nearly impossible to avoid. AL-CoFactors™ provides 12 effective, synergistic nutrients to reduce acetaldehyde toxicity including the metabolically active forms of B1, B2, B6 (R)-lipoic acid and N-acetyl cysteine, along with B3, calcium pantothenate (B5), vitamin C, molybdenum, zinc, magnesium and betaine. These neuroprotective nutrients are especially important for individuals who smoke or produce acetaldehyde in their bodies as a consequence of alcohol consumption or candidiasis. Furthermore, it is a companion product to modern-day detoxification regimens.

For general use, 3 capsules of AL-CoFactors should be taken daily as 1 capsule in the morning and 2 in the evening. Best results are obtained when the product is taken with water as it supports detoxification. Alternatively, 2 capsules should be taken before alcoholic beverage consumption, followed by 1 capsule for each 1-2 drinks consumed and one additional capsule at bedtime. This product will not keep you from becoming drunk on alcohol, but it may prevent the subsequent “brain fog.”

Acetaldehyde deactivates the enzyme Delta-6-Desaturase,²⁴ responsible for the production of gamma linolenic acid (GLA) from the fatty acid, linoleic acid. GLA is a very potent anti-inflammatory demonstrating a myriad of health benefits. As exposure to acetaldehyde may create a deficiency of this important nutrient, GLA from Black Currant Seed is recommended as a complementary product to AL-CoFactors.

References

1. Zakhari S. Overview: How is alcohol metabolized by the body? Alcohol Research & Health. 2006;29(4):245-254.

2. Edenberg H J. The genetics of alcohol metabolism: Role of alcohol dehydrogenase and aldehyde dehydrogenase variants. Alcohol Research & Health. 2007;30(1):5-13.

3. Vonlaufen A, Wilson JS, Pirola RC, Apte MV. Role of alcohol metabolism in chronic pancreatitis. Alcohol Research & Health. 2007;30(1):38-54.

4. Galland LD. Nutrition and Candida albicans, 1986 A year in Nutritional Medicine, ed. J. Bland. New Canaan. Keats Pub. 1986 pg. 203-238.

5. Truss CO. Metabolic Abnormalities in Patients with Chronic Candidiasis: The Acetaldehyde Hypothesis. J Orthomolecular Psychiatry. 1984;13(2):66-93.

6. www.fs.fed.us/t-d/pubs/htmlpubs/htm04232327/page01.htm (US Forest Service-Dept of Agriculture). What’s Burning in your Campfire? Garbage In, Toxics Out.

7 Sorrell MF, Tuma DJ. The Functional Implications of Acetaldehyde Binding to Cell Constituents. Ann NY Acad Sci. 1987;492:50-62.

8. www.EWG.org, accessed on 5/10/10.

9. U.S. Environmental Protection Agency. Integrated Risk Information System (IRIS) on Acetaldehyde. Source: http://www.epa.gov/iris/subst/0290.htm Nov. 2002.

10. Blum K, Payne J. Alcohol and the Addictive Brain. NYC: The Free Press, 1991, pp. 99-216.

11. Epp LM, Mravec B. Chronic polysystemic candidiasis as a possible contributor to onset of idiopathic Parkinson’s disease. Bratisl Lek Listy. 2006;107(6-7):227-30.

12. Maruyama W, Naoi M. Cell death in Parkinson’s disease. J Neurol 2002;249(suppl 2):183-89.

13. Martinez-Alvarado P, et al. Possible role of salsolinol quinone methide in the decrease of RCSN-3 cell survival. Biochem Biophys Res Commun 2001;283(5):1069-76.

14. Tsuboi KK, Thompson DJ, Rush EM, Schwartz HC. Acetaldehyde-Dependent Changes in Hemoglobin and Oxygen Affinity of Human Erythrocytes. Hemoglobin. 1981;5(3):241-50.

15. Tuma DJ, Jennett RB, Sorrell MF. The Interaction of Acetaldehyde with Tubulin. Ann NY Acad Sci 1987;492:277-286.

16. Takabe M, Itokawa Y. Thiamin depletion after ethanol and acetaldehyde administration to rabbits. J Nutr Sci Vitaminol (Tokyo). Oct. 1983;29(5):509-14.

17. Lonsdale D, Shamberger R. Red cell transketolase as an indicator of nutritional deficiency. Am J Clin Nutr 1980;33:205-11.

18. Williams RR, et al. Induced Thiamin (vitamin B1) Deficiency in Man. Arch Int Med. 1942;69:721-38.

19. Fradin MS. Mosquitoes and Mosquito Repellents: A Clinician’s Guide. Ann Intern Med. June 1998;128(11):931-940.

20. Molybdenum. Monograph. Altern Med Rev. 2006;11(2):156-161.

21. Schmitt WH, et al. Molybdenum for Candida albicans Patients and other Problems. The Digest of Chiropractic Economics. Jan-Feb. 1991;31(4):56-63.

22. Sprince H, Parker CM, Smith GG, Gonzales LJ. Protective Action of Ascorbic Acid and Sulfur Compounds against Acetaldehyde Toxicity: Implications in Alcoholism and Smoking. Agents and Action. May 1975;5(2):164-73.

