Are Antibacterial Soaps Harming Your Health?

Reposted from Life Extension
http://blog.lef.org/2012/09/antibacterial-soaps-bad-health.html

By Maylin Rodriguez-Paez, RN

Antibacterial soaps are all over the market, but should they be? As it turns out, an ingredient found in most of them — a chemical called triclosan — may be bad for your health.

Concerns have been raised over triclosan's use after several animal studies have linked it to severe health problems.

Triclosan is found in many household products including body washes, detergents, dishwashing liquid, and toothpastes. Unfortunately, it seeps into the human body and has been detected in urine samples and even in breast milk.¹
Because of safety concerns, the FDA is investigating triclosan; however, their research is not conclusive as of yet. Of course, we’re not going to wait for them to finish.

We don’t like it, and we think it’s pretty dangerous stuff.

Triclosan Disrupts Thyroid Function

Studies show animals exposed to triclosan have reduced thyroid hormone levels. This effect has been seen in frogs and rats.^2,3 Scientists believe this might have to do with triclosan’s resemblance to thyroid hormone.

Now to be fair, a human study found no real thyroid effects from triclosan.⁴ But until more research is conducted, we’d prefer to err on the side of caution.

Triclosan Grows Estrogen-Sensitive Tissues

Triclosan is a xenoestrogen. This means it looks and acts like estrogen. For instance, a study on rats showed that triclosan increased uterine growth.⁵
Could this result in fibroids or endometriosis in people? Maybe. Again, more research is needed.

Triclosan also disrupts the normal sexual development of young rats.⁶ This is a sure sign of hormonal imbalances brought on by triclosan exposure. This is certainly not a good thing for rats or humans.

Natural Alternatives to Antibacterial Soaps

Soaps don’t have to contain harsh ingredients to be effective. Try products with essential oils instead.

These oils not only clean the skin but may also be therapeutic. For example, tea tree essential oil has been shown to ease skin inflammation⁷ and even promote wound healing.⁸
Here are some key essential oils to look out for:

• Tea tree oil
• Grapefruit seed extract
• Cinnamon
• Oregano
• Lemon

A Safe Way to Wash your Hands

You don’t have to use antibacterial soaps to clean your hands. All you need is regular soap, good hand washing techniques, and warm water.

The key to good hand washing is to scrub your hands vigorously and to target areas like the space beneath your fingernails and the area between your fingers. “Germs” really like to hide in these places.

Wash your hands for 20 seconds or the time it takes you to sing the “Happy Birthday” song. That should do the trick.

The bottom line is this: To stay clean, skip the chemicals and stick with good old-fashioned hand soap. It’s perfectly sufficient for keeping your hands germ free!

References:

1. J Appl Toxicol. 2011 May;31(4):285-311.
2. Aquat Toxicol. 2006 Dec 1;80(3):217-27.
3. Environ Toxicol Chem. 2010 Dec;29(12):2840-4.
4. Sci Total Environ. 2012 Feb 1;416:75-9.
5. Toxicol Lett. 2012 Jan 25;208(2):142-8.
6. Toxicol Sci. 2010 Sep;117(1):45-53.
7. Skin Pharmacol Physiol. 2012;25(3):162-3.
8. Am J Infect Control. 2004 Nov;32(7):402-8.

How to Avoid Acetaminophen Toxicity

Reposted from Life Extension
http://blog.lef.org/2013/08/how-to-avoid-acetaminophen-toxicity.html

By Michael A. Smith, MD

What if a dietary supplement had been proven to cause liver damage, liver failure, and death?

What if each year this same supplement caused 100,000 calls to poison control centers, 56,000 emergency room visits, 26,000 hospitalizations, and more than 450 deaths from liver failure alone?

You know the answer. The FDA would immediately shut down the supplement company and seek to incarcerate the principals for life.

What if, on the other hand, a highly profitable drug caused this much disease and death? To no one’s surprise, the FDA’s response is to do the equivalent of nothing.

Don’t Assume Over-the-Counter Drugs are Safe

Many people assume that over-the-counter medications are safe when taken as directed. Yet even at recommended doses, aspirin can cause ulcers, antihistamines can cause sedation, and acetaminophen can cause serious liver damage.

You can read about some of these risks in the product information that accompanies over-the-counter medicines. For example, the acetaminophen package insert warns about taking the drug if you consume three or more alcoholic drinks a day.

The link between acetaminophen, alcohol, and an increased risk of liver damage was identified in the 1980s. This research identified another factor that can increase the risks associated with acetaminophen: fasting. This can refer to fasting due to abdominal upset or pain, nausea, vomiting, loss of appetite, anorexia, or malnutrition.

But most people assume the dangerous side effects occur when the drugs are abused or accidently misused. That’s not always the case.

Liver Failure at Recommended Doses

A 25-year-old, previously healthy, Swedish man developed gastroenteritis while on holiday in Turkey. For a day and a half, before flying home, the man experienced nausea and vomiting, and he was unable to keep food or liquid down.

When he arrived, after the long flight home, he was taken directly to a hospital. As his condition worsened, he was diagnosed with liver failure and transferred to await a liver transplant.

Information from his brother, who had been with him in Turkey, indicated that the he had taken 500 mg to 1,000 mg of acetaminophen two to three times each day — well below the maximum daily dose of 4,000 mg.¹
What had the Swedish man done wrong to develop liver failure? Nothing! He took acetaminophen merely to ease abdominal pain, as do thousands of people each day. He followed the rules but nearly died.

The doctors presenting this case concluded that severe liver toxicity “can occur after low, repeated doses of paracetamol.” They added that the drug should not be used under conditions of starvation, including acute gastroenteritis with nausea and vomiting.¹

Yet today, despite this report and many others, acetaminophen products do not list a warning advising people against using the drug when they are unable to eat.

Acetaminophen is a Powerful Liver Toxin

Many drugs can cause liver damage, liver failure, and death. Yet acetaminophen prompts the most calls to poison control centers — more than 100,000 per year. According to statistics published in 2006, acetaminophen accounts for about 56,000 emergency room visits, 26,000 hospitalizations, and more than 450 annual deaths from liver failure.²
In humans the metabolism of acetaminophen, even at standard doses, releases small amounts of a toxic substance, N-acetyl-p-benzoquinone imine (or NAPQI). With excessive doses, a much larger amount of this toxin is formed.^{3, 4}

In order to remove the toxin, liver cells conjugate it with glutathione. This detoxifies NAPQI and allows it to be safely removed from the body. But here’s the problem: Glutathione levels quickly become depleted in the process, especially during periods of fasting — like when you’re sick. NAPQI levels rise and liver injury ensues.

What You Can Do

Given the potential risks of overusing acetaminophen, it is wise to use it sparingly, if at all. Those who have to take acetaminophen need to be aware of the factors that can increase the risks.

These include taking acetaminophen while having three or more alcohol drinks a day, using multiple acetaminophen-containing products, or taking acetaminophen when you are unable to eat.

Be sure to carefully read the label of any over-the-counter medication. If you are taking more than one medication, make sure that only one contains acetaminophen. Read the warnings. Stay within the recommended doses of acetaminophen. Over-medicating by even small amounts raises acetaminophen’s risks.

Of course, it naturally follows that supplementing with glutathione-boosting nutrients like N-acetyl-cysteine can help, along with liver supporting nutrients like milk thistle.

Watch Out for Hidden Acetaminophen

Here are some frequently prescribed medications that contain acetaminophen. This list is not exhaustive; there are many other prescription drugs and scores of over-the-counter remedies that contain acetaminophen.

If your doctor prescribes a drug for pain, headache or muscle tension, ask your doctor or pharmacist whether it contains acetaminophen.

• Tylenol® No.2, Tylenol® No.3, Tylenol® No.4: acetaminophen and codeine
• Vicodin®, Lorcet®, Lortab®, Maxidone®, Zydone®: acetaminophen and hydrocodone
• Percocet®, Roxicet™: acetaminophen and oxycodone
• Fioricet®: acetaminophen, butalbital, and caffeine
• Darvocet-N®, Wygesic®: acetaminophen and propoxyphene

References:

1. J Intern Med. 1992 May;231(5):567-70.
2. Pharmacoepidemiol Drug Saf. 2006 Jun;15(6):398-405.
3. Proc Natl Acad Sci U S A. 1984 March; 81(5): 1327–1331.
4. Pharmacognosy Res. 2011 Oct-Dec; 3(4): 250–255.

