Chlorella 101: What you need to know about this nourishing superfood

A single-celled, water-grown micro-algae, chlorella is widely known as a powerful "superfood" supplement with extraordinary nutrient density. It is believed to have been around for eons. One of the few edible species of water-grown algae, chlorella is full of chlorophyll. It contains all of the B vitamins, vitamin C, vitamin E, beta-carotene, amino acids, magnesium, iron, trace minerals, carbohydrates and a higher amount of protein (more than 50%) than meat, per grams of weight (http://www.naturalnews.com). It also has a unique set of phytonutrients (http://www.naturalnews.com/034109_chlorella_superfood.html). It binds to toxins and carries them out of the body. It's high amount of protein makes it a staple for many people who do not eat meat. Phyllis Balch, CNC, says it is virtually a complete food.

Why take it?

One of the main uses of chlorella is to detoxify, or cleanse, the body. It has been found to chelate, or remove, heavy metals from the body according to a Russian study (http://www.naturalnews.com/035177_chlorella_cilantro_detox.html). A study involving rats demonstrated the effectiveness of using chlorella as a counteragent for heavy metal poisoning ( http://www.naturalnews.com). Chlorella-treated rats also had less tissue damage than the control group.

Heavy metals are typically very difficult to get out of your tissues. If you have mercury fillings in your teeth, work in certain industries, have received vaccinations, or have been exposed to radiation, you have heavy metals. Most people have at least some, from our environment and food supply, such as the mercury found in fish. NaturalNews' Paul Fassa reports on a Japanese study which found that all cancer cells contain mercury (http://www.naturalnews.com/035177_chlorella_cilantro_detox.html). Additionally, heavy metal toxicity has been associated with mental decline illnesses such as dementia and Alzheimer's.

Additional Benefits

Chlorella cleanses the blood and optimizes oxygen into the blood. It alkalizes the body, correcting a state of acidosis, in which most disease thrives. By definition, then, it also relieves inflammation, which is the root of much disease. It follows that chlorella is a pain reliever, reduces hypertension and enhances the immune system (http://www.naturalnews.com).

In this NaturalNews report, Donna Earnest Pravel says a study on fibromyalgia patients showed a significant reduction in pain and tenderness. In a similar study, hypertension patients were able to go off of their prescriptions upon taking chlorella (http://www.naturalnews.com).

In addition, Pravel also cites a study done on patients receiving flu shots. They took chlorella before receiving their vaccine for a few weeks. They were found to have 2 - 4 times more antibodies when tested, a few weeks after being vaccinated.

Chlorella has also been proven effective for:

• Balancing hormones (relieving PMS, regulating cycles, etc.)

• Treatment of ulcers

• Balancing the digestive system (improving digestion, relieving constipation)

• Increasing the white blood cell count (helps with infections, warding off of illness)

• Reduces or eliminates body odors

• Balances blood pressure, cholesterol, blood sugar (fighting/preventing cardiovascular disease, diabetes, obesity)

• Reduces occurrence of asthma attacks and allergies

• Treats fatigue

• Helps boost immune response

• Protects the brain and nervous system

• Supports elimination of many kinds of pollutants, from heavy metals to molds

• Boosts tissue growth, healing and repair

• Detoxifies harmful radiation, protects organs

(http://www.naturalnews.com/034109_chlorella_superfood.html, http://www.naturalnews.com/031779_spirulina_radiation.html, http://www.squidoo.com/what-is-chlorella-good-for?)

These are just some of the benefits of taking chlorella. These statements have not been validated by the FDA, but have been validated by centuries of use across many cultures.

How to get it in your diet

Chlorella requires processing due to a strong cell wall that makes it otherwise impossible to gain access to its nutrients. Be sure the products you buy do not use heat or chemicals in their processing. Fassa says a special milling process or rapid pressure change method is necessary to break down the cell wall and make the nutrients bioavailable. You can find chlorella in pill form or powder form, to add to smoothies.

The herb cilantro is also known for its ability to leech mercury out of the body. It combines nicely with chlorella as a superfood and detoxifying combo (http://www.naturalnews.com/035177_chlorella_cilantro_detox.html).

Other things you should know

According to Michelle Bosmier, because of the toxic load the average person carries, sometimes when people start a regime of chlorella they think they are experiencing side-effects. In reality, they are experiencing the effects of detoxification. The cleansing of toxins from the body may give you gas, nausea, stomach cramps, diarrhea, etc. For this reason, its good to start taking chlorella on a weekend, when you can stay close to home. If the side-effects of detoxing are too much for you, ease up on your consumption, adding it in slowly. The symptoms will pass in a couple of days.

Chlorella has a high amount of vitamin K, so it could interfere with blood thinning medications (http://www.naturalnews.com/028017_chlorella_diabetes.html). It also contains iodine, so if you are allergic, avoid it.

Chlorella is inexpensive partially because it is one of the fastest growing plants on Earth. It is the most potent source of pure chlorophyll available (http://www.naturalnews.com/034109_chlorella_superfood.html). Chlorophyll is identical to human blood except for the center element - blood's is iron; chlorophyll's is magnesium. For this reason it is uniquely wonderful for our health. It is a good addition to most diets and disaster kits. It is readily available and stores well, so stock up!

Source: http://www.naturalnews.com/036086_chlorella_superfood_algae.html#ixzz1x2HaiUxl