23. Salaspuro V. Interaction of alcohol and smoking in the pathogenesis of upper digestive tract cancers-possible chemoprevention with cysteine. Univ. Helsinki, Institute of Clinical Medicine. Doctoral dissertation. April 2006.

24. Horrobin DF. The Importance of Gamma-Linolenic Acid and Prostaglandin E1 in Human Nutrition and Medicine. J Holistic Med. 1981;3:118-39.

A large body of scientific evidence has shown that an increase in visceral (abdominal) fat also increases the risk of the metabolic syndrome, insulin resistance, diabetes and cardiovascular disease. Recently, researchers have uncovered a strong link between the accumulation of visceral fat and cognitive dysfunctions such as cognitive decline and dementia. This significant finding, reported by the Centers for Disease Control and Prevention (CDC), substantiates that 33.8 percent of American adults are obese.¹

Visceral fat, or intra-abdominal fat, is adipose tissue that surrounds the abdominal organs. This type of fat is unlike the white fat found under the skin; visceral fat is a highly metabolically active tissue with powerful, deleterious effects on human physiology. Visceral fat secretes numerous hormones, a variety of inflammatory molecules and chemical mediators known as adipokines, which are believed to be mediators of the altered cellular mechanisms, which lead to increased risks of various diseases, particularly the metabolic syndrome.² Accumulation of visceral fat may lead to central obesity, which is defined as waist circumference greater than 40 inches in men and 35 inches in women, or by the waist-to-hip ratio (waist circumference divided by hip circumference) of greater than 0.9 for men and 0.85 for women. Data indicates that 50 percent of adults have central obesity.³

One of the most alarming aspects of visceral fat is that it can have devastating effects even in normal weight people. Studies have shown that subjects with large waists had an increased risk of death—even if they were considered to be normal weight based upon their body mass index (BMI). Normal-weight males whose waists measured about 40 inches or more had double the risk of dying compared to those who had waists 34 inches or less. Females whose BMI was normal but who had waists 35 inches or more had a 79 percent increased chance of dying compared to female subjects whose waists were 28 inches or less.⁴

Belly Fat: A Worthy Opponent for Your Brain

Previous research has shown that increased BMI is associated with an increased risk of developing dementia. More recently, researchers suggested that visceral adipose tissue, rather than BMI, should be considered as an important factor in the development of dementia due to the abnormal metabolic activities of visceral fat.⁵ One study evaluated the relationship between adiposity and cognitive decline. In this study, 3,054 elderly individuals were evaluated for BMI, waist circumference, sagittal (midline) abdominal diameter, total fat mass plus their subcutaneous and visceral fat. Cognition was also assessed using the Modified Mini-Mental State Examination. The subjects were evaluated annually for 8 years. The results of the study showed that in men, all of the measures of adiposity were associated with increased cognitive decline. More specifically, the men with the highest total fat mass had the greatest decline in the Mental Status Examination scores.⁶

In another study, researchers evaluated the risk of mid-life central obesity and the risk of developing dementia later in life. Subjects included 6,583 adults that were evaluated for sagittal (midline) abdominal diameter. Approximately 36 years later, the medical records of the subjects were reviewed to determine the prevalence of dementia. The results of the study showed that 15.9 percent of the subjects developed dementia. The individuals with the highest sagittal abdominal diameter had a three-fold increase in the risk of developing dementia compared to the individuals with the lowest abdominal diameter. Even in the subjects with normal BMI, the subjects with increased sagittal abdominal diameter had nearly double the risk of developing dementia compared to the subjects with lower abdominal diameter. Furthermore, this study found that the subjects that were both obese and had an increased sagittal abdominal diameter had the highest risk of dementia, showing a 3.6-fold increased risk.³

The idea that obesity is associated with markers of brain aging gained further support in a study of 733 adults averaging 60 years of age. The subjects were evaluated for body mass index (BMI), waist circumference, waist-to-hip ratio and computed tomography (CT)-based measurements of subcutaneous and visceral adipose tissue. The subjects were also evaluated using an MRI of the brain to determine total brain volume, temporal horn volume, white matter hyper-intensity volume and MRI-defined brain infarcts (tissue death due to loss of blood supply). The study found that increased BMI, subcutaneous fat and visceral fat were associated with decreased total brain volume. More importantly, the researchers discovered that the strongest association was between increased visceral fat and decreased total brain volume, independent of the BMI.⁷ In a similar study, investigators found a significant association between increased visceral fat accumulation and changes in hippocampus volume, which is the area of the brain important for long-term memory, spatial memory and navigation.⁸

Scientists also found an association between high visceral fat accumulation in patients with type 2 diabetes and white matter lesions, an important prognostic factor for the development of stroke.⁹