Powerful Protection Against Cellular Aging

Reposted from Life Extension
http://www.lef.org/magazine/mag2012/oct2012_Powerful-Protection-Against-Cellular-Aging_01.htm

By Michael Downey

 

Conclusive evidence now indicates that PQQ (pyrroloquinoline quinone) activates cell signaling pathways that have the potential to reverse cellular aging!1
PQQ has previously been shown to promote growth of new mitochondria within aging cells,1-3 up-regulate cellular metabolism,1,2 protect neurons,4-7 and repair DNA!1,8
These and other synergistic signaling effects have the combined ability to promote longevity at the critical subcellular level.
PQQ has been found in all plant species ever tested. Scientists have gone so far as to state that PQQ may be "vital to life."3

An Essential Anti-Aging Nutrient

Scientists have found that PQQ, a critical coenzyme, plays a leading role in boosting critical cell signaling mechanisms.3
These signaling pathways regulate a variety of physiological and molecular processes throughout the body10—processes that have an impact on key biomarkers of aging, such as mitochondrial function11-16 and cellular defense against oxidative stress.10

Through these effects, the cell signaling power of PQQ targets aging at both the cellular and subcellular levels.
New research confirm that humans can obtain these multiple benefits after even just short-term supplementation.17
A wealth of studies now confirm that PQQ's cell-signaling activity translates into substantial protection against degenerative and age-related conditions, such as mitochondrial dysfunction,1 heart degeneration,18-20 brain injury, and cognitive decline.21-40 As one example, research shows that 20 mg of PQQ daily may reverse age-related cognitive decline in aging humans!
Since PQQ cannot be synthesized by your body it is necessary to obtain PQQ from outside sources.24,41-43 Fortunately, compared to other plant compounds, PQQ has greater solubility and bioavailability. PQQ is water-soluble and therefore, more easily absorbed at low supplemental intakes.1,44,45
Let's take a look at the modes of action behind PQQ's multiple effects.

PQQ and Cell Signaling

How can PQQ target multiple aging factors?
The answer lies in the potent and unique capacity of PQQ to activate cell signaling pathways, especially those directly involved in cellular energy metabolism.
Also, similar to the action of CoQ10, PQQ actively participates in the energy transfer within the mitochondria that supplies the body with most of its bioenergy.
PQQ can even trigger spontaneous mitochondrial biogenesis—the creation of fresh, new mitochondria!
Specific cell signaling molecules have been found to be directly activated by PQQ.

Cell Signaling Pathways

Early studies revealed that animals deprived of PQQ exhibit signs of accelerated aging in the form of elevated plasma glucose concentrations, impaired oxygen metabolism, stunted growth, compromised immunity, impaired reproductive capability, reduced numbers and survival rate of offspring, and a decrease in energy-producing mitochondria in their tissue. Reintroducing PQQ to their diet reversed these effects, increasing mitochondrial numbers and restoring systemic function.46-48
PQQ is now linked to favorable effects on cell development, metabolism, and mitochondrial biogenesis. It provides the potential to reverse cellular aging and age-related disease by:

• Stimulating spontaneous growth of new mitochondria within aging cells.1
• Regulating gene expression.3
• Promoting tumor cell death from apoptosis.49
• Supporting mitochondrial protection and repair.1
• Providing powerful antioxidant support to mitochondria and other body molecules—with up to 5,000 times the effect of other antioxidants,4 and protecting the brain's cells and neurotransmitter systems against neurotoxicity5,39,50 and amyloid-beta protein.36

The end result of PQQ's activity is subcellular anti-aging and enhanced longevity.
(For more on these beneficial pathways, see previous box titled, 'PQQ and Cell Signaling.')

Heart Benefits

PQQ's cell signaling activities produce measurable health improvements, especially cardio-protective and neuro-protective benefits.
For example, research with animals found that supplementation with PQQ decreased the size of the area of the heart injured by acute coronary artery blockage. This protective effect was found whether PQQ was given before or after the event—suggesting taking PQQ within the first hours following a cardiac event could deliver invaluable benefit to patients.18
Following up on this research, scientists then tested both PQQ and the common post-heart-attack treatment metoprolol (Lopressor®). They found that, while both reduced the size of the damaged area, there was a greater increase in mitochondrial energy-producing functions with PQQ.
And only PQQ lowered lipid peroxidation!
The study team concluded that "PQQ is superior to metoprolol in protecting mitochondria from ischemia/reperfusion oxidative damage."19
These same scientists found in later animal research, that "PQQ reduces oxidative stress, mitochondrial dysfunction, and cell death" in cardiac muscle cells.20

What You Need to Know

PQQ: Powerful Protection Against Cellular Aging

• Pyrroloquinoline quinone (PQQ) activates a number of vital, cell signaling pathways involved in protecting against cellular aging!
• PQQ-powered signaling mechanisms create fresh mitochondria,1-3 upregulate cellular metabolism,1,2 improve cognitive performance and protect neurons,4-7 and repair DNA damage!8
• These synergistic effects deliver substantial, subcellular anti-aging and enhanced longevity.
• Evidenced by studies verifying its wide cardioprotective and neuroprotective effects, PQQ beneficially modulates a host of key biomolecular functions!

Brain Effects

Scientists found in pre-clinical trials that PQQ reversed cognitive impairment caused by oxidative stress and improved performance on memory tests.21 PQQ was shown to protect against a pathologic gene protein associated with Parkinson's disease. 22 Much of the long-term neurological damage that arises after a stroke or spinal cord injury is caused by reactive nitrogen species which impose severe stresses on damaged neurons. However, PQQ was found to suppress reactive nitrogen species in induced strokes.24
PQQ also blocked a source of reactive nitrogen species following spinal cord injury.25 Researchers concluded that PQQ significantly reduces the size of the damaged area of the brain even if administered 3 hours after the stroke!27 Additionally, it provides potent protection against the inflammation and oxidative damage that results from the sudden return of blood and nutrients to tissues deprived of them by stroke.26 It would seem that PQQ should become a standard nutrient in the hospital emergency room setting for rapid administration to stroke victims.

PQQ and Mitochondrial Biogenesis

Greater mitochondrial damage has been found in brain cells of humans over 70 relative to those in their early 40s. Many scientists believe mitochondrial longevity and the number of functioning mitochondria determine overall human longevity.51-53
The coenzyme PQQ, has been shown to induce mitochondrial biogenesis—the growth of new mitochondria in aging cells.
While coenzyme Q10, or CoQ10, optimizes the function of mitochondria, PQQ activates genes that govern mitochondrial reproduction, protection, and repair.
To date, the only ways known to reliably stimulate mitochondrial biogenesis have been sustained calorie restriction or strenuous physical activity—potentially too rigorous for aging individuals.
With its power to safely trigger mitochondrial biogenesis, PQQ represents an extraordinary advance in the quest to reverse cellular aging.

Illustrating its cell signaling mechanism, PQQ protects neurons by modifying a key receptor site within our brain's neurotransmitter system.28,29 This inhibits excitotoxicity, a response to long-term over-stimulation of neurons that is associated with many neurodegenerative diseases and seizures.30-32
PQQ was shown to block neurotoxicity induced by other toxins, including mercury, a factor suspected to play a role in the development of Alzheimer's disease.5,33
Accumulating research indicates that PQQ serves as an intervention in Alzheimer's and Parkinson's disease—blocking development, and oxidative effects, of both the amyloid beta protein associated with Alzheimer's and the alpha-synuclein protein associated with Parkinson's, before they can cause damage.34-37
PQQ has been observed to deliver substantial cognitive benefits, including improved memory and attention.9,38 It activates the manufacture and release of an important, neuro-protective, nerve growth factor.38 Scientists tested PQQ's cognitive effects in a double-blind, placebo-controlled clinical trial conducted on humans. In this study of healthy individuals ranging from 45 to 65 years of age, 20 mg a day of PQQ produced clear improvements on standard tests of greater cognitive function. Also, the PQQ test group scored two-fold higher on memory tests than the control group.9
Scores were dramatically higher for a third group that received 300 mg per day of CoQ10 along with their 20 mg of PQQ. This underscores the powerful cognitive benefits of supplementation with agents shown to be involved in mitochondrial energy production.9

PQQ and Gene Expression

Recent rodent research on gene expression has shown that an induced deficiency of the coenzyme pyrroloquinoline quinone, or PQQ, results in an altering of the expression of a total of 438 genes.54 When the diet is then supplemented with PQQ, the genetic expression pattern reverts to normal. On investigation, the genes most affected by PQQ turned out to be those responsible for:58

• Cell signaling
• Cellular stress
• Growth of new mitochondria
• MAP kinase pathways (cell-surface-to-nucleus signaling proteins)
• Transport of metabolites

These findings shed light on PQQ's genetic involvement with cell signaling, antioxidant activity, and mitochondrial biogenesis.

Summary

Through its broad cell signaling activity, PQQ (pyrroloquinoline quinone) modulates the many pathways of aging!
Scientific findings indicate that PQQ-enhanced signaling stimulates mitochondrial biogenesis,1-3 boosts cellular metabolism,1, improves cognitive performance and protects neurotransmitters, 4-7 and repairs DNA!8
Together, these mechanisms support subcellular anti-aging and promote longevity.
Studies have shown that PQQ beneficially modulates biomolecular functions that result in substantial heart and brain defense. As one example, scientists found that PQQ helped produce remarkable reversal of cognitive decline in aging humans!9
If you have any questions on the scientific content of this article, please call a Life Extension® Health Advisor at 1-866-864-3027.