Carnosine: A Proven Longevity Factor

In our youth, carnosine shields us from the onslaught of oxidation, glycation, DNA damage, and other reactions that injure tissues and cripple organs.1   The problem is that as we grow older, carnosine levels in the body decline,2-4 leaving us vulnerable to loss of cognitive function, decreased mobility, loss of metabolic control, failing cardiovascular performance, and an increased susceptibility to cancer. In laboratory animals of different species, carnosine supplementation extends life spans. This is all adding up to a new era in the way conventional medicine thinks about aging. Scientists Explore Carnosine’s Longevity Benefits Carnosine is found throughout the body wherever there are high energy demands such as in the brain, the heart, and our muscles.5 Its function is to protect these vital areas from the metabolic demands of energy production and management.6,7   Young organisms have high levels of carnosine in those energy-demanding tissues. As part of the aging process, carnosine levels decline over time.2-4 That’s because our bodies both make less carnosine as we age, and also because the carnosine we have is increasingly vulnerable to destruction. In human conditions such as diabetes and metabolic syndrome, which produce unnaturally accelerated aging, carnosine production is decreased, and its destruction is increased.8,9   These findings suggest that a “carnosine deficiency” might be partly responsible for the visible aging and loss of function in a multitude of areas throughout the body that occurs as we get older. If we could restore our bodies’ carnosine stores to their youthful levels, we might be able to arrest part of the aging process. Here are a few of the most dramatic observations in recent years that demonstrate how carnosine supplementation extends life spans: Carnosine slows the aging of human cells in culture dishes.10,11 Scientists added carnosine to cultures of young cells. While the control cells developed the typical “old” appearance, those grown in high carnosine concentrations retained their youthful appearance.5 When these youthful-appearing cells were transferred to culture dishes lacking extra carnosine, they quickly developed the “old” appearance of control cells of the same age. Yet, when scientists took old cells, approaching the limits of their life span, and transferred them into culture dishes containing high carnosine concentrations, they found that the cells rapidly became rejuvenated to resemble young cells.10 Carnosine extends the life span of rotifers, a microscopic aquatic organism now being used as a model of aging in many laboratories.12 In this experiment, scientists tested many different antioxidant compounds, identifying carnosine as one of just four that had significant effects on the organisms’ longevity. Carnosine extends the life span of fruit flies, another organism commonly used to study aging, up to 20% in males.13,14 Normally, male fruit flies die much sooner than do females, but when fed a steady diet including a carnosine supplement, the males attained the same age as the females. Carnosine extends the life span of laboratory mice, complex, warm-blooded mammals with many of the aging features common to humans.15,16 Scientists used a strain of mice in which aging is markedly accelerated and supplemented their food with carnosine. Not only did the animals live significantly longer, they retained the physical and behavioral features of youthful animals.15 Next, the scientists tested the supplement in normal mice, finding much the same effects. Carnosine clearly improved the animals’ external appearances and maintained the animals in better condition than control animals receiving no carnosine.16 What You NEed To Know: Carnosine Provides Broad-Spectrum Defense Against Aging Carnosine is a natural anti-aging constituent in your body. Carnosine fights such age-inducing processes as oxidation, glycation, protein cross-linking, mitochondrial dysfunction, telomere shortening,64 and transition metal accumulation. Carnosine levels decline with age, leaving you with progressively weaker defenses against age-related processes. Carnosine supplementation can restore youthful carnosine levels in blood and tissues, and it extends the life spans of experimental animals of many species. Carnosine supplementation may protect against neurodegenerative diseases and stroke; it also enhances exercise performance and comfort, ameliorates diabetes and its complications, and protects heart muscle and blood vessels from atherosclerosis. Carnosine Protects Against Cardiovascular Disease Carnosine’s multi-targeted effects are most prominent in the heart and blood vessels. Carnosine has been shown to decrease mortality from strokes as well as mitigate the damaging effects of stroke on the brain itself.17-19 Studies in experimental animals show that carnosine, administered before or after a stroke is induced, protects brain cells from the so-called ischemia-reperfusion injury that occurs when tissue is first deprived of oxygen and is then subjected to high oxygen levels when blood flow is restored.17,18 That results in marked reduction in signs of oxidant damage to brain cells, and to a real and significant reduction in the size of the stroke area in the brain.18   Carnosine also protects heart muscle from ischemia (lack of blood flow), which can ultimately produce a heart attack. This protection derives from carnosine’s antioxidant actions, combined with its ability to trap oxidation-inducing transition metals, its acid-buffering capacity, and its influence on inflammatory cell activity.19 In fact, carnosine has been added to solutions used to protect heart muscle during open-heart surgery, when the heart is intentionally stopped, and there is high risk for ischemic damage.20   Carnosine’s actions on blood vessels may even prevent ischemia from occurring in the first place. Carnosine protects artery-lining endothelial cells from oxidation and glycation, both of which are early events in development of atherosclerosis.21,22 Studies show that carnosine prevents formation of dangerous “foam cells,” fat-laden scavenger cells that trigger the inflammatory response that produces deadly arterial plaque.23   Excessive muscle tone in arteries raises blood pressure and reduces blood flow to heart muscle and brain cells; carnosine reduces arterial tone by multiple mechanisms.24 It modulates calcium ion signaling in the smooth muscle cells that control vascular tone and enhances production of beneficial endothelial nitric oxide synthetase (eNOS) that induces arteries to relax.25   Given carnosine’s beneficial impact on skeletal muscle and exercise performance, it is hardly surprising to learn that carnosine also enhances heart muscle contractility. This is again a multifactorial effect, produced in part by carnosine’s ability to control calcium flow, and partly by its antioxidant, acid buffering, and anti-glycation activities.19,26,27 Carnosine Fights Diabetes and Its Consequences The global obesity epidemic brings with it the growing threat of type 2 diabetes and all of its devastating consequences that include cardiovascular disease, kidney failure, nerve damage, and eye disorders. Studies show that diabetics’ cells have lower-than-normal carnosine levels, similar to levels in older adults.10 That may be one reason that diabetes produces accelerated aging.28   Yet carnosine supplementation can restore youthful carnosine levels in vital tissues, and offers protection against many of the components of diabetes. Carnosine lowers elevated blood sugar levels, reduces long-term formation of dangerous advanced glycation end-products, limits oxidant stress and elevated inflammation, and prevents protein cross-linking, not only in diabetics, but also in otherwise healthy aging adults.29-33   Additionally, carnosine works ‘behind the scenes’ to offer important protection for diabetics’ physiological destruction from high blood sugar: Carnosine protects kidney cells from the effects of high glucose levels, helping to reduce the risk of diabetic kidney disease, or nephropathy.34-36 Carnosine reduces oxidation and glycation of low-density lipoprotein (LDL) which bodes well for reduction of diabetes-induced atherosclerosis.37,23 Carnosine reduces protein cross-linking in the lens of the eye and helps to reduce the risk of cataract, a common diabetic complication.38,39 Carnosine supplementation also prevents the microscopic blood vessel damage that produces diabetic retinopathy, a major cause of blindness in diabetics.40 Carnosine supplements prevent loss of sensory nerve function (neuropathy) in diabetic animals.41 Carnosine Protects Brain Cells, Preserves Cognition So far, drug treatment has shown only minimal effectiveness at slowing the progression of cognitive decline. Carnosine’s many therapeutic targets make it exceptionally promising for all of these conditions.42 Alzheimer’s disease is the most widely feared and the most common of the neurodegenerative disorders. Scientists have found that Alzheimer’s patients have even lower levels of carnosine in their brains and spinal fluid than those of other older adults.43 It is not yet clear whether this is a cause or an effect of Alzheimer’s, but many intriguing observations suggest a role for carnosine in prevention of the disease. Alzheimer’s disease is the result of multiple causes, virtually all of which have some connection to carnosine and its function in the brain. Noted expert Alan R. Hipkiss of London’s Queen Mary’s School of Medicine and Dentistry recently summarized the relationship between Alzheimer’s and falling levels of carnosine in the body. Hipkiss observed that those parts of the