Summer is Here … Protect Your Skin from the Inside Out

Summer is Here ... Protect Your Skin from the Inside OutExcessive sun exposure can lead to premature aging of the skin; which means more wrinkles and discolorations. Although topical sunscreens remain the top choice of consumers, there is a new oral method for protecting your skin … Polypodium leucotomos.

Much has been written about how the sun’s burning ultraviolet rays harm our health and appearance. Yet despite the warnings, more than two million people in the US will be diagnosed with skin cancer this year alone. Rates of melanoma — the most dangerous form of skin cancer — have not only doubled over the past 10-20 years, but continue to rise 3% to 7% annually.1

A recent study found that a new oral supplement sourced from the fern, Polypodium leucotomos, could potentially become an important anti-aging ingredient for the skin.2  Extracts from the fern have been used in South America for many years to protect against the damaging effects caused by excessive sun exposure.

This amazing fern also protects skin cells from the consequences of excessive ultraviolet radiation by reducing sun-induced injury.3 Additionally, it helps ease skin inflammation and blocks protein-destroying skin enzymes.3,4

Polypodium leucotomos extract also contains a high percentage of potent antioxidants (phenolics) which block the formation of dangerous free radicals and the oxidative damage that results from excessive sun exposure.5

Remember, for long periods of sun exposure, you should defend your skin against premature aging with an oral extract from Polypodium leucotomos and a topical sunscreen to ensure complete sun protection.

References

  1. Available at: http://www.medscape.com/viewarticle/470300_2. Accessed May 3, 2010.
  2. Philips N, Conte J, Chen YJ, et al. Beneficial regulation of matrixmetalloproteinases and their inhibitors, fibrillar collagens and transforming growth factor-beta by Polypodium leucotomos, directly or in dermal fibroblasts, ultraviolet radiated fibroblasts, and melanoma cells. Arch Dermatol Res. 2009 Aug;301(7):487-95.
  3. J Photochem Photobiol B. 2006 Mar 1;82(3):173-9.
  4. J Dermatol Sci. 2003 Jun;32(1):1-9.
  5. Ann Intern Med. 1971 Dec;75(6):873-80.

Stress, Immortality, and the Hormesis Hypothesis

Stress, Immortality, and the Hormesis Hypothesis

By Steven V. Joyal, MD

Stress, Immortality, and the Hormesis HypothesisIs low-level stress the secret to immortality?

Longevity scientists have long been puzzled by the fact that stress, when carefully applied, very often results in prolongation of lifespan rather than causing premature death.

We need to be careful by the manner in which we characterize or define stress in the context of lifespan extension. Stress, as a critical causal factor in lifespan extension, is best defined by the term hormesis. When stress, either internal or external, is applied to a living system at a relatively low level so that a beneficial biological adaptation occurs, we define this as hormesis. The capacity of a biological system to adapt and thrive in response to stress is critical to survival. In fact, aging itself can be characterized as the inability to adapt and respond successfully to stress.

We must differentiate chronic stress that overwhelms a biological system and results in damage and decay from the type of low-level stress of hormesis that contributes to a beneficial biological response. For example, chronic stress that causes large bursts of the hormones cortisol and “fight or flight” catecholamines like adrenaline accelerates the aging process and reduces lifespan. In contrast, low-dose radiation with gamma rays and beta radiation has been shown in several studies to stimulate natural chemical and biological processes that are actually protective against cancer.1-4 This may seem surprising to some, but low-level gamma radiation, rather than causing cancer and premature death, has been shown to suppress cancer induction from chemical carcinogens, oncogenic retroviruses, and viral oncogenes like ras and src.5,6

Significant lifespan extension as a result of calorie restriction is probably the best evidence in support of the hormesis hypothesis as applied to longevity. Animals that are calorie restricted are able to significantly suppress chemical and radiation-induced cancers as opposed to peer controls fed ad libitum. Calorie restriction in animals results in an increase in resistance to oxidative stress and the negative effects of excess inflammation as well as the deleterious impact of exhaustive physical exercise.