Protecting Mitochondrial DNA

Degradation of mitochondrial DNA leads to mitochondria senescence and death—and extinction of the "host" organism.
As the power generators responsible for almost all bioenergetic production, mitochondria are the site of enormous oxidative activity. A nearly incalculable number of electrons are constantly flowing within the mitochondria, throwing off an equally enormous number of free radicals.
As a result, mitochondria are much more vulnerable to biochemical insults than other cellular structures.
And as scientists have discovered over the past several decades, mitochondrial DNA—relative to genetic DNA in the cell's nucleus (nuclear DNA)—possesses few defenses against free radical damage.55,56
Nuclear DNA is protected by numerous guardian proteins—histones and repair enzymes—that blunt the impact of free radicals. Similar repair systems do not exist to protect mitochondrial DNA.55-57
Also, nuclear DNA is housed within a protective double-membrane that separates it from the rest of the cell. This double-membrane is complemented by a dense matrix of filament proteins called the nuclear lamina, a kind of hard shell casing to further buffer DNA from external impacts.
By comparison, mitochondrial DNA is left almost entirely exposed. It is attached directly to the inner membrane where the mitochondria's electrochemical furnace rages continuously, generating an enormous volume of toxic reactive oxygen species.
The mitochondria rank among the physiological structures most vulnerable to destruction from oxidative damage.
And scientific studies link genetic mutation within the mitochondria to human aging.57-59
PQQ's formidable free radical-scavenging capacity furnishes the mitochondria with superior antioxidant protection.
As a bioactive coenzyme, PQQ supports optimal function within the mitochondria which is responsible for supplying the body with most of its bioenergy.60
Unlike other antioxidant compounds, PQQ's ex-ceptional stability allows it to carry out thousands of these electron transfers without undergoing molecular breakdown.
In fact, PQQ is up to 5,000 times more efficient in sustaining antioxidant capacity than other common antioxidant compounds, such as ascorbic acid.4

References

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2. Liang H, Ward WF. PGC-1alpha: a key regulator of energy metabolism. Adv Physiol Educ. 2006 Dec;30(4):145-51.
3. Rucker R, Chowanadisai W, Nakano M. Potential physiological importance of pyrroloquinoline quinone. Altern Med Rev. 2009;14:268-77.
4. Stites TE, Mitchell AE, Rucker RB. Physiological importance of quinoenzymes and the O-quinone family of cofactors. J Nutr. 2000 Apr;130(4):719-27.
5. Zhang P, Xu Y, Sun J, Li X, Wang L, Jin L. Protection of pyrroloquinoline quinone against methylmercury-induced neurotoxicity via reducing oxidative stress. Free Radical Research. 2009 Mar;43(3):224-33.
6. Hara H, Hiramatsu H, Adachi T. Pyrroloquinoline quinone is a potent neuroprotective nutrient against 6-hydroxydopamine-induced neurotoxicity. Neurochemical Research. 2007 Mar;32(3):489-95.
7. Zhang JJ, Zhang RF, Meng XK. Protective effect of pyrroloquinoline quinone against Abeta-induced neurotoxicity in human neuroblastoma SH-SY5Y cells. Neurosc Lett. 2009 Oct 30;464(3):165-9.
8. Available at: http://www.ncbi.nlm.nih.gov/gene/1387. Accessed July 5, 2012.
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10. Misra HS, Rajpurohit YS, Khairnar NP. Pyrroloquinoline-quinone and its versatile roles in biological processes. J Biosci. 2012 Jun;37(2):313-25.
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12. Linnane AW, Marzuki S, Ozawa T, Tanaka M. Mitochondrial DNA mutations as an important contributor to ageing and degenerative diseases. Lancet. 1989 Mar 25;1(8639):642-5.
13. Lanza IR, Nair KS. Mitochondrial metabolic function assessed in vivo and in vitro. Curr Opin Clin Nutr Metab Care. 2010 Sept;13(5):511.
14. Mota MP, Peixoto FM, Soares JF, et al. Influence of aerobic fitness on age-related lymphocyte DNA damage in humans: relationship with mitochondria respiratory chain and hydrogen peroxide production. Age (Dordr). 2010 Sept;32(2):337-46.
15. Tranah G. Mitochondrial-nuclear epistasis: Implications for human aging and longevity. Ageing Res Rev. 2010 Jun 25.
16. Cho DH, Nakamura T, Lipton SA. Mitochondrial dynamics in cell death and neurodegeneration. Cell Mol Life Sci. 2010 Oct;67(20):3435-47.
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18. Zhu BQ, Zhou HZ, Teerlink JR, Karliner JS. Pyrroloquinoline quinone (PQQ) decreases myocardial infarct size and improves cardiac function in rat models of ischemia and ischemia/reperfusion. Cardiovasc Drugs Ther. 2004 Nov;18(6):421-31.
19. Zhu BQ, Simonis U, Cecchini G, et al. Comparison of pyrroloquinoline quinone and/or metoprolol on myocardial infarct size and mitochondrial damage in a rat model of ischemia/reperfusion injury. J Cardiovasc Pharmacol Ther. 2006 Jun;11(2):119-28.
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21. Ohwada K, Takeda H, Yamazaki M, et al. Pyrroloquinoline quinone (PQQ) prevents cognitive deficit caused by oxidative stress in rats. J Clin Biochem Nutr. 2008 Jan;42:29-34.
22. Nunome K, Miyazaki S, Nakano M, Iguchi-Ariga S, Ariga H. Pyrroloquinoline quinone prevents oxidative stress-induced neuronal death probably through changes in oxidative status of DJ-1. Biol Pharm Bull. 2008 Jul;31(7):1321-6.
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25. Hirakawa A, Shimizu K, Fukumitsu H, Furukawa S. Pyrroloquinoline quinone attenuates iNOS gene expression in the injured spinal cord. Biochem Biophys Res Commun. 2009 Jan 9;378(2):308-12.
26. Jensen FE, Gardner GJ, Williams AP, Gallop PM, Aizenman E, Rosenberg PA. The putative essential nutrient pyrroloquinoline quinone is neuroprotective in a rodent model of hypoxic/ischemic brain injury. Neuroscience. 1994 Sep;62(2):399-406.
27. Zhang Y, Feustel PJ, Kimelberg HK. Neuroprotection by pyrroloquinoline quinone (PQQ) in reversible middle cerebral artery occlusion in the adult rat. Brain Res. 2006 Jun 13;1094(1):200-6.
28. Aizenman E, Hartnett KA, Zhong C, Gallop PM, Rosenberg PA. Interaction of the putative essential nutrient pyrroloquinoline quinone with the N-methyl-D-aspartate receptor redox modulatory site. J Neurosci. 1992 Jun;12(6):2362-9.
29. Aizenman E, Jensen FE, Gallop PM, Rosenberg PA, Tang LH. Further evidence that pyrroloquinoline quinone interacts with the N-methyl-D-aspartate receptor redox site in rat cortical neurons in vitro. Neurosci Lett. 1994 Feb 28;168(1-2):189-92.
30. Hossain MA. Molecular mediators of hypoxic-ischemic injury and implications for epilepsy in the developing brain. Epilepsy Behav. 2005 Sep;7(2):204-13.
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36. Zhang JJ, Zhang RF, Meng XK. Protective effect of pyrroloquinoline quinone against Abeta-induced neurotoxicity in human neuroblastoma SH-SY5Y cells. Neurosci Lett. 2009 Oct 30;464(3):165-9.
37. Kim J, Kobayashi M, Fukuda M, et al. Pyrroloquinoline quinone inhibits the fibrillation of amyloid proteins. Prion. 2010 Jan;4(1):26-31.
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50. Hara, H, Hiramatsu H, Adachi T. Pyrroloquinoline quinone is a potent neuroprotective nutrient against 6-hydroxydopamine-induced neurotoxicity. Neurochem Res 2007 Mar;32(3):489-95.
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56. Miquel J. An update on the mitochondrial-DNA mutation hypothesis of cell aging. Mutat Res.1992 Sep;275(3-6):209-16.
57. Wei YH, Ma YS, Lee HC, Lee CF, Lu CY. Mitochondrial theory of aging matures—roles of mtDNA mutation and oxidative stress in human aging. Zhonghua Yi Xue Za Zhi (Taipei). 2001 May;64(5):259-70.
58. Lee HC, Wei YH. Oxidative stress, mitochondrial DNA mutation, and apoptosis in aging. Exp Biol Med (Maywood). 2007 May;232(5):592-606.
59. Wei YH, Lee HC. Oxidative stress, mitochondrial DNA mutation, and impairment of antioxidant enzymes in aging. Exp Biol Med (Maywood). 2002 Oct;227(9):671-82.
60. Bauerly K, Harris C, Chowanadisai W, et al. Altering pyrroloquinoline quinone nutritional status modulates mitochondrial, lipid, and energy metabolism in rats. PLoS One. 2011;6(7):e21779. Epub 2011 Jul 21.