brain that are first affected in early Alzheimer’s disease are also those in which carnosine is normally found in highest concentrations.44 That suggests that, as carnosine levels fall with age, those brain areas become the most vulnerable to the Alzheimer’s-related damage. In addition, he notes that the abnormal protein, amyloid beta, which is seen exclusively in Alzheimer’s diseased brains is typically full of zinc ions. Carnosine is capable of binding up zinc and keeping it from damaging tissues in excess.44,45 Again, the implication is that falling levels of carnosine allow brain tissue to fall victim to an unnatural accumulation of a toxic substance. Finally, Hipkiss notes that the so-called “neurofibrillary tangles” found in the brains of Alzheimer’s disease patients contain proteins that are extensively cross-linked.44 Carnosine is an effective inhibitor of protein cross-linking everywhere in the body.46   Mitochondrial dysfunction is yet another contributor to Alzheimer’s disease; the oxidant stress it produces may be involved in formation of the Alzheimer’s protein amyloid beta.47 Experimental studies show that supplementing Alzheimer’s disease mice with carnosine potently reduces amyloid beta accumulation and completely rescues their brains from mitochondrial dysfunction.31 These biochemical relationships are now showing real effects in experimental models of neurodegenerative diseases of aging. Researchers fed aged rats a supplement rich in carnosine, which also contained vitamin D3 as well as blueberry and green tea polyphenols, or a control substance.48 The animals were then trained in finding their way to a platform submerged in water. By the end of the training period, the treated group of impaired older animals performed better than the controls in the same age category. Supplemented animals also were found to have increased production of new brain cells and fewer markers of brain cell inflammation and deterioration than controls. Similar anti-oxidative and anti-inflammatory effects were seen in the brains of mice with an experimental form of Parkinson’s disease.49   Strokes cause brain cells to die from oxidant damage. Recent studies show that carnosine’s antioxidant effects provide some protection against both ischemic stroke (in which too little blood reaches brain tissue), and hemorrhagic strokes (in which bleeding exposes brain tissue to damage from free blood). In one study, rats were supplemented with a carnosine-blueberry-green tea-vitamin D3 mixture for two weeks prior to experimentally-induced ischemic stroke, at which time a major brain artery was surgically blocked.50 Pre- and post-surgery behavioral testing demonstrated that, compared with control animals, supplemented rats had a 12% reduction in motor asymmetry, and a 24% reduction in neurologic dysfunction following the stroke. Supplemented rats also had up to a 3-fold increase in new brain cell proliferation after the stroke, compared with controls. Other studies of ischemic stroke demonstrate a strong reduction in oxidative stress and brain cell death by apoptosis in animals supplemented with carnosine.51 Importantly, carnosine also provides protection following ischemia from so-called glutamate excitotoxicity, the same sort of neuronal “overdrive” that is thought to further contribute to Alzheimer’s disease.52   In experimental models of hemorrhagic stroke, carnosine treatment led to restoration of normal neurotransmitter receptors damaged by the presence of blood in brain tissue.53 Carnosine also prevented some of the dangerous swelling that often follows a hemorrhagic stroke.53 Carnosine Targets Six Multiple Molecular Aging Mechanisms Initially, researchers considered carnosine as just an antioxidant molecule. But, while it has good antioxidant effects, carnosine is by no means the most powerful antioxidant in the body. What caught the researchers’ attention was that supplementation with other, more potent, antioxidants did not produce the dramatic increase in longevity seen with carnosine.62,65 Clearly, something else is going on. Few scientists, however, were prepared for the revelation that carnosine actually targets six major processes involved in the aging process. Let’s look briefly at each one, to see how carnosine exerts its overall effects. Oxidation at the cellular and tissue levels is one of the major contributors to the aging of organisms. Carnosine scavenges oxygen and nitrogen free radicals, and reduces their destructive impact on fat and DNA molecules.1,62,66,67 These effects are a powerful means of stopping atherosclerosis and cancer formation, respectively. Glycation, the formation of molecular compounds of glucose with vital biomolecules such as enzymes and other proteins, is another major cause of aging. Glycated proteins induce potent oxidant stress and trigger inflammatory responses that hasten the aging process. Glycated proteins also form “cross-links” that bind them together, reducing their youthful flexibility and function. Carnosine takes a “sacrificial hit” and allows itself to be glycated, sparing other vital structures and preventing dangerous protein cross-linking.5,67,68 Accumulation of excess metals 44,69 Carnosine chelates, or binds to, ions of copper, zinc, and iron, which in excess are known to induce production of amyloid beta and other proteins found in Alzheimer’s and Parkinson’s diseases.66,70-72 Cross-linked proteins are the result of accumulated oxidant damage and glycation in youth. They are eliminated by intracellular structures called proteasomes.65 With increasing age, however, proteasomal degradation drops off, allowing the dysfunctional proteins to accumulate and interfere with cellular function. Carnosine can react with these abnormal proteins, hastening their elimination.65,70 Telomeres are the repeating DNA sequences at the ends of chromosomes that function as a kind of “molecular clock,” becoming shortened with each cycle of cell replication. When telomeres become too short, cells die. Carnosine reduces damage to telomeres and slows their rate of shortening in experimental systems.64 Mitochondrial dysfunction accelerates aging by depriving cells of the energy they need, and by adding to their oxidative burden as mitochondria lose their efficiency.73 Carnosine alleviates all of these alterations, especially in vulnerable brain cells where mitochondrial dysfunction contributes to Alzheimer’s and other neurodegenerative diseases.47,73,74 Carnosine Enhances Exercise Performance While excess body fat increases the risk of diabetes, regular exercise reduces the risk of both obesity and diabetes. Carnosine supports exercise performance by buffering the rising levels of acid that accumulate in working muscle.55,56 Accumulating acid in muscles produces the fatigue and pain that ultimately limits our workouts.54,57,58   Increasing muscle carnosine levels is now a well-established means of improving exercise performance and reducing fatigue, both in trained and untrained individuals.6,59,60 In older adults, in whom frailty and the risk of falls increases with muscle weakness, it can be a critical factor in promoting safety and independent living.61   In one study of people 55-92 years old, raising muscle carnosine content increased their fatigue threshold by 29% from pre- to post-supplementation, with no change seen in the placebo group.62 A similar study among 60-80 year-olds demonstrated a significant increase in the time subjects could exercise before becoming exhausted.63 Summary The past decade has led to a broad array of findings regarding carnosine’s multiple protective effects, arising from its ability to fight multiple processes that cause aging. Carnosine defends against oxidant damage, glycation of vital proteins, acid accumulation in muscle and heart, dangerous transition metal ions, age-induced protein cross-linking, mitochondrial dysfunction, and age-accelerating telomere shortening.64   These multitargeted actions collaborate to prevent age-related diseases such as cognitive decline and dementia, to promote exercise comfort and performance, to slow progression of metabolic conditions such as diabetes, and to defend against atherosclerosis and heart disease. It’s no wonder carnosine is referred to as the “antiaging dipeptide.”26  If you have any questions on the scientific content of this article, please call a Life Extension® Health Advisor at 1-866-864-3027.  References:
1. Hipkiss AR. Carnosine, a protective, anti-ageing peptide? Int J Biochem Cell Biol. 1998 Aug;30(8):863-8. 2. Boldyrev AA, Yuneva MO, Sorokina EV, et al. Antioxidant systems in tissues of senescence accelerated mice. Biochemistry (Mosc). 2001 Oct;66(10):1157-63. 3. Bellia F, Calabrese V, Guarino F, et al. Carnosinase levels in aging brain: redox state induction and cellular stress response. Antioxid Redox Signal. 2009 Nov;11(11):2759-75. 4. Everaert I, Mooyaart A, Baguet A, et al. Vegetarianism, female gender and increasing age, but not CNDP1 genotype, are associated with reduced muscle carnosine levels in humans. Amino Acids. 2011 Apr;40(4):1221-9. 5. Bellia F, Vecchio G, Cuzzocrea S, Calabrese V, Rizzarelli E. Neuroprotective features of carnosine in oxidative driven diseases. Mol Aspects Med. 2011 Aug;32(4-6):258-66. 6. Baguet A, Bourgois J, Vanhee L, Achten E, Derave W. Important role of muscle carnosine in rowing performance. J Appl Physiol. 2010 Oct;109(4):1096-101. 7. Calabrese V, Cornelius C, Cuzzocrea S, Iavicoli I, Rizzarelli E, Calabrese EJ. Hormesis, cellular stress response and vitagenes as critical determinants in aging and longevity. Mol Aspects Med. 2011 Aug;32(4-6):279-304. 8. Riedl E, Koeppel H, Pfister F, et al. N-glycosylation of carnosinase influences protein secretion and enzyme activity: implications for hyperglycemia. Diabetes. 2010 Aug;59(8):1984-90. 9. Gayova E, Kron I, Suchozova K, Pavlisak V, Fedurco M, Novakova B. Carnosine in patients with type I diabetes mellitus. Bratisl Lek Listy. 1999 Sep;100(9):500-2. 10. McFarland GA, Holliday R. Retardation of the senescence of cultured human diploid fibroblasts by carnosine. Exp Cell Res. 1994 Jun;212(2):167-75. 11. McFarland GA, Holliday R. Further evidence for the rejuvenating effects of the dipeptide L-carnosine on cultured human diploid fibroblasts. Exp Gerontol. 1999 Jan;34(1):35-45. 12. Snell TW, Fields AM, Johnston RK. Antioxidants can extend lifespan of Brachionus manjavacas (Rotifera), but only in a few combinations. Biogerontology. 2012 Jan 24. 13. Yuneva AO, Kramarenko GG, Vetreshchak TV, Gallant S, Boldyrev AA. Effect of carnosine on Drosophila melanogaster life span. Bull Exp Biol Med. 2002 Jun;133(6):559-61. 14. Stvolinsky S, Antipin M, Meguro K, Sato T, Abe H, Boldyrev A. Effect of carnosine and its Trolox-modified derivatives on life span of Drosophila melanogaster. Rejuvenation Res. 2010 Aug;13(4):453-7. 15. Boldyrev AA, Gallant SC, Sukhich GT. Carnosine, the protective, anti-aging peptide. Biosci Rep. 1999 Dec;19(6):581-7. 16. Gallant S, Semyonova M, Yuneva M. Carnosine as a potential anti-senescence drug. Biochemistry (Mosc). 2000 Jul;65(7):866-8. 17. Dobrota D, Fedorova T, Stvolinsky S, et al. Carnosine protects the brain of rats and Mongolian gerbils against ischemic injury: after-stroke-effect. Neurochem Res. 2005 Oct;30(10):1283-8. 18. Rajanikant GK, Zemke D, Senut MC, et al. 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Mech Ageing Dev. 2005 Oct;126(10):1034-9. 31. Nagai K, Niijima A, Yamano T, et al. Possible role of L-carnosine in the regulation of blood glucose through controlling autonomic nerves. Exp Biol Med (Maywood). 2003 Nov;228(10):1138-45. 32. Hipkiss AR, Brownson C, Carrier MJ. Carnosine, the anti-ageing, anti-oxidant dipeptide, may react with protein carbonyl groups. Mech Ageing Dev. 2001 Sep 15;122(13):1431-45. 33. Aldini G, Facino RM, Beretta G, Carini M. Carnosine and related dipeptides as quenchers of reactive carbonyl species: from structural studies to therapeutic perspectives. Biofactors. 2005;24(1-4):77-87. 34. Janssen B, Hohenadel D, Brinkkoetter P, et al. Carnosine as a protective factor in diabetic nephropathy: association with a leucine repeat of the carnosinase gene CNDP1. Diabetes. 2005 Aug;54(8):2320-7. 35. Sauerhofer S, Yuan G, Braun GS, et al. L-carnosine, a substrate of carnosinase-1, influences glucose metabolism. Diabetes. 2007 Oct;56(10):2425-32. 36. Riedl E, Pfister F, Braunagel M, et al. Carnosine prevents apoptosis of glomerular cells and podocyte loss in STZ diabetic rats. Cell Physiol Biochem. 2011;28(2):279-88. 37. Lee YT, Hsu CC, Lin MH, Liu KS, Yin MC. Histidine and carnosine delay diabetic deterioration in mice and protect human low density lipoprotein against oxidation and glycation. Eur J Pharmacol. 2005 Apr 18;513(1-2):145-50. 38. Yan H, Harding JJ. Carnosine protects against the inactivation of esterase induced by glycation and a steroid. Biochim Biophys Acta. 2005 Jun 30;1741(1-2):120-6. 39. Yan H, Guo Y, Zhang J, Ding Z, Ha W, Harding JJ. Effect of carnosine, aminoguanidine, and aspirin drops on the prevention of cataracts in diabetic rats. Mol Vis. 2008;14:2282-91. 40. Pfister F, Riedl E, Wang Q, et al. Oral carnosine supplementation prevents vascular damage in experimental diabetic retinopathy. Cell Physiol Biochem. 2011;28(1):125-36. 41. Kamei J, Ohsawa M, Miyata S, Tanaka S. Preventive effect of L-carnosine on changes in the thermal nociceptive threshold in streptozotocin-induced diabetic mice. Eur J Pharmacol. 2008 Dec 14;600(1-3):83-6. 42. Shen Y, Hu WW, Chen Z. Carnosine and diseases of central nervous system. Zhejiang Da Xue Xue Bao Yi Xue Ban. 2007 Mar;36(2):199-203. 43. Fonteh AN, Harrington RJ, Tsai A, Liao P, Harrington MG. Free amino acid and dipeptide changes in the body fluids from Alzheimer’s disease subjects. Amino Acids. 2007 Feb;32(2):213-24. 44. Hipkiss AR. Could carnosine or related structures suppress Alzheimer’s disease? J Alzheimers Dis. 2007 May;11(2):229-40. 45. Matsukura T, Tanaka H. Applicability of zinc complex of L-carnosine for medical use. Biochemistry (Mosc). 2000 Jul;65(7):817-23. 46. Wang AM, Ma C, Xie ZH, Shen F. Use of carnosine as a natural anti-senescence drug for human beings. Biochemistry (Mosc). 2000 Jul;65(7):869-71. 47. Corona C, Frazzini V, Silvestri E, et al. Effects of dietary supplementation of carnosine on mitochondrial dysfunction, amyloid pathology, and cognitive deficits in 3xTg-AD mice. PLoS One. 2011;6(3):e17971. 48. Acosta S, Jernberg J, Sanberg CD, et al. NT-020, a natural therapeutic approach to optimize spatial memory performance and increase neural progenitor cell proliferation and decrease inflammation in the aged rat. Rejuvenation Res. 2010 Oct;13(5):581-8. 49 Tsai SJ, Kuo WW, Liu WH, Yin MC. Antioxidative and anti-inflammatory protection from carnosine in the striatum of MPTP-treated mice. J Agric Food Chem. 2010 Oct 6. 50. Yasuhara T, Hara K, Maki M, et al. Dietary supplementation exerts neuroprotective effects in ischemic stroke model. Rejuvenation Res. 2008 Feb;11(1):201-14. 51. Pekcetin C, Kiray M, Ergur BU, et al. Carnosine attenuates oxidative stress and apoptosis in transient cerebral ischemia in rats. Acta Biol Hung. 2009 Jun;60(2):137-48. 52. Shen Y, He P, Fan YY, et al. Carnosine protects against permanent cerebral ischemia in histidine decarboxylase knockout mice by reducing glutamate excitotoxicity. Free Radic Biol Med. 2010 Mar 1;48(5):727-35. 53. Khama-Murad A, Mokrushin AA, Pavlinova LI. Neuroprotective properties of l-carnosine in the brain slices exposed to autoblood in the hemorrhagic stroke model in vitro. Regul Pept. 2011 Feb 25;167(1):65-9. 54. Begum G, Cunliffe A, Leveritt M. Physiological role of carnosine in contracting muscle. Int J Sport Nutr Exerc Metab. 2005 Oct;15(5):493-514. 55. Baguet A, Koppo K, Pottier A, Derave W. Beta-alanine supplementation reduces acidosis but not oxygen uptake response during high-intensity cycling exercise. Eur J Appl Physiol. 2010 Feb;108(3):495-503. 56. Sale C, Saunders B, Harris RC. Effect of beta-alanine supplementation on muscle carnosine concentrations and exercise performance. Amino Acids. 2010 Jul;39(2):321-33. 57. Tallon MJ, Harris RC, Boobis LH, Fallowfield JL, Wise JA. The carnosine content of vastus lateralis is elevated in resistance-trained bodybuilders. J Strength Cond Res. 2005 Nov;19(4):725-9. 58. Giannini Artioli G, Gualano B, Smith A, Stout J, Herbert Lancha AJ. The role of beta-alanine supplementation on muscle carnosine and exercise performance. Med Sci Sports Exerc. 2009 Dec 9. 59. Derave W, Everaert I, Beeckman S, Baguet A. Muscle carnosine metabolism and beta-alanine supplementation in relation to exercise and training. Sports Med. 2010 Mar 1;40(3):247-63. 60. Hobson RM, Saunders B, Ball G, Harris RC, Sale C. Effects of beta-alanine supplementation on exercise performance: a meta-analysis. Amino Acids. 2012 Jan 24. 61. Stout JR, Graves BS, Smith AE, et al. The effect of beta-alanine supplementation on neuromuscular fatigue in elderly (55-92 Years): a double-blind randomized study. J Int Soc Sports Nutr. 2008;5:21. 62. Hyland P, Duggan O, Hipkiss A, Barnett C, Barnett Y. The effects of carnosine on oxidative DNA damage levels and in vitro life span in human peripheral blood derived CD4+T cell clones. Mech Ageing Dev. 2000 Dec 20;121(1-3):203-15. 63. Del Favero S, Roschel H, Solis MY, et al. Beta-alanine (Carnosyn) supplementation in elderly subjects (60-80 years): effects on muscle carnosine content and physical capacity. Amino Acids. 2011 Dec 6. 64. Shao L, Li QH, Tan Z. L-carnosine reduces telomere damage and shortening rate in cultured normal fibroblasts. Biochem Biophys Res Commun. 2004 Nov 12;324(2):931-6.67. 65. Hipkiss AR, Brownson C, Bertani MF, Ruiz E, Ferro A. Reaction of carnosine with aged proteins: another protective process? Ann N Y Acad Sci. 2002 Apr;959:285-94. 66. Hipkiss AR, Preston JE, Himsworth DT, et al. Pluripotent protective effects of carnosine, a naturally occurring dipeptide. Ann N Y Acad Sci. 1998 Nov 20;854:37-53. 67. Reddy VP, Garrett MR, Perry G, Smith MA. Carnosine: a versatile antioxidant and antiglycating agent. Sci Aging Knowledge Environ. 2005 May 4;2005(18):pe12. 68. Hipkiss AR, Michaelis J, Syrris P. Non-enzymatic glycosylation of the dipeptide L-carnosine, a potential anti-protein-cross-linking agent. FEBS Lett. 1995 Aug 28;371(1):81-5. 69. Kang JH. Protective effects of carnosine and homocarnosine on ferritin and hydrogen peroxide-mediated DNA damage. BMB Rep. 2010 Oct;43(10):683-7. 70. Hipkiss AR. On the enigma of carnosine’s anti-ageing actions. Exp Gerontol. 2009 Apr;44(4):237-42. 71. Hipkiss AR. Carnosine and its possible roles in nutrition and health. Adv Food Nutr Res. 2009;57:87-154. 72. Boldyrev AA, Stvolinsky SL, Fedorova TN, Suslina ZA. Carnosine as a natural antioxidant and geroprotector: from molecular mechanisms to clinical trials. Rejuvenation Res. 2010 Apr-Jun;13(2-3):156-8. 73. Cheng J, Wang F, Yu DF, Wu PF, Chen JG. The cytotoxic mechanism of malondialdehyde and protective effect of carnosine via protein cross-linking/mitochondrial dysfunction/reactive oxygen species/MAPK pathway in neurons. Eur J Pharmacol. 2011 Jan 10;650(1):184-94. 74. Hipkiss AR. Aging, proteotoxicity, mitochondria, Glycation, NAD and Carnosine: Possible Inter-relationships and resolution of the oxygen paradox. Front Aging Neurosci. 2010;2:10. Author: Susan Evans Source:  http://www.lef.org/magazine/mag2012/jun2012_Carnosine-Proven-Longevity-Factor_01.htm