VFM-100™, Visceral Fat and the Brain

VFM-100 is a lipid-soluble extract of the roots from Glycyrrhiza glabra; this extract is standardized for the bioactive flavonoid glabridin. Both animal and human studies demonstrate that glabridin reduces both visceral and body fat. Glabridin has the additional ability to decrease the synthesis of fat, as well as to increase the activity of enzymes in the liver that are responsible for fat breakdown.¹⁰ Animal models have shown that the flavonoid-rich oil from Glycyrrhiza glabra, when supplemented to diabetic obese mice that were fed a high-fat diet for 4 weeks, resulted in significantly decreased body weight gain, reduced weight of abdominal adipose tissues and lower blood glucose levels compared to the mice fed a high-fat diet without the Glycyrrhiza glabra flavonoid oil.¹¹ A similar study showed that in obese mice fed a high-fat diet, supplementation with Glycyrrhiza glabra flavonoid oil decreased body weight gain, weight of abdominal adipose tissue and the size of the adipose cells.¹²

Human studies with Glycyrrhiza glabra flavonoid oil support these findings. A randomized, double-blind, placebo-controlled study was conducted in which overweight subjects were supplemented with 300 mg per day of Glycyrrhiza glabra flavonoid oil. After 12 weeks of supplementation, there was a significant difference in the changes in both body weight and BMI in the group receiving the flavonoid oil, but not in the placebo group. Furthermore, the weight-reducing effect of the Glycyrrhiza glabra flavonoid oil was specifically due to a reduction in body fat.¹³ A second clinical trial supplemented 300 mg, 600 mg or 900 mg of Glycyrrhiza glabra flavonoid oil per day to obese subjects for 8 weeks’ duration. All of the Glycyrrhiza glabra groups showed a significant reduction in fat mass when compared with the levels at the beginning of the study. In addition, the group supplemented with the 900 mg daily dose showed a significant decrease in body weight, BMI and visceral fat mass.¹⁴

Confirming the emerging link between visceral fat and brain health is a study showing that glabridin and flavonoid-rich extracts of Glycyrrhiza glabra also support cognitive function. In this study, glabridin was supplemented to mice and compared to the effects of piracetam, a known cognitive enhancer. The mice were subsequently exposed to the drug scopolamine to induce amnesia. The results showed that both glabridin and piracetam improved memory tests and passive-avoidance tests in the animals, suggesting that glabridin is an effective memory enhancer. Additionally, glabridin was compared to the drug metrifonate, a known cholinesterase inhibitor. Both glabridin and metrifonate reduced cholinesterase activity in the treated mice, which suggests glabridin may also improve the biochemical pathology and learning decrements associated with cognitive decline.¹⁵

Another study examined the effectiveness of glabridin in preventing brain injury after a stroke. Strokes were induced in mice by occluding the middle cerebral artery. The glabridin that was administered to the mice with strokes resulted in a significant decrease in the volume of damaged tissue, less cellular damage, decreased apoptosis (programmed cell death) and reductions in levels of brain malonyldialdehyde, a chemical correlate of oxidative stress. Additionally, glabridin increased levels of antioxidants in the brain, including both superoxide dismutase and reduced glutathione (GSH), suggesting that glabridin has antioxidant, neuroprotective activity.¹⁶ Animal models have also demonstrated that Glycyrrhiza glabra extracts provide an antidepressant-like effect,¹⁷ improve learning and memory¹⁸ and decrease plaque deposition in the brain, which is associated with cognitive decline.¹⁹

Conclusion

Recent research has uncovered powerful, new evidence, which documents that visceral fat also is associated with cognitive dysfunction, in addition to its known adverse effects on blood sugar regulation and the health of the cardiovascular system. This compelling evidence further supports the importance of reducing visceral fat, using Glabridin in conjunction with regular exercise to optimize health and extend longevity.

References

1. Flegal KM, Carroll MD, Ogden CL, Curtin LR. Prevalence and Trends in Obesity Among US Adults, 1999-2008. JAMA. 2010;303(3):235-241.

2. Matsuzawa Y. Establishment of a concept of visceral fat syndrome and discovery of adiponectin. Proc Jpn Acad Ser B Phys Biol Sci. 2010;86(2):131-41.

3. Whitmer RA, Gustafson DR, Barrett-Connor E, et al. Central obesity and increased risk of dementia more than three decades later. Neurology. 2008 Sep 30;71(14):1057-64.

4. Pischon T, Boeing H, Hoffmann K, Bergmann M, Schulze MB, Overvad K, van der Schouw YT, Spencer E, Moons KG, Tjønneland A, Halkjaer J, Jensen MK, Stegger J, Clavel-Chapelon F, Boutron-Ruault MC, Chajes V, Linseisen J, et al. General and abdominal adiposity and risk of death in Europe. New England Journal of Medicine. November 13, 2008;359(20):2105-2120.

5. Cereda E, Sansone V, Meola G, et al. Increased visceral adipose tissue rather than BMI as a risk factor for dementia. Age Ageing. 2007 Sep;36(5):488-91.

6. Kanaya AM, Lindquist K, Harris TB, et al. Total and regional adiposity and cognitive change in older adults: The Health, Aging and Body Composition (ABC) study. Arch Neurol. 2009 Mar;66(3):329-35.

7. Debette S, Beiser A, Hoffmann U, et al. Visceral fat is associated with lower brain volume in healthy middle-aged adults. Ann Neurol. 2010 May 20. Published Online Ahead of Print.