The beneficial biological response to oxidative stress in calorie restriction is particularly impressive. Animals under calorie restriction have reduced levels of oxidatively damaged proteins, lipids, and DNA. Calorie restricted animals have an amazing capacity to beneficially modify gene expression involved in glucose metabolism, protein synthesis, and cellular energy capacity. Gene expression in calorie restricted animals shows adaptations involving enhancement of detoxification, anti-inflammatory pathways, and DNA repair enzymes.

Do the impressive adaptive benefits of calorie restriction share a common pathway?

The hormesis hypothesis helps provide an answer.

The mild stress of calorie restriction rapidly turns on a variety of gene pathways critical for essential defense and survival of the organism. Gene expression studies show that calorie restricted animals rapidly turn on genes related to stress response and energy metabolism. For example, Lee et al showed that of 6,437 genes activated by calorie restriction, nearly 30% were related to energy metabolism and stress response.7 Hormesis as an explanation for the biological benefits of calorie restriction implies an adaptive mechanism through evolutionary biology. In order to survive, living systems must adapt to an ever-changing barrage of internal and external insults. The low-level stress of calorie restriction produces gene expression changes that create a variety of positive adaptive responses for longevity.

In addition to calorie restriction, other strategies may help mimic the hormetic response. Consistent, mild-to-moderate (never exhaustive) exercise triggers a variety of adaptive mechanisms similar to calorie restriction. Exercise adaptation includes improvements in insulin signaling, mitochondrial energy metabolism, and resistance to oxidative stress, all of which are also known to occur with calorie restriction.

Nutrients, too, have hormetic properties. One example is vitamin D. The past decade has seen a veritable explosion of research supporting beneficial biological roles for vitamin D in the immune system, cardiovascular system, central nervous system, and endocrine system, in addition to control of the cell cycle and cancer pathogenesis.8 There is compelling evidence that vitamin D acts as a hormetic agent. Low doses of vitamin D exert stimulatory effects upon wound healing, while large doses may inhibit psoriatic plaque. A longitudinal, nested, case-control study of prostate cancer showed that both low (</=19 nmol/l) and high (>/=80 nmol/l) 25(OH)-vitamin D serum concentrations were associated with higher prostate cancer risk, while serum concentrations of 25(OH)-vitamin D within the 40-60 nmol/l range comprised the lowest risk of prostate cancer.9 A biphasic, U-shaped response curve is a characteristic of hormesis.

Clearly, more research is needed to understand how best to evaluate the hormesis hypothesis as applied to calorie restriction, physical exercise, and nutrients like vitamin D in the context of longevity science. In the interim, we are left with the intriguing possibility that stress, when applied carefully and strategically, may be the key to living healthier, longer.

References:

  1. Mitchel REJ. Low doses of radiation are protective in vitro and in vivo: Evolutionary origins. Dose-response. 2006;4(2):75–90.
  2. Mitchel REJ. Low doses of radiation reduce risk in vivo. Dose-Response. 2007;5(1):1–10.
  3. Sakai K, Nomura T, Ina Y. Enhancement of bio-protective functions by low dose/dose-rate radiation. Dose-Response. 2006;4(4):327–332.
  4. Sakai K, Hoshi Y, Nomura T, Oda T, Iwasaki T, Fujita K, Yamada T, Tanooka H. Suppression of carcinogenic process in mice by chronic low dose rate gamma-irradiation. Int J Low Radiat. 2003;1(1):142–146.
  5. Bauer G. Low dose radiation and intercellular induction of apoptosis: potential implications for control of oncogenesis. Int J Radiat Biol. 2007;83(11–12):873–888.
  6. Jürgensmeier JM, Schmitt CP, Viesel E, Höfler P, Bauer G. Transforming growth factor beta treated normal fibroblast eliminate transformed fibroblasts by induction of apoptosis. Cancer Res. 1994;54(2):393–398.
  7. Lee CK, Klopp RG, Weindruch R, Prolla TA. Gene expression profile of aging and its retardation by caloric restriction. Science. 1999;285(5432):1390-3.
  8. Norman AW. From vitamin D to hormone D: fundamentals of the vitamin D endocrine system essential for good health. Am J Clin Nutr. 2008;88(2):491S-499S.
  9. Tuohimaa P, Tenkanen L, Ahonen M, Lumme S, Jellum E, Hallmans G, Stattin P, Harvei S, Hakulinen T, Luostarinen T, Dillner J, Lehtinen M, Hakama M. Both high and low levels of blood vitamin D are associated with a higher prostate cancer risk: a longitudinal, nested case-control study in the Nordic countries. Int J Cancer. 2004;108(1):104-8.