Newly Discovered Health Benefits of Vitamin C

Reposted from Life Extension
http://www.lef.org/magazine/mag2008/apr2008_Newly-Discovered-Benefits-Of-Vitamin-C_01.htm

By Julius Goepp, MD

Vitamin C is rapidly finding new applications in protecting against endothelial dysfunction, high blood pressure, and the blood vessel changes that precede heart disease.1-3 Additional research is discovering that vitamin C can be helpful in preventing asthma,4 protecting against cancer,5 and supporting healthy blood sugar levels in diabetics.6 While often taken for granted, vitamin C is a critical supplement in your program to improve cardiac health and avoid degenerative diseases. Vitamin C—Breakthroughs in Cardiovascular Health One of the most intensely studied areas of vitamin C benefits is in the area of cardiovascular health. Researchers are finding that vitamin C impacts several aspects of cardiac health, ranging from blood pressure to endothelial health. Perhaps it’s not surprising that as the relationship between oxidative damage, inflammation, and atherosclerosis becomes increasingly investigated by science, vitamin C is seen as a key protective element against many aspects of cardiovascular disease. For years, scientists have warned us against the dangerous buildup of plaque that can lead to a heart attack or stroke. Researchers are investigating the possibilities that vitamin C may play a role in reducing our risk of plaque buildup. In the early stages of atherosclerosis, white blood cells called monocytes migrate and stick to the walls of the endothelium. Once this process begins, our vessel walls begin to thicken and lose their elasticity, which paves the way for atherosclerosis. Interestingly, British researchers studied the effects of vitamin C supplementation (250 mg/day) on this adhesion process in 40 healthy adults.7 Before the study, subjects with low pre-supplementation levels of vitamin C had 30% greater monocyte adhesion than normal, putting them at higher risk for atherosclerosis. Impressively, after six weeks of supplementation, the rate of this dangerous monocyte adhesion actually fell by 37%. The researchers went on to demonstrate that the same small dose of vitamin C was able to normalize a molecule that white blood cells use to adhere to the endothelium.8 The findings indicated that through supplementation with vitamin C, scientists were able to regulate how specific genes produce vital proteins, thereby reducing the risk of cardiovascular disease at the molecular level. Building on this important work, scientific researchers in 2005 studied the impact of antioxidant supplementation on degenerative aortic stenosis, an age-associated heart valve disorder that has an inflammatory component.9 The scientists studied 100 patients with mild-to-moderate aortic stenosis, randomly assigning 41 of them to receive vitamins C (1,000 mg/day) and E (400 IU/day), 39 to receive vitamin C only (1,000 mg/day), and 20 to serve as untreated controls. Both supplemented groups experienced significant reductions in levels of several important adhesion molecules, potentially reducing further inflammatory damage to the heart valves. And just as vitamin C helps preserve vascular integrity, it is also proving beneficial in combating other risk factors for endothelial dysfunction and cardiovascular disease. What You Need to Know: Vitamin C Ascorbic acid, or vitamin C, is a potent antioxidant with increasingly diverse uses in health promotion and disease prevention. Every step in the progression of atherosclerosis can benefit from the antioxidant power of vitamin C, from preventing endothelial dysfunction and altering lipid profiles and coagulation factors to preventing blood vessel changes that can lead to strokes and other vascular catastrophes. Vitamin C supplements reduce cellular DNA damage that is the vital first step in cancer initiation and also reduce the inflammatory changes that allow a malignant cell to grow into a dangerous tumor. Vitamin C supplements enhance the health-promoting effects of exercise and reduce exercise-induced oxidative damage. Vitamin C supplements also dramatically combat the oxidative damage caused by smoking and exposure to tobacco smoke. In respiratory conditions, vitamin C supplements help avert or shorten the duration of common colds and may mitigate the risk of serious respiratory conditions like asthma. Vitamin C supplements can speed the clearance of the stomach disease-causing bacterium Helicobacter pylori and cut the risk of gastric cancer it causes. Lipid Profiles, Blood Pressure, and Body Mass Index Most people have learned to pay attention to the amount and kinds of fats and cholesterol in their blood (lipid profiles), their blood pressure, and their body mass index (BMI), the most meaningful measure of how weight and health are related. This group of parameters not only influences endothelial function but is instrumental in laying down atherosclerotic plaque, helping set the stage for atherosclerosis. Data from just the past few years reveal that vitamin C plays an important role in helping to prevent such a scenario. In 2000, British researchers reported a six-month, double-blind study of vitamin C 500 mg/day versus placebo in 40 men and women, aged 60-80 years.2 The study was a “crossover” design in which subjects took the assigned pills for three months, stopped them for one week, and then reversed their assignments for another three months; this is a particularly strong study design because it helps to eliminate individual differences. The results were impressive—daytime systolic blood pressure dropped by an average of 2 mm Hg, with the greatest drop seen in subjects who had the highest initial pressures. Women in the study also had a modest increase in their beneficial high-density lipoprotein (HDL) levels. The authors concluded that these effects might “contribute to the reported association between higher vitamin C intake and lower risk of cardiovascular disease and stroke.” Researchers in South Carolina conducted a 2002 study of 31 patients with a mean age of 62 years, who were randomly assigned to take 500, 1,000, or 2,000 mg of vitamin C daily for eight months.10 This research group actually found a drop in both systolic (4.5 mm Hg) and diastolic (2.8 mm Hg) blood pressure over the course of supplementation, although there was no change in blood lipid levels. Interestingly, this study found no differences between the groups taking the various doses, though the number of subjects was small and a larger study might have demonstrated important dose-related differences. Body mass index (BMI) and waist circumference correlate well with risk for cardiovascular diseases and diabetes.11 A landmark 2007 study from nutritionists at the University of Arizona explored the relationships between vitamin C levels, body mass index, and waist circumference.12 In 118 sedentary, non-smoking adults, 54% of whom were classified as obese and 24% overweight by BMI standards, lower vitamin C levels were significantly correlated with higher BMI, percentage of body fat, and waist circumference. Women with higher vitamin C levels also had higher levels of the fat-suppressing hormone, adiponectin. This remarkable study demonstrated a vital relationship between vitamin C levels and obesity-related risk factors for cardiovascular disease. Vascular Stiffness and Coagulation The development of atherosclerosis involves dysfunction of the vascular endothelium. As plaque accumulates and as vessel walls thicken, blood vessels become increasingly stiff, making them less able to participate in blood pressure control and to deliver appropriate amounts of blood flow. Endothelial dysfunction increases the tendency for arterial blockage due to a blood clot, or thrombosis. Like several other “atherogenic” changes, these effects are related to the impact of free-radical damage.13 Vitamin C’s antioxidant characteristics are showing great power in reducing or even reversing some of these ominous vascular changes. Medical researchers explored the impact of vitamin C supplements on both arterial stiffness and platelet aggregation (an important early step in clot formation).13 They provided vitamin C in a single 2,000 mg oral dose, or placebo, to healthy male volunteers. Just six hours after supplementation, measures of arterial stiffness decreased by 10% in the supplemented group, and platelet aggregation (as stimulated chemically) by 35%, with no changes at all seen in the placebo group. As the authors point out, this impressive impact of vitamin C even in healthy subjects may imply an even greater effect in patients with atherosclerosis or cardiovascular risk factors, and that “vitamin C supplementation might prove an effective therapy in cardiovascular disease.” Many other studies have further advanced our understanding of how vitamin C might reduce atherosclerosis risk factors.1,8,14-16 Finnish researchers studied 440 adults aged 45-69 years with elevated total serum cholesterol.3 Subjects took daily doses of just 500 mg slow-release vitamin C and 272 IU vitamin E and were followed for six years for evidence of progression of atherosclerotic changes in blood vessels. The chief study outcome was the intima-media thickness, or IMT (an indicator of stroke risk) of the carotid arteries, which supply blood to the brain. Supplementation with vitamins C and E significantly decreased the rate of IMT increase over the six-year period by 26%. Importantly, this effect was even larger in people with low baseline vitamin C levels and those with pre-existing plaques in their coronary arteries. In other words, supplementation seemed to provide the greatest benefit to those with the greatest need. This study shows that supplementation with vitamin C slows down the progression of stroke-inducing atherosclerosis. Maximizing Healthy Lifestyle Choices In our efforts to reduce the risk of heart disease, regular exercise plays an important part in maintaining a healthy lifestyle. The increased delivery of oxygen-rich blood to tissues is a vital part of the process—but it can also produce destructive free radicals.17 Clearly, the solution is not to stop exercising! Rather, a series of recent studies shows how supplementation with vitamin C can mitigate free-radical damage from intense exercise. British researchers evaluated the effects of just two weeks of modest vitamin C supplementation (200 mg twice daily) on the recovery from an unaccustomed bout of exercise.18 Eight healthy men were given either a placebo or vitamin C supplementation each day, and after 14 days performed a 90-minute-long running test. The supplemented group had less muscle soreness, better muscle function, and lower blood levels of the oxidative stress-induced molecule malondialdehyde. And although both groups experienced post-exercise elevations in levels of the inflammatory cytokine interleukin-6, increases in the supplemented group were smaller than in the placebo recipients. The scientists concluded that “prolonged vitamin C supplementation has some modest beneficial effects on recovery from unaccustomed exercise.”18 Timing is critical, however. When