Government-distributed spam canned meat products linked to causing doubled risk of diabetes

A new study published in the American Journal of Clinical Nutrition has found that processed, canned meat products -- these are collectively known as "spam," as is the brand-name version of the canned meat popularly known as "SPAM" -- are linked to a double risk of developing diabetes. Particularly among American Indians who consume lots of spam given them by the U.S. government, diabetes risk is exceptionally high.

Researchers from the University of Washington School of Medicine surveyed 2,000 Native Americans from Arizona, Oklahoma, and North and South Dakota as part of a study that aimed to figure out why diabetes rates are so high among this particular ethnic group. What they came to discover was that canned meat products, which are typically very high in processed sodium and other additives and preservatives, were very clearly linked to elevated rates of diabetes.

Among the 500 study participants who consumed the most canned meat products, a whopping 85 percent of them developed diabetes in the time leading up to the five-year study follow-up. In contrast, only 44 percent of those among the 500 who ate the least amount of canned meat products developed diabetes. None of the participants had diabetes at the start of the study.

"A lot of communities in this study are in very rural areas with limited access to grocery stores ... and they want to eat foods that have a long shelf life," explained Amanda Fretts, lead author of the study, to Reuters.

Though the researchers say they are unsure exactly why canned meat products are linked to diabetes, the high salt content in canned meat products could be at least one factor. A single 12-ounce can of Hormel's SPAM Classic, for instance, contains nearly 5,000 milligrams (mg) of sodium, which is basically all processed salt rather than nutritive sea salt (http://www.hormelfoods.com/brands/spam/default.aspx).

But another cause could have to do with the "unique" way canned meat is processed, as researchers did not see a similar rise in diabetes rates among those who consumed unprocessed meats. Some varieties of Hormel's SPAM products, for instance, contain "mechanically separated" meat products similar to those used in McDonald's chicken McNuggets ( http://www.huffingtonpost.com).

Sources for this article include:

http://www.reuters.com

Source: http://www.naturalnews.com/034923_processed_meat_diabetes_government.html#ixzz1m6TmKNpf

Why McDonald's Happy Meal hamburgers won't decompose - the real story behind the story

It's always entertaining when the mainstream media "discovers" something they think is new even though the natural health community has been talking about for years. The New York Times, for example, recently ran a story entitled When Drugs Cause Problems They Are Supposed to Prevent (http://www.nytimes.com/2010/10/17/h...). We've been covering the same topic for years, reporting on how chemotherapy causes cancer, osteoporosis drugs cause bone fractures and antidepressant drugs cause suicidal behavior.

The latest "new" discovery by the mainstream media is that McDonald's Happy Meal hamburgers and fries won't decompose, even if you leave them out for six months. This story has been picked up by CNN, the Washington Post and many other MSM outlets which appear startled that junk food from fast food chains won't decompose.

The funny thing about this is that the natural health industry already covered this topic years ago. Remember Len Foley's Bionic Burger video? It was posted in 2007 and eventually racked up a whopping 2 million views on YouTube (http://www.youtube.com/watch?v=mYyD...). And this video shows a guy who bought his McDonald's hamburgers in 1989 -- burgers that still haven't decomposed in over two decades!