Men should not stop using Avodart because of heart attack fears! Life Extension’s Rebuttle

Life Extension’s rebuttal by William Faloon in reference to published clinical study in Thursday’s New England Journal of Medicine on Avodart and increased risk for sudden myocardial infarction.

I suspect none of the study participants where using testosterone creams, even though they were ALL likely to be testosterone deficient. You will soon read the findings of an internal study we did on Life Extension Foundation members that found 86% of men have less than optimal testosterone levels.

The significance of this is that testosterone deficiency predisposes a man to heart failure. By taking a drug like Avodart when in a testosterone deficient state, the heart muscle will be robbed completely of this vital anabolic hormone. That may be why this study showed higher heart failure rates in the Avodart group.

 Those with prostate cancer often intentionally suppress their testosterone levels and have to be extra vigilant in protecting against heart attack. Log on to http://www.lef.org/magazine/mag2009/mag2009_05.htm for information on how to protect against multiple risk factors underlying coronary atherosclerosis.

 Aging men (without prostate cancer) should do whatever is necessary to maintain free testosterone blood levels of 20-25 pg/mL, while keeping DHT blood levels at the very low end of the reference range.

This provides the heart, brain and other vital parts their testosterone requirements while protecting the prostate gland against the adverse effects of excess DHT.

 The Avodart study exposes the flaws in so many of these single agent trials. We know, for example, that 25-hydroxyvitamin D serum levels strongly predict prostate cancer risk. If this potent confounding factor was not accounted for, then the results shown with Avodart have little meaning.

If, for example the placebo group’s median 25-hydoxyvitamin D level was 35 ng/mL, and the Avodart group was only 25 ng/mL, this would skew the results in a way to show Avodart less effective than it may really be. Dietary intakes of cruciferous vegetables would have an equally significant confounding effect.

 Bill Faloon

Statin Drugs May Increase Diabetes Risk

Statin Drugs May Increase Diabetes Risk

New data from a large review (meta-analysis) of major statin trials suggests that the cholesterol lowering drugs (statins) slightly increase the risk of developing diabetes. The results of the study were published online February 17, 2010 in The Lancet.

“We found that there was indeed a risk of diabetes, about 9%, but it isn’t a worrying increase as had been suggested by other studies,” said lead investigator Dr David Preiss (University of Glasgow, Scotland). “Then again, it wasn’t a completely flat result. We did see [risk].”

Investigators stress that clinical practice should remain unchanged in patients with moderate or high cardiovascular risk, given the benefits of statins seen in these populations.

However, statin medications are increasingly prescribed for low risk patients. The risk for developing diabetes is greater than the benefits of statin drugs in the low risk group.

Bottom line … protect yourself against diabetes if you’re taking a statin drug. The following nutrients help to maintain healthy blood sugar levels and may provide the protection you need:

1. Soluble Fiber

Soluble fibers, such as apple pectin and glucomannan, help control blood sugar spikes after eating a meal. Nutritionists suggest supplementing with five grams 20 minutes before each meal.