the researchers repeated their study with subjects who took vitamin C only after exercise, no benefit was seen.19 Oxidative stress during exercise induces significant changes in proteins, producing compounds known as protein carbonyls.20 Measuring levels of protein carbonyls is therefore a useful indicator of oxidation.21 Exercise scientists at the University of North Carolina studied the impact of vitamin C supplementation (500 or 1,000 mg/day for two weeks) compared with placebo on oxidative stress indicators in 12 healthy men.22 As expected, exercise acutely reduced total blood levels of antioxidants in both groups. Levels of protein carbonyls increased by nearly four-fold in the placebo group, while vitamin C recipients experienced little or no elevation. This vital study demonstrates that vitamin C can protect against exercise-induced protein oxidation in a dose-dependent fashion. Muscle soreness after exercising can be a big disincentive to continue on a healthy fitness program. That’s why the subsequent findings of that UNC group are so important. The scientists gave vitamin C supplements (3,000 mg/day) or placebo to a group of 18 healthy men for two weeks before and four days after performing 70 repetitions of an elbow extension exercise.23 Not surprisingly, considerable muscle soreness ensued, but it was significantly reduced in the supplemented group. The release of creatine kinase, an indicator of muscle damage, was also attenuated with vitamin C, compared with the placebo group. Blood levels of natural antioxidants fell significantly in placebo subjects, while vitamin C supplementation completely prevented this change. Results such as these suggest that the supplemented group would be much more enthusiastic about exercising the next day! Minimizing Unhealthy Lifestyle Choices Vitamin C may offer important protective benefits for smokers and those who are passively exposed to tobacco smoke. Smoking has been linked with elevated levels of C-reactive (CRP) protein, an inflammatory marker linked with an elevated risk of cardiovascular disease. As Life Extension readers know, it is crucial to monitor your CRP levels through regular blood testing and to keep your CRP under control in order to limit cardiovascular problems. Fortunately, vitamin C has been shown to play a role in helping to combat excessive CRP levels. Researchers in Berkeley evaluated the impact of antioxidant supplementation on blood levels of CRP in both active and passive smokers.24 They studied 160 healthy adults who were actively or passively exposed to cigarette smoke and randomly assigned to receive placebo, vitamin C (515 mg/day), or an antioxidant mixture (including vitamins C, E, and lipoic acid). Subjects in the vitamin C group underwent a significant 24% reduction in their plasma CRP concentrations, while neither of the other groups showed a significant change. This remarkable result provides strong support for chronic supplementation with vitamin C, whether or not you smoke. Smoking causes cancer in part by directly damaging DNA, which is a vital first step in the onset of cancer. In studying the effect of vitamin C supplements on reducing DNA damage in blood cells, Danish researchers gave relatively low doses (500 mg/day) of vitamin C as plain-release or slow-release tablets combined with vitamin E (182 mg/day), or placebo, for four weeks to a group of male smokers.25 The slow-release formulation of vitamin C reduced the number of DNA damage sites measured in white blood cells just four and eight hours after a single tablet, a positive result that was still evident at four weeks. The plain-release tablets also exerted a protective effect at four hours, suggesting benefits of long-term vitamin C supplementation in minimizing DNA damage. Once DNA is damaged, however, smoking induces pro-inflammatory changes that can allow a malignant cell to become a dangerous tumor as well as causing blood vessel damage associated with atherosclerosis. Vitamin C supplementation is a logical approach to reducing the impact of these inflammatory changes, as was shown recently by a British investigative team.15 They studied 10 smokers with the high-risk lipoprotein ApoE4 gene as well as 11 non-smokers, all of whom took just 60 mg/day of vitamin C for four weeks. Remarkably, these high-risk smokers on this low-dose regimen responded with a marked reduction in levels of a host of pro-inflammatory cytokines. As the authors themselves pointed out, this study identified core molecular mechanisms that help explain the known benefits of vitamin C supplementation in smokers. Literally scores of other studies have been published demonstrating the benefits of vitamin C supplements in smokers and those passively exposed to cigarette smoke. One study found that 500 mg of vitamin C twice daily for just two weeks reduced the depletion of vitamin E caused by smoking by up to 50%.26 Two other studies investigating low and high doses of vitamin C supplementation revealed its benefits in improving endothelial function, a cornerstone of cardiovascular health, known to be impaired in smokers. The first study showed that just 60 mg of vitamin C daily given to a group of smokers for 12 weeks improved endothelial function as assessed by flow-mediated vasodilation.27 In the second study, Dutch researchers found that 2,000 mg/day of vitamin C for two weeks reversed endothelial dysfunction caused by the abnormal migration of monocytes7 implicated in atherosclerosis.28 Furthermore, Berkeley public health researchers successfully reduced levels of F2-isoprostanes, a sign of oxidative stress and cell damage, in a group of 67 passive smokers who were given vitamin C supplements daily for two months. The researchers stressed the value of these findings in preventing tobacco smoke-induced health damage in non-smokers.14 Vitamin C and the Importance of Antioxidants Oxidative damage and the resultant inflammatory changes are now known to lie at the root of most common chronic conditions in humans, such as cardiovascular disease and cancer.5,35,48-51 Although for many years it was thought that tissue ischemia (lack of oxygen-rich blood) caused the damage from acute conditions such as myocardial infarction (heart attack) and stroke, today we recognize instead that it is the sudden restoration of vital oxygen and the consequent production of reactive oxygen species that wreak major havoc on surviving tissue.52 This so-called ischemia/reperfusion injury is also now recognized as a critical factor in brain injury following bleeding and head trauma.53 Reactive oxygen species are harmful in other ways as well—they contribute to the DNA damage that is the first step in converting healthy cells into malignant cancers54,55 and they impair many of the checks and balances inherent in our immune systems, rendering us potentially vulnerable to deadly infections and their consequences.56,57 Finally, healthy lifestyle choices such as exercise17,18 and unhealthy activities such as smoking and excessive alcohol consumption14,24,58 produce reactive oxygen species that must be controlled to prevent tissue injury. Scientists studying all of these conditions are rapidly developing a strong appreciation for vitamin C’s powerful potential as a preventive and often therapeutic supplement. Other Recent Advances in Vitamin C Therapy Nutritional researchers are constantly uncovering new health benefits for vitamin C. Recent findings include vitamin C’s role in the following applications: Respiratory illnesses: The impact of vitamin C in staving off the common cold has been hotly debated for more than three decades. Large, well-designed studies continue to show, however, that regular vitamin C supplements reduce the frequency29 and duration of the common cold.30 More serious illnesses also benefit from the antioxidant effects of vitamin C, particularly asthma.31-33 Asthmatic children given an antioxidant supplement containing 250 mg vitamin C and 50 mg vitamin E had markedly decreased responses to environmental asthma triggers.4 And vitamin C supplements (1,000 mg/day) also reduced the amount of long-term inhaled corticosteroids needed by adults with asthma.34 Cancer: Exciting new work is showing that vitamin C supplementation may decrease the toxic effects of chemotherapy drugs (such as damage to heart tissue)35 and increase the anti-tumor activity of chemotherapy.36 Further, promising studies show that vitamin C may synergize with other antioxidant and anti-inflammatory nutraceuticals to help fight cancer.37,38 Chronic supplementation with vitamin C and other antioxidants might also serve a vital chemopreventive role, reducing the risk of actually developing cancer in the first place.5,39-41 Diabetes: Human studies have now demonstrated that vitamin C supplements may help lower blood glucose levels in diabetics, with additional beneficial reductions in low-density lipoprotein (LDL) and plasma free radicals.6,42 Stomach Health: Supplementing with vitamin C can also protect against oxidative damage wrought by the bacterium Helicobacter pylori, a major cause of gastritis and stomach ulcers. Vitamin C supplements can also reduce the dose of antibiotics needed to eradicate the organism39,43 and may directly prevent the gastritis it causes.44 And there’s encouraging evidence that higher vitamin C levels are associated with lower long-term gastric cancer risk.45 Supplementing with Vitamin C The recommended intake to prevent overt vitamin C deficiency is 90 mg/day for men and 75 mg/day for women who do not smoke; for smokers, 125 mg/day for men and 110 mg/day for women are recommended. Clinical studies suggest that the amount of vitamin C required for optimal health is at least 400 mg/day, with some studies suggesting doses as high as several thousand milligrams daily.46 Many health practitioners recommend supplementing with at least 1,000 mg of vitamin C daily. While vitamin C is generally considered safe and well-tolerated, a few words of caution apply. Individuals who have certain hematologic disorders such as thalassemia, anemia, or glucose-6-phosphate deficiency should consult a physician before supplementing with vitamin C, as should pregnant or nursing women.47 Summary Modern science is now eagerly embracing vitamin C’s enormous potential as an antioxidant capable of preventing and, in some cases, reversing a host of human ills. Helping to maximize the beneficial effects of exercise while minimizing the impact of destructive toxins like tobacco smoke, vitamin C also acts at the most fundamental levels to prevent endothelial changes that lead to atherosclerosis, while also blocking harmful DNA degradation that triggers malignant change and sets the stage for cancer. And as scientists learn still more about the vital role of oxidative damage in diseases ranging from asthma to stomach ailments, vitamin C’s importance is growing literally by the day. There is no doubt that future research will uncover even more astonishing findings on the health benefits of vitamin C. If you have any questions on the scientific content of this article, please call a Life Extension Health Advisor at 1-800-226-2370.