8. Anan F, Masaki T, Shimomura T, et al. Abdominal visceral fat accumulation is associated with hippocampus volume in non-dementia patients with type 2 diabetes mellitus. Neuroimage. 2010 Jan 1;49(1):57-62.

9. Anan F, Masaki T, Eto T, et al. Visceral fat accumulation is a significant risk factor for white matter lesions in Japanese type 2 diabetic patients. Eur J Clin Invest. 2009 May;39(5):368-74.

10. Kamisoyama H, Honda K, Tominaga Y, et al. Investigation of the anti-obesity action of licorice flavonoid oil in diet-induced obese rats. Biosci Biotechnol Biochem. 2008 Dec;72(12):3225-31.

11. Nakagawa K, Kishida H, Arai N, et al. Licorice flavonoids suppress abdominal fat accumulation and increase in blood glucose level in obese diabetic KK-A(y) mice. Biol Pharm Bull. 2004 Nov;27(11):1775-8.

12. Aoki F, Honda S, Kishida H, et al. Suppression by licorice flavonoids of abdominal fat accumulation and body weight gain in high-fat diet-induced obese C57BL/6J mice. Biosci Biotechnol Biochem. 2007 Jan;71(1):206-14.

13. Tominaga Y, Mae T, Kitano M, et al. Licorice flavonoid oil effects body weight loss reduction in overweight subjects. J Health Sci. 2006;52(6):672-683.

14. Tominaga Y, Nakagawa K, Mae T, et al. Licorice flavonoid oil reduces total body fat and visceral fat in overweight subjects: A randomized, double-blind, placebo-controlled study. Obes Res Clin Pract. 2009; 3(3):169-78.

15. Cui YM, Ao MZ, Li W, et al. Effect of glabridin from Glycyrrhiza glabra on learning and memory in mice. Planta Med. 2008 Mar;74(4):377-80.

16. Yu XQ, Xue CC, Zhou ZW, et al. In vitro and in vivo neuroprotective effect and mechanisms of glabridin, a major active isoflavan from Glycyrrhiza glabra (licorice). Life Sci. 2008 Jan 2;82(1-2):68-78.

17. Dhingra D, Sharma A. Antidepressant-like activity of Glycyrrhiza glabra L. in mouse models of immobility tests. Prog Neuropsychopharmacol Biol Psychiatry. 2006 May;30(3):449-54.

18. Parle M, Dhingra D, Kulkarni SK. Memory-strengthening activity of Glycyrrhiza glabra in exteroceptive and interoceptive behavioral models. J Med Food. 2004 Winter;7(4):462-6.

19. Zhu Z, Li C, Wang X, et al. 2,2’,4’-trihydroxychalcone from Glycyrrhiza glabra as a new specific BACE1 inhibitor efficiently ameliorates memory impairment in mice. J Neurochem. 2010 Apr 19. Published Online Ahead of Print.

Sleep apnea is a disorder characterized by the cessation of breathing or in some cases underbreathing during periods throughout sleep. Apnea is a Greek word that literally means “without breath.” Apnea results in the afflicted individual suffering from reduced oxygen levels (hypoxia). Sleep apnea is one of the least thought about reasons for a variety of health concerns that at first glance seem unrelated to sleep disorders and is a common reason for fatigue. The disorder also has been shown to be life threatening, increasing morbidity and mortality.¹ In the U.S., it is estimated that obstructive sleep apnea is responsible for 38,000 cardiovascular deaths per year.²

Sleep apnea is a very common problem among my patients. Although obesity is a risk factor for sleep apnea, I have found that even some of my normal weight patients test positive for this condition. As a matter of practice, I test all of my heart disease patients for sleep apnea, due to the strong connection between the two conditions.

A Hidden Epidemic

The National Institutes of Health estimates 12 million Americans have overt sleep apnea,³ including 1 out of 25 middle-aged men and 1 out of 50 middle-aged women. The incidence also increases with age, with at least 1 out of 10 people over the age of 65 developing the disorder. Women are much more likely to develop sleep apnea after menopause.³

It is thought that the occurrence of sleep apnea is much more widespread than the estimates show since many people who have the disorder go undiagnosed.⁴

In men over age 40, obesity, smoking and alcohol use increase the risk for obstructive sleep apnea⁵ and the condition occurs more frequently in African-Americans than in Caucasians.³

Obesity is the strongest risk factor. As body mass index increases by 1 standard deviation, the obstructive sleep apnea risk increases fourfold. Another strong risk factor is neck circumference, an indication that upper body or central weight gain puts people more at risk than overall obesity.⁶ Other risk factors for sleep apnea includes hypothyroidism, menopause and andropause and anatomical abnormalities.^7-9

Although people who have sleep apnea may not have any of these specific symptoms, common symptoms of sleep apnea include fatigue, excessive daytime sleepiness, headache (especially in the morning), restless leg syndrome symptoms, impaired thinking, chronic snoring, waking up abruptly with shortness of breath, episodes of breathing cessation during sleep, sore or dry mouth upon awakening, insomnia, depression and personality changes.¹⁰ In children, symptoms include attention deficit disorder, decreased intelligence, hyperactivity and aggressiveness.¹¹ Depression, insomnia and hypothyroidism are more common in women with sleep apnea than men.¹² I routinely observe more premature hormone cessation in both men and women with apnea, presenting with earlier menopause, andropause and adrenal fatigue.