Now, he has an entire museum of non-decomposed burgers in his basement.

Did the mainstream media pick up on this story? Nope. Not a word. The story was completely ignored. It was only in 2010 when an artist posted a story about a non-decomposing McDonald's hamburger from six months ago that the news networks ran with the story.

Check out the video link above and you'll see an entire museum of Big Macs and hamburgers spanning the years -- none of which have decomposed.

This is especially interesting because the more recent "Happy Meal Project" which only tracks a burger for six months has drawn quite a lot of criticism from a few critics who say the burgers will decompose if you give them enough time. They obviously don't know about the mummified burger museum going all the way back to 1989. This stuff never seems to decompose!

Why don't McDonald's hamburgers decompose?

So why don't fast food burgers and fries decompose in the first place? The knee-jerk answer is often thought to be, "Well they must be made with so many chemicals that even mold won't eat them." While that's part of the answer, it's not the whole story.

The truth is many processed foods don't decompose and won't be eaten by molds, insects or even rodents. Try leaving a tub of margarine outside in your yard and see if anything bothers to eat it. You'll find that the margarine stays seems immortal, too!

Potato chips can last for decades. Frozen pizzas are remarkably resistant to decomposition. And you know those processed Christmas sausages and meats sold around the holiday season? You can keep them for years and they'll never rot.

With meats, the primary reason why they don't decompose is their high sodium content. Salt is a great preservative, as early humans have known for thousands of years. McDonald's meat patties are absolutely loaded with sodium -- so much so that they qualify as "preserved" meat, not even counting the chemicals you might find in the meat.

To me, there's not much mystery about the meat not decomposing. The real question in my mind is why don't the buns mold? That's the really scary part, since healthy bread begins to mold within days. What could possibly be in McDonald's hamburger buns that would ward off microscopic life for more than two decades?

As it turns out, unless you're a chemist you probably can't even read the ingredients list out loud. Here's what McDonald's own website says you'll find in their buns:

Enriched flour (bleached wheat flour, malted barley flour, niacin, reduced iron, thiamin mononitrate, riboflavin, folic acid, enzymes), water, high fructose corn syrup, sugar, yeast, soybean oil and/or partially hydrogenated soybean oil, contains 2% or less of the following: salt, calcium sulfate, calcium carbonate, wheat gluten, ammonium sulfate, ammonium chloride, dough conditioners (sodium stearoyl lactylate, datem, ascorbic acid, azodicarbonamide, mono- and diglycerides, ethoxylated monoglycerides, monocalcium phosphate, enzymes, guar gum, calcium peroxide, soy flour), calcium propionate and sodium propionate (preservatives), soy lecithin.

Great stuff, huh? You gotta especially love the HFCS (diabetes, anyone?), partially-hydrogenated soybean oil (anybody want heart disease?) and the long list of chemicals such as ammonium sulfate and sodium proprionate. Yum. I'm drooling just thinking about it.

Now here's the truly shocking part about all this: In my estimation, the reason nothing will eat a McDonald's hamburger bun (except a human) is because it's not food!

No normal animal will perceive a McDonald's hamburger bun as food, and as it turns out, neither will bacteria or fungi. To their senses, it's just not edible stuff. That's why these bionic burger buns just won't decompose.

Which brings me to my final point about this whole laughable distraction: There is only one species on planet Earth that's stupid enough to think a McDonald's hamburger is food. This species is suffering from skyrocketing rates of diabetes, cancer, heart disease, dementia and obesity. This species claims to be the most intelligent species on the planet, and yet it behaves in such a moronic way that it feeds its own children poisonous chemicals and such atrocious non-foods that even fungi won't eat it (and fungi will eat cow manure, just FYI).

Care to guess which species I'm talking about?

Author: Mike Adams
Source: http://www.naturalnews.com/030074_Happy_Meal_decompose.html#ixzz1jHcVk4Se

Erectile Dysfunction - Natural Therapies

Natural Therapies for Relieving Erectile Dysfunction

Until recently, the very mention of erectile dysfunction or impotence could bring about a blush to even the most manly of men. Embarrassing as it may be, erectile dysfunction affects more than 18 million men in America. It can vary in severity from an inability to achieve, maintain and sustain an erection, to an inability to achieve an orgasm, even though a healthy sexual desire exists. Because of the sensitive nature of this disorder, it often goes unreported. 

 

Achieving a Normal Erection

Achieving a normal erection is a complex process. It involves psychological impulses from the brain, adequate levels of testosterone (male sex hormone), a functioning nervous system, and healthy vascular tissue of the penis. Electrical impulses from the brain, when stimulated, cause the nerves in the penis to release nitric oxide. This, in turn, increases the production of guanylate MonoPhosphate (cGMP) in the muscle cells of the corpora cavernosa (the tissue of the penis, consisting of smooth muscles, fibrous tissues, spaces, veins and arteries). The cGMP triggers the muscles of the corpora cavernosa to relax and fill with blood, which causes the penis to expand.

 

Erectile Dysfunction Factors

Because of the intricate nature of the physiological processes involved, a number of different factors can interfere with a man's ability to achieve a normal and healthy erection. The most common of these is aging. As a man gets older, his ability to produce nitric oxide decreases, thus affecting the proper functioning of the corpora cavernosa.

 

Diabetes and Erectile Dysfunction

A number of health issues can also underscore this disorder. The most frequently seen are diabetes mellitus and hypertension. Diabetes, for example, can damage the sensory nerves in the body. In turn, individuals who suffer from hypertension exhibit low nitric oxide production. Other factors that can contribute to erectile dysfunction include cardiovascular disease, nerve or spinal cord damage, cigarette smoking, low testosterone levels, prescription medications, depression, stress and anxiety.

Until recently, it was believed that little could be done to help a man who is suffering from erectile dysfunction, but there are a number of natural alternative health remedies that can be tried before having to rely on the “little blue pill."

 

Alternative Remedies and Wellness Recommendations for Erectile Dysfunction

• If you think your stress, anxiety or depression is affecting you physically, perhaps psychological counseling, meditation, bio-feedback or hypnotherapy can help.
  
  
• If you are taking prescription medications such as MAO inhibitors or anti-hypertensives, talk to your doctor about their possible side effects.
  
  
• Have your hormone levels checked. You might be suffering from low testosterone levels. In some men, low levels of the hormone dehydroepiandrosterone (DHEA) have also been reported. DHEA is essential for the production of testosterone.
  
  
• Quit smoking.
  
  
• Try supplementing with the amino acid L-arginine. Nitric oxide formation depends on sufficient levels of L-arginine in the body and has been found particularly effective for men with abnormal nitric oxide metabolism.
  
  
• Yohimbe bark has a history of helping men with erectile dysfunction. Yohimbe dilates blood vessels and may help regardless of the underlying cause. If you are on prescription medications, talk to your doctor before taking yohimbe.
  
  
• Muria puama can be used to increase the libido and erectile strength. It works best when combined with yohimbe bark. This combination can be found in Nature's Sunshine's X-Action for Men.
  
  
• In Mexico, the herb damiana is used as a male aphrodisiac and is an herb traditionally recommended for men with erectile dysfunction.
  
  
• In Peru, maca is known as a potent aphrodisiac. Maca is often called the herbal Viagra and does not alter circulation. Instead it works to regulate hormones and bring the body back into balance.
  
  
• Asian (panax) ginseng is an herb that has long been used to support male potency.
  