2. Chromium

Chromium is a trace mineral critical for maintaining healthy blood sugar levels. It helps the transport of blood sugar (glucose) into cells, and thereby supports already-normal insulin action. Foods rich in chromium include eggs, lean beef, spinach, and apples.

3. Cinnamon

Cinnamon supports healthy glucose metabolism. It’s believed that a water-soluble cinnamon extract is the most effective form for daily supplementation. Additionally, cinnamon has been shown to support levels of triglycerides and cholesterol that are already within normal ranges.

4. Lipoic Acid

Lipoic acid helps protect against oxidative stress generated by high glucose levels. Foods rich in lipoic acid include dark green leafy vegetables, broccoli, and organ meat. If you decide to supplement, take the active form of lipoic acid. It’s known as the “R” form and is responsible for lipoic acid’s benefits.

Natural Support for Diabetic Nerves that Hurt

Natural Support for Diabetic Nerves that Hurt
Millions of people suffer needlessly from diabetic neuropathy because conventional medicine has nothing to offer but toxic medications that don’t work.

Fortunately, natural nerve support is available for nerve damage caused by high blood sugar. You can stop the pain and improve your quality of life by supplementing with specific nutrients proven to support healthy nerves.

1. Acetyl-L-carnitine

Acetyl-L-carnitine has been shown to limit the neuropathy associated with diabetes. In two randomized, placebo-controlled clinical trials, acetyl-L-carnitine, in daily doses of 500 mg and 1000 mg, was shown to yield significant reductions in pain.

2. Lipoic Acid

As a powerful antioxidant, lipoic acid positively affects important aspects of diabetes, including prevention, blood sugar control, and the development of long-term complications such as disease of the heart, kidneys, and small blood vessels.

It has also been shown to reduce the pain associated with diabetic neuropathy.

Clinical trials of people with diabetes who had symptoms caused by nerve damage affecting the heart showed significant improvement taking 800 mg of oral alpha-lipoic acid daily without significant side effects.

3. Curcumin

Researchers are continually discovering more benefits from curcumin, which is the yellow pigment that gives turmeric its distinctive golden hue.

In a study of inherited peripheral neuropathies, curcumin was shown to relieve neuropathy by causing the release of disease-associated proteins that are produced by a mutated gene.

4. Omega-6 Fats

Diabetics are not able to make the omega-6 fat, GLA, and it must be supplemented. GLA improves diabetic neuropathy if given long enough to work.

In one double-blind, placebo-controlled study, 111 people with mild diabetic neuropathy received either 480 mg GLA daily or a placebo.

After 12 months, the group taking GLA was doing significantly better than the placebo group. Good results were seen in two smaller studies as well.

5. Omega-3 Fats

The omega-3s are found in high quantities in coldwater fish such as salmon and are widely consumed for their anti-inflammatory powers.

Omega-3s are essential fatty acids and are important components of cell membranes, including the delicate myelin sheath that protects nerves.

Studies have shown that omega-3 fatty acids, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are able to reduce demyelination in the nerves of diabetic animals, which reduces neuropathic pain.

For more information on diabetic neuropathy, visit our protocol at http://www.lef.org/protocols/neurological/neuropathy_01.htm.

Stop Smoking! But Watch Out for Diabetes…

Stop Smoking! But Watch Out for Diabetes Smoking cessation predicts higher short-term risk for the development of type 2 diabetes, according to the results of a prospective cohort study reported in the January 5, 2010, issue of the Annals of Internal Medicine.

“Cigarette smoking is an established predictor of incident type 2 diabetes mellitus, but the effects of smoking cessation on diabetes risk are unknown,” writes Hsin-Chieh Yeh, Ph.D., from Johns Hopkins University in Baltimore, Maryland, and colleagues from the Atherosclerosis Risk in Communities (ARIC) Study.

The goal of this study was to test the hypothesis that smoking cessation would increase diabetes risk in the short term, possibly caused by weight gain related to quitting smoking.

The study cohort consisted of 10,892 middle-aged adults free of diabetes at study enrollment from 1987 to 1989.