Different Types of Sleep Apnea

There are three types of sleep apnea: obstructive, central, or mixed. In obstructive sleep apnea (OSA), which is the most common, patients upper airways are obstructed, causing airflow to stop during sleep despite respiratory effort. In central sleep apnea, there is a lack of central nervous system initiation, causing complete or partial lack of respiratory drive combined with at least 10 seconds of absence of breath during sleep. Only 10 percent of patients with sleep apnea have central sleep apnea;¹³ however, central sleep apnea syndrome is seen in approximately 40 percent of patients with congestive heart failure.¹⁴ Mixed sleep apnea is a combination of lack of respiratory effort and upper airway obstruction.

Health Concerns Associated with Sleep Apnea

Sleep apnea predisposes sufferers to a number of health concerns:

Cardiovascular Conditions

Sleep apnea elevates inflammation markers such as C-reactive protein, higher levels of which are linked to atherosclerosis and coronary artery disease.¹⁵ Individuals who have OSA also show increased platelet activity and aggregation (where blood cells clump together, clogging the arteries), higher levels of fibrinogen (a clotting factor) and a decrease in fibrinolytic (clot breakdown) activity.¹⁶

Furthermore, cardiac arrhythmias including premature ventricular contractions (PVCs) as well as both bradycardia and tachycardia are increased in sleep apnea.^17-18 Approximately 50 percent of individuals with OSA also have high blood pressure, which may be related to the fact that many OSA patients are obese.¹⁹ Research has shown that OSA severity is directly linked to severity of both sleep apnea and daytime hypertension.²⁰ Researchers also have determined that obstructive sleep apnea is an independent risk factor for strokes or transient ischemic attacks.²¹

Blood Sugar Concerns

Individuals who have sleep apnea are at a greater risk for abnormal glucose metabolism, insulin resistance and type 2 diabetes.^22-23 Treatment with a positive airway pressure device in individuals with OSA and type 2 diabetes resulted in an increase in insulin sensitivity and a decrease in levels of HbA1c, a marker for high blood sugar.²⁴

Gastroesophageal Reflux (GERD)

Those suffering from GERD experience an increased risk of OSA. Studies show that GERD becomes worse when the Apnea-Hypopnea Index (AHI) increases.²⁵

Decreased Mood and Well-Being

In veterans with sleep apnea, researchers noted a significant increase in mood disorders, such as depression, anxiety, dementia, psychosis and post-traumatic stress disorder.²⁶ Treatment with a positive airway pressure device, meanwhile, can reduce symptoms of depression.²⁷

Diagnosing Sleep Apnea

To test for the presence of sleep apnea, physicians will commonly either send patients to a sleep lab or monitor the patient with an at-home oximeter unit or portable cardiorespiratory device. Once the presence of sleep apnea is confirmed, conventional physicians may either suggest surgery or have the patient use positive airway pressure devices (CPAP, BiPAP, APAP), or oral appliances designed to open the airway during sleep. Positive airway pressure devices, which supply air pressure to force the respiratory passages open during sleep, are prescribed for more severe forms of sleep apnea while oral appliances are generally used in mild-to-moderate sleep apnea.

While these devices are effective at clearing the obstructed airway during sleep, they do not fully address the primary cause behind the sleep apnea nor the complications associated with the disorder.

Natural Support

The first approach I use with my sleep apnea patients is to monitor their hormone levels through a salivary hormone test (Comprehensive Hormone Panel) to check for imbalanced levels of cortisol and other hormones due to the increase in sleep apnea after menopause and andropause. Sleep apnea patients also have been found to have high cortisol levels and normal cortisol levels have been restored after CPAP treatment.²⁸

I find that supporting the health of my sleep apnea patients with various natural substances can be especially helpful. If cortisol levels are found to be high, I suggest using Cortisol Control, which is a combination of Relora®, a proprietary blend of Magnolia (Magnolia officinalis) bark and an extract from Phellodendron (Phellodendron amurense), and Sensoril®, a patented Ashwagandha (Withania somnifera) root and leaf extract. Relora and Sensoril lower cortisol levels and reduce the detrimental effects of stress.^29-30

N-acetyl cysteine (NAC) may help with the intermittent hypoxia (low oxygen) that occurs during obstructive sleep apnea. When animals were given NAC, the deleterious effects of intermittent hypoxia on respiratory muscle function were blocked, likely due to NAC’s ability to increase glutathione levels.³¹ NAC also protected heart cells of animals against the damaging effects of low oxygen conditions.³²

Melatonin is another natural substance that counteracts the damaging effects of hypoxic conditions. When researchers exposed hamsters to low oxygen conditions, the animals developed high blood pressure, fasting hyperglycemia, elevated levels of damaging compounds known as Reactive Oxygen Species (ROS) and narrowing of the blood vessels (vasoconstriction). Melatonin decreased blood pressure, blood glucose and ROS and widened the blood vessels (vasodilation).³³