  
• Sarsaparilla has a history of being used as a tonic for male sexual potency and is thought to assist in the production of testosterone.
  
  
• Some men find relief when taking ginkgo biloba. Ginkgo biloba supports blood circulation and may help by increasing blood flow to the penis. This supplement is not recommended if you are taking any kind of prescription blood thinner.
  
  
• Traditionally used to lessen the symptoms of an enlarged prostate, saw palmetto stimulates a low libido and increases sexual energy.

Source: About.com
Author: Dr. Rita Louise

Glycemic Index and Glycemic Load

Glycemic Index

In the past, carbohydrates were classified as simple or complex based on the number of simple sugars in the molecule. Carbohydrates composed of one or two simple sugars like fructose or sucrose (table sugar; a disaccharide composed of one molecule of glucose and one molecule of fructose) were labeled simple, while starchy foods were labeled complex because starch is composed of long chains of the simple sugar, glucose. Advice to eat less simple and more complex carbohydrates (i.e., polysaccharides) was based on the assumption that consuming starchy foods would lead to smaller increases in blood glucose than sugary foods (1). This assumption turned out to be too simplistic since the blood glucose (glycemic) response to “complex” carbohydrates has been found to vary considerably. A more accurate indicator of the relative glycemic response to dietary carbohydrates should be glycemic load, which incorporates the relative quality and quantity of carbohydrates in the diet.

Measuring the Glycemic Index of Foods
To determine the glycemic index of a food, volunteers are typically given a test food that provides 50 grams of carbohydrate and a control food (white bread or pure glucose) that provides the same amount of carbohydrate on different days (2). Blood samples for the determination of glucose are taken prior to eating and at regular intervals after eating over the next several hours. The changes in blood glucose over time are plotted as a curve. The glycemic index is calculated as the area under the glucose curve after the test food is eaten, divided by the corresponding area after the control food is eaten. The value is multiplied by 100 to represent a percentage of the control food. For example, a baked potato has a glycemic index of 76 relative to glucose and 108 relative to white bread, which means that the blood glucose response to the carbohydrate in a baked potato is 76% of the blood glucose response to the same amount of carbohydrate in pure glucose and 108% of the blood glucose response to the same amount of carbohydrate in white bread (3). In contrast, cooked brown rice has a glycemic index of 55 relative to glucose and 79 relative to white bread (4). In the traditional system of classifying carbohydrates, both brown rice and potato would be classified as complex carbohydrates despite the difference in their effects on blood glucose levels.

Physiological Responses to High- versus Low-Glycemic Index Foods
By definition, the consumption of high-glycemic index foods results in higher and more rapid increases in blood glucose levels than the consumption of low-glycemic index foods. Rapid increases in blood glucose are potent signals to the beta-cells of the pancreas to increase insulin secretion (2). Over the next few hours, the high insulin levels induced by consumption of high-glycemic index foods may cause a sharp decrease in blood glucose levels (hypoglycemia). In contrast, the consumption of low-glycemic index foods results in lower but more sustained increases in blood glucose and lower insulin demands on pancreatic beta-cells (5).

Glycemic Load

The glycemic index compares the potential of foods containing the same amount of carbohydrate to raise blood glucose. However, the amount of carbohydrate consumed also affects blood glucose levels and insulin responses. The glycemic load of a food is calculated by multiplying the glycemic index by the amount of carbohydrate in grams provided by a food and dividing the total by 100 (1). Dietary glycemic load is the sum of the glycemic loads for all foods consumed in the diet. The concept of glycemic load was developed by scientists to simultaneously describe the quality (glycemic index) and quantity of carbohydrate in a meal or diet.

Disease Prevention

Type 2 Diabetes Mellitus
After a high-glycemic load meal, blood glucose levels rise more rapidly and insulin demand is greater than after a low-glycemic load meal. High blood glucose levels and excessive insulin secretion are thought to contribute to the loss of the insulin-secreting function of the pancreatic beta-cells that leads to irreversible diabetes (6). High dietary glycemic loads have been associated with an increased risk of developing type 2 diabetes mellitus (DM) in several large prospective studies. In the Nurses’ Health Study (NHS), women with the highest dietary glycemic loads were 37% more likely to develop type 2 DM over a 6-year period than women with the lowest dietary glycemic loads (7). Additionally, women with high-glycemic load diets that were low in cereal fiber were more than twice as likely to develop type 2 DM than women with low-glycemic load diets that were high in cereal fiber. The results of the Health Professionals Follow-up Study (HPFS), which followed male health professionals over six years were similar (8). In the NHS II study, a prospective study of younger and middle-aged women, those who consumed foods with the highest glycemic index values and the least cereal fiber were also at significantly higher risk of developing type 2 DM over the next eight years (9). The foods that were most consistently associated with increased risk of type 2 DM in the NHS and HPFS cohorts were potatoes (cooked or French-fried), white rice, white bread, and carbonated beverages (6).The Black Women's Health study, a prospective study in a cohort of 59,000 U.S. black women, found that women who consumed foods with the highest glycemic index values had a 23% greater risk of developing type 2 DM over eight years of follow-up compared to those who consumed foods with the lowest glycemic index values (10). In the American Cancer Society Cancer Prevention Study II, which followed 124,907 men and women for nine years, high glycemic load was associated with a 15% increased risk of type 2 DM (11). Further, in a cohort of over 64,000 Chinese women participating in the Shanghai Women's Health Study, high glycemic load was associated with a 34% increase in risk of type 2 DM; this positive association was much stronger among overweight women (12).


A U.S. ecological study of national data from 1909 to 1997 found that increased consumption of refined carbohydrates in the form of corn syrup, coupled with declining intake of dietary fiber, has paralleled the increase in prevalence of type 2 DM (13). Today, high-fructose corn syrup (HFCS) is used as a sweetener and preservative in many commercial products sold in the United States, including soft drinks and other processed foods. To make HFCS, the fructose content of corn syrup (100% glucose) has been artificially increased; common formulations of HFCS now include 42%, 55%, or 90% fructose (13). When consumed in large quantities on a long-term basis, HFCS is unhealthful and may contribute to other chronic diseases besides type 2 DM, including obesity and cardiovascular disease.

Cardiovascular Disease
Impaired glucose tolerance and insulin resistance are known to be risk factors for cardiovascular disease and type 2 DM. In addition to increased blood glucose and insulin concentrations, high dietary glycemic loads are associated with increased serum triglyceride concentrations and decreased HDL cholesterol concentrations; both are risk factors for cardiovascular disease (14, 15). High dietary glycemic loads have also been associated with increased serum levels of C-reactive protein (CRP), a marker of systemic inflammation that is also a sensitive predictor of cardiovascular disease risk (16). In the NHS cohort, women with the highest dietary glycemic loads had a risk of developing coronary heart disease (CHD) over the next ten years that was almost twice as high as those with the lowest dietary glycemic loads (17). The relationship between dietary glycemic load and CHD risk was more pronounced in overweight women, suggesting that people who are insulin resistant may be most susceptible to the adverse cardiovascular effects of high dietary glycemic loads (1). A similar finding was reported in a cohort of middle-aged Dutch women followed for nine years (18). More recently, a prospective study in an Italian cohort of 47,749 men and women, who were followed for almost eight years, found that a high glycemic load was associated with an increased risk of CHD in women but not in men (47). Yet, studies to date have reported mixed results, and more research is needed to determine if low glycemic index diets decrease the risk for CHD (19).