Interview at baseline and at subsequent follow-up determined smoking status. Incident diabetes was identified by fasting glucose assays through 1998 and by self-report of physician diagnosis or use of diabetes medications through 2004.

In the first three years of follow-up, 380 participants quit smoking. Compared with adults who never smoked, the incident of diabetes among former smokers was two times higher. The authors concluded, “Smoking cessation leads to higher short-term risk.”

For smokers at risk for diabetes, smoking cessation should be coupled with strategies for diabetes prevention and early detection.

What You Should Do

You should protect against diabetes after you quit smoking. Here are two strategies to consider…

1. Start a Borderline Diabetic Diet

A borderline diabetic diet reverses prediabetes. Preventing full-blown diabetes is ONLY possible with early dietary intervention. Start this diet before you quit smoking.

The diet consists of avoiding anything “white” and focusing on a higher protein based-diet.  Eating whole grains is allowed to a lesser extent.

2. Stop Blood Sugar Spikes

The diabetic diet guidelines begin with minimizing sugar spikes after meals. Carbohydrates result in a sharp rise in blood sugar levels. This is quickly followed by a rise in insulin levels.

The more insulin that’s released the greater the chance for developing insulin resistance … the hallmark of type 2 diabetes.

Eat 10-15 grams of soluble fiber and try supplementing with 1 ounce of apple cider vinegar 10 minutes before each meal.

The Best Foods for Diabetics on Insulin

The best foods for diabetics on insulin are rich in nutrients that improve insulin sensitivity.  I call them “insulin promoters” because they promote more efficient cellular uptake of glucose from the blood. 

Eating a diet rich in promoters enhances the effects of insulin therapy by targeting insulin resistance, the hallmark of type 2 diabetes.  Taking insulin when resistant to its effects simply won’t work. 

You have to re-sensitize your body to insulin with foods rich in promoters in order to gain optimal blood sugar control.  I suggest adding the following foods, rich in insulin promoters, to your diabetic diet today.

The Best Insulin Promoters

The best insulin promoters contain high levels of lipoic acid.  As a powerful antioxidant, lipoic acid positively affects blood sugar control and the development of long-term complications. 

It’s believed that lipoic acid promotes optimal glucose control by protecting insulin receptors located on the surface of muscle cells.  Successful insulin therapy is totally dependent on healthy receptors, making lipoic acid a key component of a diabetic diet. 

It’s effectiveness as an insulin promoter is best supported by the recent approval in Germany for its use in the prevention and treatment of diabetes.

Foods rich in lipoic acid include:

1. Collard greens
2. Lean red meats (organ meats)
3. Brewer’s yeast
4. Cruciferous Vegetables (cabbage, broccoli, cauliflower)

I also suggest taking a lipoic acid supplement.  Take the “R” form of lipoic acid.  This is the more active form found in nature.  Take between 200 mg and 300 mg/day.

The Second Best Insulin Promoters

The second best insulin promoters are foods rich in chromium.  It’s an essential trace mineral that plays a significant role in sugar metabolism.

Chromium helps control blood sugar levels in type 2 diabetes and improves metabolism of carbohydrates, proteins, and lipids.  A study of type 2 diabetics compared two forms of chromium (brewer’s yeast and chromium chloride). 

Both forms of chromium significantly improved blood sugar control by promoting the uptake of glucose into the tissues after eating a carbohydrate rich meal.  Fasting blood glucose levels were also lowered during a 2 month follow-up period.

Foods rich in chromium include (in order of most to least):

1. Egg yolk
2. Brewer’s yeast
3. Breads (whole grain, wheat, sprouted, rye)
4. Apples
5. Spinach
6. Oranges

Summary

Insulin promoters, rich in lipoic acid and chromium, are the best foods for diabetics on insulin.  If you’re taking insulin, your diet should include foods like collard greens, broccoli, apples, and whole grain. 

If loaded with insulin promoters, the foods you eat could be the difference between disease and health.