Green tea also is emerging as a substance that may stop the side effects associated with sleep-apnea-related hypoxia. In an animal model of sleep apnea, green tea stopped some of the cognitive dysfunction that occurs during hypoxic conditions.³⁴

L-Tryptophan is another nutrient I use to support the health of patients during sleep. In one study, 12 subjects with obstructive apnea and 3 with central apnea were given an average dose of 2,500 mg L-tryptophan at bedtime. L-tryptophan resulted in significant improvement in the obstructive sleep apnea patients, who experienced the most dramatic improvement in non-REM sleep.³⁵

Due to the oxidative stress that occurs in sleep apnea, I have found that antioxidants such as vitamin C and vitamin E can be very helpful. In a study of obstructive sleep apnea subjects, lipid peroxidation (which occurs due to free radical damage to the lipids in the body) was significantly increased compared to normal subjects and levels of the antioxidant glutathione were significantly reduced. CPAP therapy as well as vitamin C and vitamin E given for 45 days reduced the lipid peroxidation and restored the glutathione concentrations in OSA subjects. After antioxidant intake, OSA patients slept better with decreased Epworth sleepiness scores and the number of sleep apnea episodes, and they spent more time in stages 3 and 4 sleep. Additionally, the optimum CPAP device pressure was significantly lowered after the subjects consumed the antioxidants.³⁶

Conclusion

Sleep apnea is an underdiagnosed problem and can be the overlooked culprit behind a number of concerns, including coronary artery disease. It not only affects the person suffering from the sleep apnea, but also sleeping companions who experience sleep disruption due to their partner’s nightly snoring or worry about the one they care about.

After testing determines patients have sleep apnea, I have found that monitoring cortisol and hormone levels with a salivary hormone test and supporting their health with Cortisol Control (if levels test high), NAC, melatonin, green tea extract, L-tryptophan and vitamins C and E can have profound effects on their health. These supplements are not intended to be used as a substitution of conventionally accepted apnea therapy, but rather as adjunctive support. Sufficient oxygen is essential for the performance of every cell within your body; therefore, any changes to current or future pressure of a positive pressure device needs to be adjusted by one’s attending sleep specialist provider.

References

1. Fletcher EC. Obstructive sleep apnoea and cardiovascular morbidity. Monaldi Arch Chest Dis. 1996;51:77-80.

2. Barthel SW, Strome M. Snoring, obstructive sleep apnea, and surgery. Med Clin North Am. 1999 Jan;83(1):85-96.

3. National Institutes of Health website, www.nhlbi.nih.gov, accessed June 15, 2010.

4. American Sleep Apnea Association website, www.sleepapnea.org, accessed June 15, 2010.

5. Kara CO, Zencir M, Topuz B, et al. The prevalence of snoring in the adult population. Kulak Burun Bogaz Ihtis Derg. 2005;14(1-2):18-24.

6. Schafer H, Pauleit D, Sudhop T, et al. Body fat distribution, serum leptin, and cardiovascular risk factors in men with obstructive sleep apnea. Chest. 2002;122:829-839.

7. Resta O, Pannacciulli N, Di Gioia G, et al. High prevalence of previously unknown subclinical hypothyroidism in obese patients referred to a sleep clinic for sleep disordered breathing. Nutr Metab Cardiovasc Dis. 2004;14:248-253.

8. Resta O, Bonfitto P, Sabato R, et al. Prevalence of obstructive sleep apnoea in a sample of obese women: Effect of menopause. Diabetes Nutr Metab. 2004;17:296-303.

9. Gazayerli M, Bleibel W, Elhorr A, et al. A correlation between the shape of the epiglottis and obstructive sleep apnea. Surg Endosc. 2006 Mar 16. Published Online Ahead of Print.

10. Cutler MJ, Hamden, AL, et al. Sleep apnea: From the nose to the heart. J Am Board Fam Pract. 2002;15:128-141.

11. Balbani AP, Weber SA, Montovani JC. Update in obstructive sleep apnea syndrome in children. Rev Bras Otorrinolaryngol (Engl Ed). 2005; 71:74-80.

12. Shepertycky MR, Banno K, Kryger MH. Differences between men and women in the clinical presentation of patients diagnosed with obstructive sleep apnea syndrome. Sleep. 2005;28:309314.

13. Cutler MJ, Hamden, AL, et al. Sleep apnea: From the nose to the heart. J Am Board Fam Pract. 2002;15:128141.

14. Müller M, de Jong M, Jaarsma T, Koops A, Voors AA, Nieuwenhuis JA, Wijkstra PJ. Central sleep apnoea syndrome in chronic heart failure: an underestimated and treatable comorbidity. Neth Heart J. 2010 May;18(5):260-3.

15. Kokturk O, Ciftci TU, Mollarecep E, Ciftci B. Elevated C-reactive protein levels and increased cardiovascular risk in patients with obstructive sleep apnea syndrome. Int Heart J 2005;46:801809.