References

1. Rossig L, Hoffmann J, Hugel B, et al. Vitamin C inhibits endothelial cell apoptosis in congestive heart failure. Circulation. 2001 Oct 30;104(18):2182-7. 2. Fotherby MD, Williams JC, Forster LA, Craner P, Ferns GA. Effect of vitamin C on ambulatory blood pressure and plasma lipids in older persons. J Hypertens. 2000 Apr;18(4):411-5. 3. Salonen RM, Nyyssonen K, Kaikkonen J, et al. Six-year effect of combined vitamin C and E supplementation on atherosclerotic progression: the Antioxidant Supplementation in Atherosclerosis Prevention (ASAP) Study. Circulation. 2003 Feb 25;107(7):947-53. 4. Romieu I, Sienra-Monge JJ, Ramirez-Aguilar M, et al. Antioxidant supplementation and lung functions among children with asthma exposed to high levels of air pollutants. Am J Respir Crit Care Med. 2002 Sep 1;166(5):703-9. 5. Guz J, Dziaman T, Szpila A. Do antioxidant vitamins influence carcinogenesis?. Postepy Hig Med Dosw.(Online.). 2007;61:185-98. 6. Afkhami-Ardekani M, Shojaoddiny-Ardekani A. Effect of vitamin C on blood glucose, serum lipids & serum insulin in type 2 diabetes patients. Indian J Med Res. 2007 Nov;126(5):471-4. 7. Woollard KJ, Loryman CJ, Meredith E, et al. Effects of oral vitamin C on monocyte: endothelial cell adhesion in healthy subjects. Biochem Biophys Res Commun. 2002 Jun 28;294(5):1161-8. 8. Rayment SJ, Shaw J, Woollard KJ, Lunec J, Griffiths HR. Vitamin C supplementation in normal subjects reduces constitutive ICAM-1 expression. Biochem Biophys Res Commun. 2003 Aug 22;308(2):339-45. 9. Tahir M, Foley B, Pate G, et al. Impact of vitamin E and C supplementation on serum adhesion molecules in chronic degenerative aortic stenosis: a randomized controlled trial. Am Heart J. 2005 Aug;150(2):302-6. 10. Hajjar IM, George V, Sasse EA, Kochar MS. A randomized, double-blind, controlled trial of vitamin C in the management of hypertension and lipids. Am J Ther. 2002 Jul;9(4):289-93. 11. Haffner SM. Relationship of metabolic risk factors and development of cardiovascular disease and diabetes. Obesity (Silver Spring). 2006 Jun;14 Suppl 3:121S-7S. 12. Johnston CS, Beezhold BL, Mostow B, Swan PD. Plasma vitamin C is inversely related to body mass index and waist circumference but not to plasma adiponectin in nonsmoking adults. J Nutr. 2007 Jul;137(7):1757-62. 13. Wilkinson IB, Megson IL, MacCallum H, et al. Oral vitamin C reduces arterial stiffness and platelet aggregation in humans. J Cardiovasc Pharmacol. 1999 Nov;34(5):690-3. 14. Dietrich M, Block G, Benowitz NL, et al. Vitamin C supplementation decreases oxidative stress biomarker f2-isoprostanes in plasma of nonsmokers exposed to environmental tobacco smoke. Nutr Cancer. 2003;45(2):176-84. 15. Majewicz J, Rimbach G, Proteggente AR, et al. Dietary vitamin C down-regulates inflammatory gene expression in apoE4 smokers. Biochem Biophys Res Commun. 2005 Dec 16;338(2):951-5. 16. Carnes CA, Chung MK, Nakayama T, et al. Ascorbate attenuates atrial pacing-induced peroxynitrite formation and electrical remodeling and decreases the incidence of postoperative atrial fibrillation. Circ Res. 2001 Sep 14;89(6):E32-8. 17. Khassaf M, McArdle A, Esanu C, et al. Effect of vitamin C supplements on antioxidant defence and stress proteins in human lymphocytes and skeletal muscle. J Physiol. 2003 Jun 1;549(Pt 2):645-52. 18. Thompson D, Williams C, McGregor SJ, et al. Prolonged vitamin C supplementation and recovery from demanding exercise. Int J Sport Nutr Exerc Metab. 2001 Dec;11(4):466-81. 19. Thompson D, Williams C, Garcia-Roves P, et al. Post-exercise vitamin C supplementation and recovery from demanding exercise. Eur J Appl Physiol. 2003 May;89(3-4):393-400. 20. Murali G, Panneerselvam C. Age-associated oxidative macromolecular damages in rat brain regions: role of glutathione monoester. J Gerontol A Biol Sci Med Sci. 2007 Aug;62(8):824-30. 21. Yuan Q, Zhu X, Sayre LM. Chemical nature of stochastic generation of protein-based carbonyls: metal-catalyzed oxidation versus modification by products of lipid oxidation. Chem Res Toxicol. 2007 Jan;20(1):129-39. 22. Goldfarb AH, Patrick SW, Bryer S, You T. Vitamin C supplementation affects oxidative-stress blood markers in response to a 30-minute run at 75% VO2max. Int J Sport Nutr Exerc Metab. 2005 Jun;15(3):279-90. 23. Bryer SC, Goldfarb AH. Effect of high dose vitamin C supplementation on muscle soreness, damage, function, and oxidative stress to eccentric exercise. Int J Sport Nutr Exerc Metab. 2006 Jun;16(3):270-80. 24. Block G, Jensen C, Dietrich M, et al. Plasma C-reactive protein concentrations in active and passive smokers: influence of antioxidant supplementation. J Am Coll Nutr. 2004 Apr;23(2):141-7. 25. Moller P, Viscovich M, Lykkesfeldt J, et al. Vitamin C supplementation decreases oxidative DNA damage in mononuclear blood cells of smokers. Eur J Nutr. 2004 Oct;43(5):267-74. 26. Bruno RS, Leonard SW, Atkinson J, et al. Faster plasma vitamin E disappearance in smokers is normalized by vitamin C supplementation. Free Radic Biol Med. 2006 Feb 15;40(4):689-97. 27. Young JM, Shand BI, McGregor PM, Scott RS, Frampton CM. Comparative effects of enzogenol and vitamin C supplementation versus vitamin C alone on endothelial function and biochemical markers of oxidative stress and inflammation in chronic smokers. Free Radic Res. 2006 Jan;40(1):85-94. 28. Stadler N, Eggermann J, Voo S, Kranz A, Waltenberger J. Smoking-induced monocyte dysfunction is reversed by vitamin C supplementation in vivo. Arterioscler Thromb Vasc Biol. 2007 Jan;27(1):120-6. 29. Sasazuki S, Sasaki S, Tsubono Y, et al. Effect of vitamin C on common cold: randomized controlled trial. Eur J Clin Nutr. 2006 Jan;60(1):9-17. 30. Van SM, Josling P. Preventing the common cold with a vitamin C supplement: a double-blind, placebo-controlled survey. Adv Ther. 2002 May;19(3):151-9. 31. Romieu I, Trenga C. Diet and obstructive lung diseases. Epidemiol Rev. 2001;23(2):268-87. 32. Trenga CA, Koenig JQ, Williams PV. Dietary antioxidants and ozone-induced bronchial hyperresponsiveness in adults with asthma. Arch Environ Health. 2001 May;56(3):242-9. 33. Tecklenburg SL, Mickleborough TD, Fly AD, Bai Y, Stager JM. Ascorbic acid supplementation attenuates exercise-induced bronchoconstriction in patients with asthma. Respir Med. 2007 Aug;101(8):1770-8. 34. Fogarty A, Lewis SA, Scrivener SL, et al. Corticosteroid sparing effects of vitamin C and magnesium in asthma: a randomised trial. Respir Med. 2006 Jan;100(1):174-9. 35. Bast A, Haenen GR, Bruynzeel AM, Van d, V. Protection by flavonoids against anthracycline cardiotoxicity: from chemistry to clinical trials. Cardiovasc Toxicol. 2007;7(2):154-9. 36. bdel-Latif MM, Raouf AA, Sabra K, Kelleher D, Reynolds JV. Vitamin C enhances chemosensitization of esophageal cancer cells in vitro. J Chemother. 2005 Oct;17(5):539-49. 37. Chen J, Kang J, Da W, Ou Y. Combination with water-soluble antioxidants increases the anticancer activity of quercetin in human leukemia cells. Pharmazie. 2004 Nov;59(11):859-63. 38. Chen J, Wanming D, Zhang D, Liu Q, Kang J. Water-soluble antioxidants improve the antioxidant and anticancer activity of low concentrations of curcumin in human leukemia cells. Pharmazie. 2005 Jan;60(1):57-61. 39. Correa P, Fontham ET, Bravo JC, et al. Chemoprevention of gastric dysplasia: randomized trial of antioxidant supplements and anti-helicobacter pylori therapy. J Natl Cancer Inst. 2000 Dec 6;92(23):1881-8. 40. Maramag C, Menon M, Balaji KC, Reddy PG, Laxmanan S. Effect of vitamin C on prostate cancer cells in vitro: effect on cell number, viability, and DNA synthesis. Prostate. 1997 Aug 1;32(3):188-95. 41. Wei DZ, Yang JY, Liu JW, Tong WY. Inhibition of liver cancer cell proliferation and migration by a combination of (-)-epigallocatechin-3-gallate and ascorbic acid. J Chemother. 2003 Dec;15(6):591-5. 42. Paolisso G, Balbi V, Volpe C, et al. Metabolic benefits deriving from chronic vitamin C supplementation in aged non-insulin dependent diabetics. J Am Coll Nutr. 1995 Aug;14(4):387-92. 43. Chuang CH, Sheu BS, Kao AW, et al. Adjuvant effect of vitamin C on omeprazole-amoxicillin-clarithromycin triple therapy for Helicobacter pylori eradication. Hepatogastroenterology. 2007 Jan;54(73):320-4. 44. Sun YQ, Girgensone I, Leanderson P, Petersson F, Borch K. Effects of antioxidant vitamin supplements on Helicobacter pylori-induced gastritis in Mongolian gerbils. Helicobacter. 2005 Feb;10(1):33-42. 45. Waring AJ, Drake IM, Schorah CJ, et al. Ascorbic acid and total vitamin C concentrations in plasma, gastric juice, and gastrointestinal mucosa: effects of gastritis and oral supplementation. Gut. 1996 Feb;38(2):171-6. 46. Available at: http://lpi.oregonstate.edu/infocenter/vitamins/vitaminC/. Accessed January 25, 2008. 47. Available at: http://pdrhealth.com/search/search-results.aspx?searchTerm=vitamin+c. Accessed January 25, 2008. 48. Lenton KJ, Sane AT, Therriault H, et al. Vitamin C augments lymphocyte glutathione in subjects with ascorbate deficiency. Am J Clin Nutr. 2003 Jan;77(1):189-95. 49. Tipoe GL, Leung TM, Hung MW, Fung ML. Green tea polyphenols as an anti-oxidant and anti-inflammatory agent for cardiovascular protection. Cardiovasc Hematol Disord Drug Targets. 2007 Jun;7(2):135-44. 50. Comelli MC, Mengs U, Schneider C, Prosdocimi M. Toward the definition of the mechanism of action of silymarin: activities related to cellular protection from toxic damage induced by chemotherapy. Integr Cancer Ther. 2007 Jun;6(2):120-9. 51. Nicolls MR, Haskins K, Flores SC. Oxidant stress, immune dysregulation, and vascular function in type I diabetes. Antioxid Redox Signal. 2007 Jul;9(7):879-89. 52. Sureda A, Batle JM, Tauler P, et al. Hypoxia/reoxygenation and vitamin C intake influence NO synthesis and antioxidant defenses of neutrophils. Free Radic Biol Med. 2004 Dec 1;37(11):1744-55. 53. Polidori MC, Mecocci P, Frei B. Plasma vitamin C levels are decreased and correlated with brain damage in patients with intracranial hemorrhage or head trauma. Stroke. 2001 Apr;32(4):898-902. 54. Mallette FA, Ferbeyre G. The DNA damage signaling pathway connects oncogenic stress to cellular senescence. Cell Cycle. 2007 Aug 1;6(15):1831-6. 55. Krohn K, Maier J, Paschke R. Mechanisms of disease: hydrogen peroxide, DNA damage and mutagenesis in the development of thyroid tumors. Nat Clin Pract Endocrinol Metab. 2007 Oct;3(10):713-20. 56. Wintergerst ES, Maggini S, Hornig DH. Contribution of selected vitamins and trace elements to immune function. Ann Nutr Metab. 2007;51(4):301-23. 57. Hughes DA. Effects of dietary antioxidants on the immune function of middle-aged adults. Proc Nutr Soc. 1999 Feb;58(1):79-84. 58. El-Taukhy MA, Salama SM, bou-Shousha SA, Ismail SS, Saleh M. Effects of chronic ethanol and vitamin C administration on production of tumor necrosis factor-alpha and interleukin-6 in rats. Egypt J Immunol. 2006;13(1):1-10.