Obesity
In the first two hours after a meal, blood glucose and insulin levels rise higher after a high-glycemic load meal than they do after a low-glycemic load meal containing equal calories. However, in response to the excess insulin secretion, blood glucose levels drop lower over the next few hours after a high-glycemic load meal than they do after a low-glycemic load meal. This may explain why 15 out of 16 published studies found that the consumption of low-glycemic index foods delayed the return of hunger, decreased subsequent food intake, and increased satiety (feeling full) when compared to high-glycemic index foods (20). The results of several small, short-term trials (1-4 months) suggest that low-glycemic load diets result in significantly more weight or fat loss than high-glycemic load diets (21-23). Although long-term randomized controlled trials of low-glycemic load diets in the treatment of obesity are lacking, the results of short-term studies on appetite regulation and weight loss suggest that low glycemic-load diets may be useful in promoting long-term weight loss and decreasing the prevalence of obesity. A recent review of six randomized controlled trials concluded that overweight or obese individuals who followed a low-glycemic index/load diet experienced greater weight loss than individuals on a comparison diet that was either a high-glycemic index diet or an energy-restricted, low-fat diet (24). The length of the dietary interventions in these trials ranged from five weeks to six months.

Cancer
Evidence that high overall dietary glycemic index or high dietary glycemic loads are related to cancer risk is inconsistent. Prospective cohort studies in the U.S., Denmark, France, and Australia have found no association between overall dietary glycemic index or dietary glycemic load and breast cancer risk (25-28). In contrast, a prospective cohort study in Italy reported a positive association between breast cancer risk and high-glycemic index diets as well as high dietary glycemic loads (29). A prospective study in Canada found that postmenopausal but not premenopausal women with high overall dietary glycemic index values were at increased risk of breast cancer, particularly those who reported no vigorous physical activity (30), while a prospective study in the U.S. found that premenopausal but not postmenopausal women with high overall dietary glycemic index values and low levels of physical activity were at increased risk of breast cancer (31). In a French study of postmenopausal women, both glycemic index and glycemic load were positively associated with risk of breast cancer but only in a subgroup of women who had the highest waist circumference (median of 84 cm [33 inches]) (28). Higher dietary glycemic loads were associated with moderately increased risk of colorectal cancer in a prospective study of U.S. men, but no clear associations between dietary glycemic load and colorectal cancer risk were observed in a prospective studies of U.S. men (32), U.S. women (32-35), Swedish women (36), and Dutch men and women (37). However, one prospective cohort study of U.S. women found that higher dietary glycemic loads were associated with increased risk of colorectal cancer (38). One meta-analysis of case-control and cohort studies suggested that glycemic index and glycemic load were positively associated with colorectal cancer (39), but a more recently published meta-analysis did not find glycemic index or load to be significantly associated with colorectal cancer (40). Two separate meta-analyses reported that high dietary glycemic loads were associated with increased risk of endometrial cancer (39, 41). Although there is some evidence that hyperinsulinemia (elevated serum insulin levels) may promote the growth of some types of cancer (42), more research is needed to determine the effects of dietary glycemic load and/or glycemic index on cancer risk.

Gallbladder Disease
Results of two studies indicate that dietary glycemic index and glycemic load may be positively related to risk of gallbladder disease. Higher dietary glycemic loads were associated with significantly increased risks of developing gallstones in a cohort of men participating in the Health Professionals Follow-up Study (43) and in a cohort of women participating in the Nurses' Health Study (44). Likewise, higher glycemic index diets were associated with increased risks of gallstone disease in both studies (43-44). However, more epidemiological and clinical research is needed to determine an association between dietary glycemic index/load and gallbladder disease.

Disease Treatment

Diabetes Mellitus
Low-glycemic index diets appear to improve the overall blood glucose control in people with type 1 and type 2 diabetes mellitus (DM). A meta-analysis of 14 randomized controlled trials that included 356 diabetic patients found that low-glycemic index diets improved short-term and long-term control of blood glucose levels, reflected by clinically significant decreases in fructosamine and hemoglobin A1C levels (45). Episodes of serious hypoglycemia are a significant problem in people with type 1 DM. In a study of 63 men and women with type 1 DM, those randomized to a high-fiber, low-glycemic index diet had significantly fewer episodes of hypoglycemia than those on a low-fiber, high-glycemic index diet (46).

Lowering Dietary Glycemic Load

Some strategies for lowering dietary glycemic load include:
• Increasing the consumption of whole grains, nuts, legumes, fruits, and nonstarchy vegetables
• Decreasing the consumption of starchy high-glycemic index foods like potatoes, white rice, and white bread
• Decreasing the consumption of sugary foods like cookies, cakes, candy, and soft-drinks
See the table below for the glycemic index and glycemic load values of selected foods (4). Foods with higher glycemic index values are at the top of the table, while foods with lower glycemic index values are at the bottom of the table. To look up the glycemic index values for other foods, visit the University of Sydney’s GI Web site.

Glycemic Index and Glycemic Load Values for Selected Foods (Relative to Glucose)
Food	Glycemic Index (Glucose=100)	Serving size	Carbohydrate per serving (g)	Glycemic Load per serving
Dates, dried	103	2 oz	40	42
Cornflakes	81	1 cup	26	21
Jelly beans	78	1 oz	28	22
Puffed rice cakes	78	3 cakes	21	17
Russet potato (baked)	76	1 medium	30	23
Doughnut	76	1 medium	23	17
Soda crackers	74	4 crackers	17	12
White bread	73	1 large slice	14	10
Table sugar (sucrose)	68	2 tsp	10	7
Pancake	67	6" diameter	58	39
White rice (boiled)	64	1 cup	36	23
Brown rice (boiled)	55	1 cup	33	18
Spaghetti, white; boiled 10-15 min	44	1 cup	40	18
Spaghetti, white; boiled 5 min	38	1 cup	40	15
Spaghetti, whole wheat; boiled	37	1 cup	37	14
Rye, pumpernickel bread	41	1 large slice	12	5
Oranges, raw	42	1 medium	11	5
Pears, raw	38	1 medium	11	4
Apples, raw	38	1 medium	15	6
All-Bran™ cereal	38	1 cup	23	9
Skim milk	32	8 fl oz	13	4
Lentils, dried; boiled	29	1 cup	18	5
Kidney beans, dried; boiled	28	1 cup	25	7
Pearled barley; boiled	25	1 cup	42	11
Cashew nuts	22	1 oz	9	2
Peanuts	14	1 oz	6	1

 

References

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Written in December 2005 by:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University

Updated in February 2009 by:
Victoria J. Drake, Ph.D.
Linus Pauling Institute
Oregon State University

Reviewed in February 2009 by:
Simin Liu, M.D., M.S., M.P.H., Sc.D.
Professor and Director, Program on Genomics and Nutrition
Professor of Epidemiology and Medicine
UCLA School of Public Health

Last updated 4/38/2010  Copyright 2003-2011  Linus Pauling Institute

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Disclaimer

The Linus Pauling Institute Micronutrient Information Center provides scientific information on health aspects of micronutrients and phytochemicals for the general public. The information is made available with the understanding that the author and publisher are not providing medical, psychological, or nutritional counseling services on this site. The information should not be used in place of a consultation with a competent health care or nutrition professional.
The information on micronutrients and phytochemicals contained on this Web site does not cover all possible uses, actions, precautions, side effects, and interactions. It is not intended as medical advice for individual problems. Liability for individual actions or omissions based upon the contents of this site is expressly disclaimed.