16. Kasasbeh E, Chi DS, Krishnaswamy G. Inflammatory aspects of sleep apnea and their cardiovascular consequences. South Med J. 2006;99:58–67.

17. Guilleminault C, Connolly SJ, Winkle RA. Cardiac arrhythmia and conduction disturbances during sleep in 400 patients with sleep apnea syndrome. Am J Cardiol 1983;52:490494.

18. Harbison J, O’Reilly P, McNicholas WT. Cardiac rhythm disturbances in the obstructive sleep apnea syndrome: Effects of nasal continuous positive airway pressure therapy. Chest 2000;118:591-595.

19. Millman RP, Redline S, Carlisle CC, et al. Daytime hypertension in obstructive sleep apnea: Prevalence and contributing risk factors. Chest. 1991;99:861-866.

20. Carlson JT, Hedner JA, Ejnell H, et al. High prevalence of hypertension in sleep apnea patients independent of obesity. Am J Respir Crit Care Med. 1994;150:72-77.

21. Yaggi HK, Concato J, Kernan WN, et al. Obstructive sleep apnea as a risk factor for stroke and death. N Engl J Med. 2005;353:2034-2041.

22. Punjabi NM, Polotsky VY. Disorders of glucose metabolism in sleep apnea. J Appl Physiol. 2005;99:1998-2007.

23. Harsch IA, Hahn EG, Konturek PC. Insulin resistance and other metabolic aspects of the obstructive sleep apnea syndrome. Med Sci Monitor. 2005;11:RA70-RA75.

24. Hassaballa HA, Tulaimat A, Herdegen JJ, Mokhlesi B. The effect of continuous positive airway pressure on glucose control in diabetic patients with severe obstructive sleep apnea. Sleep Breath. 2005;9:176180.

25. Demeter P, Visy KV, Magyar P. Correlation between severity of endoscopic findings and apnea–hypopnea index in patients with gastroesophageal reflux disease and obstructive sleep apnea. World J Gastroenterol. 2005;11:839-841.

26. Sharafkhaneh A, Giray N, Richardson P, et al. Association of psychiatric disorders and sleep apnea in a large cohort. Sleep. 2005;28:1405-1411.

27. Schwartz DJ, Kohler WC, Karatinos G. Symptoms of depression in individuals with obstructive sleep apnea may be amenable to treatment with continuous positive airway pressure. Chest. 2005;128:1304-1309.

28. Henley DE, Russell GM, Douthwaite JA, Wood SA, Buchanan F, Gibson R, Woltersdorf WW, Catterall JR, Lightman SL. Hypothalamic-pituitary-adrenal axis activation in obstructive sleep apnea: the effect of continuous positive airway pressure therapy. J Clin Endocrinol Metab. 2009 Nov;94(11):4234-42.

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

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

31. Dunleavy M, Bradford A, O’Halloran KD. Oxidative stress impairs upper airway muscle endurance in an animal model of sleep-disordered breathing. Adv Exp Med Biol. 2008;605:458-62.

32. Liu JN, Zhang JX, Lu G, Qiu Y, Yang D, Yin GY, Zhang XL. The effect of oxidative stress in myocardial cell injury in mice exposed to chronic intermittent hypoxia. Chin Med J (Engl). 2010 Jan 5;123(1):74-8.

33. Bertuglia S, Reiter RJ. Melatonin reduces microvascular damage and insulin resistance in hamsters due to chronic intermittent hypoxia. J Pineal Res. 2009 Apr;46(3):307-13.

34. Burckhardt IC, Gozal D, Dayyat E, Cheng Y, Li RC, Goldbart AD, Row BW. Green tea catechin polyphenols attenuate behavioral and oxidative responses to intermittent hypoxia. Am J Respir Crit Care Med. 2008 May 15;177(10):1135-41.

35. Schmidt HS. L-tryptophan in the treatment of impaired respiration in sleep. Bull Eur Physiopathol Respir. 1983 Nov-Dec;19(6):625-9.

36. Singh TD, Patial K, Vijayan VK, Ravi K. Oxidative stress and obstructive sleep apnoea syndrome. Indian J Chest Dis Allied Sci. 2009 Oct-Dec;51(4):217-24.

In this article, I am going to discuss one of the most versatile products in the new Crayhon Research line, Peltier™ Electrolytes, a particularly appropriate product to discuss in the summer. Keeping hydrated, especially in the heat of the season, is especially hard for most people and water is not the most effective way to keep from being dehydrated. Sports drinks are somewhat better but often times are just sugar water or worse, colored, artificially sweetened water. There is a better way to keep yourself hydrated and that is Peltier Electrolytes.

Historically, humankind has eaten foods and drank fluids rich in electrolytes. They boiled bones in soups to pull out the rich mineral content, they ate root vegetables grown in mineral rich soils and they drank waters from streams and wells that also were rich in trace mineral content. Over the past hundred or so years, due to the greater demand on our agricultural system, our soil has been depleted in many of the essential minerals. Our water supply is chlorinated, ozonated and purified, which, while safer from a hygiene perspective, is virtually devoid of electrolytes.