HIgh Fructose Corn Syrup: A Sweet and Dangerous Lie

Reposted from Life Extension
http://blog.lef.org/2011/11/high-fructose-corn-syrup-dangers.html

By Michael A. Smith, MD

If I'm to believe the TV commercial I just watched, high fructose corn syrup (HFCS) is totally safe to consume in moderate amounts. Of course, this is according to the Corn Refiners Association which paid big money for the ad.

Now I'm not all that cynical by nature, but since the Corn Refiners Association certainly seems to have a vested interest in protecting its product, I think it might be best for us to investigate the safety of HFCS for ourselves. Let's do it.

Nothing but the Facts about High Fructose Corn Syrup

High fructose corn syrup is produced when corn syrup goes through enzymatic processing to convert some of its glucose into fructose in order to make it taste sweeter. In the United States, consumer foods and products often use high fructose corn syrup as a sweetener.

It's become absurdly common in processed foods and beverages including breads, cereals, breakfast bars, energy bars, candies, lunch meats, dairy products, canned foods, and, well ... pretty much everything.

There are two common types of HFCS:

1. HFCS 42 — The more common of the two, this is a blend of 42% fructose and 53% glucose. The rest is water. It’s found in pre-packaged foods, canned foods and baked items.

2. HFCS 55 — This syrup is composed of 55% fructose and 42% glucose. The rest is water. HFCS 55 is used mostly in soda and flavored drinks.

Believe it or not, the Centers for Disease Control and Prevention (CDC) first exposed the dangers of HFCS. They actually released information showing a strong correlation between obesity and total fructose consumption, including HFCS. The data they put together showed a rise in obesity mirrored by the rise in total fructose, free fructose and HFCS consumption.¹
The CDC is not saying that this is a cause-effect relationship. As we all know, there are many factors that contribute to obesity. However, they are citing HFCS as a contributor to obesity. So what else can be linked to HFCS consumption? Keep on reading to find out.

Processed Fructose Disrupts Fat Metabolism

Unlike glucose, processed fructose is readily converted to fat by the liver, leading to an excessive concentration of fats and lipoproteins in the body.² High and prolonged ingestion of processed fructose increases unfavorable lipid profiles in the body — specifically a rise in blood triglycerides — and disrupts insulin sensitivity.^3,4
A recent study of 48 adults showed that consumption of HFCS-sweetened beverages for 2 weeks at 25% of daily energy requirements increased risk factors for cardiovascular disease comparably with fructose and more than glucose in young adults.⁵
With changes in lipid profiles and an increased risk for heart disease, it seems pretty clear that fructose ingestion is a contributor to plaque buildup and narrowing of the blood vessels — a ticking time bomb for the development of both strokes and heart attacks.

Please note: fructose is a natural sugar found in fruit. But the amount of fructose in fruit is far less than in HFCS and has far less of an impact on lipid profiles.