Improving Fatigued, Stiff and Sore Muscles

Hypohydration, where the amount of fluid lost is greater than fluid intake, is very common in the summer, but also happens in every season. Headaches are a common side effect of hypohydration and dehydration states but are typically not relieved by the use of plain water.¹ The need to balance electrolytes seems to provide greater benefits when headaches are caused by hypohydration.² Another major issue that occurs in a state of dehydration is muscle fatigue and pain. What research has shown is that it isn’t just the lack of fluid in the muscle that contributes to fatigue; it is the lack of potassium, which is a major component of Peltier.^3-4

Electrolyte balance is critical to human health. In the book Human Nutrition, the authors state “…the level of one or more electrolytes in the body can stray far from the optimum before we become sufficiently aware of the problem to remedy it.”⁵ By using Peltier Electrolytes, you can help balance the major electrolytes before there is a problem to remedy. Also, according to one of the leading nutritional textbooks used by universities worldwide: “The maintenance of body fluid and electrolytes is of vital importance for sound health and nutrition.”⁶

Peltier comes as a liquid concentrate and as a capsule (Peltier Ultra). There are three liquid formulas available, each with a unique formulation. The Sports Formula is for active people who need to keep the lactic acid buildup in their muscles at bay as well as hydrate all the compartments of the body. Water and sports drinks may help improve hydration in circulating blood but you need electrolyte salts like sodium, potassium, magnesium, chlorides, bicarbonates and phosphates to get the fluids into muscle tissue. Elite athletes to weekend warriors have noticed dramatically improved performance and less fatigue while exercising. One college wrestling coach whose team was using Peltier reported better workouts, fewer injuries and better performance throughout the academic year.

The Executive Formula is one that has a higher proportion of potassium than the other formulas making it ideal for people under stress or who have tight muscles. People who have used it in the past have noted a calming effect after taking it and more relaxed neck, shoulder and back muscles. A number of chiropractors have noted that their adjustments held longer on patients taking Peltier Executive formula.

The third formula is Peltier Standard, which is helpful for the general population. It has a balance of all the electrolyte minerals and can be used with just about anybody.

One of the interesting notes about using Peltier is the different taste sensations that people have when first using it. Some will note a very thick, heavy and sometimes salty taste. This is normal but is indicative of depleted electrolytes. As they continue to take Peltier over time, the taste should even out and become quite mild and often times quite pleasing. If there is a problem with the taste, it can be added to juice or milk or other fluids that can help mask the taste. Using cold water or pre-mixing the electrolytes and storing them in the refrigerator can also help to improve the taste sensation.

Screening for Dehydration

So what is the best way to test for dehydration? Some doctors will do a blood test and look for elevations in red blood cell count, hematocrit, hemoglobin and albumin or a high specific gravity in one’s urine (measuring urine concentration), but that is impractical when trying to determine daily hydration levels.⁷ There is a simple way to screen for daily hydration that can be done in a doctor’s office and people with normal blood pressure also can be trained to do it at home.

• In a seated position, the individual should place his or her right hand palm down on their right leg.
• Note the veins on the back of the hand. They should be fluffy and sticking out. If they are not, the person is severely dehydrated.
• The individual should slowly raise his or her hand while looking at the veins on the back of their hand.
• If the veins disappear before the person reaches his or her chin, they are dehydrated.
• If the veins continue to stay puffy after the hand is over the head, this is a sign of hypertension, which may or may not correspond to blood pressure.

For people showing signs of dehydration, adding a tablespoon of Peltier Electrolytes to 8 ounces of water should work. The recommended dosage of Peltier Electrolytes is ½ ounce or 1 tablespoon per 8 ounces of water one to three times daily. What makes Peltier even more versatile is that you can use it in cooking as well. Add it to soup, chili, rice or anything that uses water and salt. It is a great alternative to the use of regular table salt as it is low in sodium and high in potassium, which makes it beneficial to individuals with high blood pressure.

Bottom line is that Peltier™ is a versatile and effective means of rehydration as well as being the perfect way to balance an individual’s electrolytes without any chance of causing imbalances.

References

1. Blau JN, Kell CA, Sperling JM. Water-deprivation headache: A new headache with Two Variants. Headache. 2004. 44(1);79-83.

2. Driskell JA, Wolinsky I. Macroelements, Water, and Electrolytes in Sports Nutrition. CRC Press, Boca Raton, FL, 1999.

3. McKenna MJ. Effects of training on potassium homeostasis during exercise in man. J Mol Cardiol. 1995. 27;241.

4. Marcos E, Ribas J. Kinetics of plasma potassium concentrations during exhausting exercise in trained and untrained men. Eur J Appl Physiol. 1995. 71;207.

5. Guthrie HA and Picciano MF. Human Nutrition. Mosby-Yearbook. St. Louis, 1995.

6. Advanced Nutrition and Human Metabolism, 2nd Ed. Groff, Gropper and Hunt, West Publishing Company, St. Paul, 1995.

7. Fischbach F, Ed. A Manual of Laboratory and Diagnostic Tests, 4th Ed. J.B Lippincott. Philadelphia, PA. 1992.