More Health Consequences of High Fructose Corn Syrup

Let's keep this as simple as possible. Here's a straightforward list of additional health consequences that can be linked to HFCS (some based on animal models):

• Insulin resistance⁶
• Type 2 diabetes⁶
• Metabolic syndrome⁷
• Non-alcoholic fatty liver disease⁸
• Gout⁹

Practical Steps for Avoiding HFCS

Here at Life Extension^®, we like to promote a practical, preventive approach to health. And let’s be honest — eliminating "corn sugar" entirely from your diet probably isn't very practical. In any case, the first thing you need to do is identify the foods that are loaded with HFCS. You should consider completely avoiding these products if possible:

• Pre-packaged Baked Items
• Pre-packaged Stuffing & Breads
• Crackers & Related Snacks
• Shake’n Bake Products
• Fruit Punch
• Juice Boxes
• Specialty Coffee Drinks (Frappuccinos)
• Energy Drinks
• Soda
• Canned fruits
• Canned vegetables
• Candies & Cookies
• All Cereals (including healthy ones, see below)
• Ketchup
• Condiments
• Lunch Meats
• Processed Cheeses
• Pickled vegetables
• Jams & Jellies

Now, let's take a look at some of the so-called “healthy” foods. Surprise, surprise! Many of these low fat foods simply replace the fat with processed HFCS! Definitely avoid these foods as much as possible:

• Low Fat Yogurt
• Low Fat Salad Dressings
• Low Fat Ice Cream Products
• Heart Healthy Cereals
• Low Calorie Snacks
• Low Fat Peanut Butter

Nutritional Steps to Take — Protect Against AGEs

Since fructose promotes problems with insulin sensitivity and may disrupt normal sugar metabolism, it’s important to protect yourself against the formation of advanced glycation end-products (AGEs). These aging molecules are linked to many of the side effects of diabetes.¹⁰ The following supplements help to promote healthy sugar metabolism and may prevent the formation and buildup of AGEs. People who consume a lot of HFCS should definitely consider them:

1. Benfotiamine — a form of vitamin B1 that blocks three of the major pathways in which sugar causes damage.¹¹ We suggest 100 to 400 mg/day.

2. Carnosine — a small protein that suppresses diabetes complications by preventing glycation. We suggest 1,000 mg/day.^12,13
3. Pyridoxal 5’-phosphate — The latest information shows that pyridoxal 5’-phosphate may also be of significant help in preventing the formation of these aging molecules and diabetes. We suggest 100 mg/day.¹⁴

"Corn Sugar" — A Sweet Name for a False Sense of Safety

Remember, no matter how creative the Corn Refiners Association gets with its branding efforts, HFCS is not something that you should be eating regularly, if at all.

Despite what those bright and creative ads are trying to tell you, "corn sugar," a.k.a. high fructose corn syrup, is NOT the same as glucose or regular sugar. As a matter of fact, processed fructose is even worse for us that we previously thought.

No amount of clever branding is going to change that. Our advice? Be proactive about your health and avoid HFCS at all costs.

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What do you think about HFCS infiltrating our food choices? Share your take in the comments below.

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4. Front Biosci. 2003 Jan 1;8:d464-76.
5. J Clin Endocrinol Metab. 2011 Oct;96(10):E1596-605.
6. Clin Transl Sci. 2011 Aug;4(4):243-52.
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8. J Hepatol. 2008 Jun;48(6):993-9.
9. Curr Opin Rheumatol. 2011 Mar;23(2):192-202.
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12. Sci Aging Knowledge Environ. 2005 May 4;2005(18):pe12.
13. FEBS Lett. 2007 Mar 6;581(5):1067-70.
14. Ann N Y Acad Sci. 2008 Apr;1126:288-90.

Six Healthy Reasons To Eat Kale

Reposted from Life Extension
http://blog.lef.org/2012/10/healthy-reasons-eat-kale.html

Maylin Rodriguez-Paez, RN

These days, it’s tough to find full agreement about what’s healthy and what’s not.

Fortunately, most of us can agree on at least one thing - kale is good for you.

More than just a health fad, kale has earned its healthy reputation for several reasons.

In this post, we’ll dig into some of the most compelling health benefits that kale has to offer.

Our goal? To inspire you to start including it in your diet regularly.

1. Kale Has Cancer Fighting Properties

Don’t let the appearance of kale fool you. It looks a heck of a lot like lettuce, but it’s actually a cruciferous vegetable.

Cruciferous vegetables have been studied extensively for their anti-cancer properties. In fact, a high intake has been associated with a lower risk of breast, prostate, colon, and lung cancer.¹

In part, the cancer fighting properties they offer come from their glucosinolates,² which are compounds that give them their bitter taste and pungent smell.

2. Kale is One of the Most Nutrient-Dense Foods

Kale is considered one of the most nutrient-dense foods on the planet, due to its rich concentration of fiber, vitamins, minerals, and antioxidants.

It competes very well when compared to other vegetables. In fact, it actually contains more polyphenols than cauliflower and broccoli.³
According to the Aggregate Nutrient Density Index Scale — which measures foods based on their nutrient content — kale has a score of 1000, which is the highest score a food can get.⁴

Some of the notable antioxidants found in kale include:

• chlorogenic acid⁵
• anthocyanins⁶ (purple variety)
• quercetin⁷
• kaempferol⁸

Kale is also a particularly rich source of:⁹

• vitamin C
• magnesium
• beta carotene
• manganese
• folate
• potassium
• vitamin K

Not bad, right?

3. Kale Enhances your Body’s Detoxification Process

Kale is often hailed as a detoxifying food, and it’s for good reason. When it’s chewed or mechanically processed, a chemical reaction occurs that turns certain glucosinolates into sulforaphane.

Sulforaphane enhances the production of your liver’s detoxifying enzymes, helping to remove dangerous chemicals and carcinogenic toxins from your body.^10-12

In addition, kale also boosts glutathione, one of the body’s main detoxifying antioxidantsl.¹³

4. Kale Helps Lower Cholesterol

A three month clinical trial showed that kale juice helped improve cholesterol levels.¹³ This effect is due to kale’s ability to bind to bile, a compound which removes cholesterol from your body.¹⁴

If you don’t like the idea of kale juice, just eat it steamed instead. Either way, its cholesterol managing properties¹⁴ will stay intact.

5. Kale is Good for Your Eyes

Kale is also a rich source of lutein and zeaxanthin.⁹ These antioxidants are naturally found in the eye where they protect against harmful UV rays.

Research shows that diets rich in these compounds can protect against macular degeneration¹⁵ and cataracts.¹⁶

6. Kale is a Great Source of Calcium

A single serving of kale provides about 91 mg of calcium,⁹ which is about 10% of your daily needs. This is good news for vegans and anyone who purposely avoids milk.

There is a common misconception that calcium in green vegetables is poorly absorbed. This may be true in some cases, but not for kale.

In fact, according to a clinical study, kale contains a highly absorbable form of calcium, even more so than milk.¹⁷

Recipe: Kale Chips

Once in a while, it’s fun to experiment a little with healthy foods. Here’s an excellent kale chips recipe, courtesy of OregonLive. It makes for a great potato chip substitute – give it a try!

Ingredients:

• 2 bunches kale (about 1 1/2 pounds)
• 1-2 tablespoons extra virgin olive oil
• Salt to taste

Instructions:

• Heat the oven to 200 degrees. Wash the kale and dry it in a salad spinner. Lay out a few clean tea towels and thoroughly pat the leaves dry.
• Put the kale in a large bowl and then drizzle the pile with one tablespoon of the olive oil. Lay the slicked-up leaves one by one on the empty baking sheet so that they don't overlap.
• Bake in a 200 degree oven for 30 minutes. Rotate the pans from top to bottom and bake another 30 minutes. For good measure, turn off the oven and leave the pans in for another hour. If they are still soft after all this, just turn the oven back to 200 degrees and dry them out for another 15 minutes or so.
• Store the cooled kale chips in an airtight container for up to a month.

Enjoy!

References:

1. Available at: http://www.cancer.gov/cancertopics/factsheet/diet/cruciferous-vegetables. Accessed October 20,2012.
2. Trends Mol Med. 2012 Jun;18(6):337-47.
3. Biosci Biotechnol Biochem. 2011;75(1):40-6.
4. Available at: http://www.drfuhrman.com/library/andi-food-scores.aspx. Accessed October 20, 2012.
5. Acta Sci Pol Technol Aliment. 2012 Jul-Sep;11(3):239-48.
6. Plant Cell Rep. 2012 Feb;31(2):281-9.
7. J Food Sci. 2011 Mar;76(2):H31-7.
8. Mini Rev Med Chem. 2011 Apr;11(4):298-344.
9. Available at: http://nutritiondata.self.com/facts/vegetables-and-vegetable-products/2461/2 Accessed October 20, 2012.
10. J Med Food. 2005;8(2):198-203.
11. Carcinogenesis. 2007 Jul;28(7):1485-90.
12. Biomed Environ Sci. 2008 Apr;21(2):91-7.
13. Nutr Res. 2008 Jun;28(6):351-7.
14. Acta Ophthalmol. 2012 Jan 23. doi: 10.1111/j.1755-3768.2011.02357.
15. Ophthalmic Res. 2010;44(3):166-72. Epub 2010 Sep 9.
16. Am J Clin Nutr. 1990 Apr;51(4):656-7.