Osteoporosis: Vitamin K for Bone Quality and Strength

Research has recognized an important role for vitamin K, which is to contribute substantially to the integrity of bones.

Vitamin K is a fat-soluble vitamin; therefore, poor absorption of fat can contribute to a deficiency of vitamin K. Some health conditions that can cause impaired absorption of fat include pancreatic disease, celiac disease, and gallbladder disease.

The World Health Organisation estimates there are 200 million Osteoporosis sufferers worldwide and, according to Osteoporosis Australia, 25 percent of Australian women and 17 percent of men will develop a bone fracture due to osteoporosis, with total incidence expected to rise 83 percent by 2011.

The Nurses Health Study followed 72,327 women between 38 and 63 years of age for 10 years. The researchers found that women with the lowest intake of vitamin K had a 30% higher risk of hip fracture than women with the highest intake of vitamin K. They concluded there was a lower risk of hip fracture in middle-aged and older women with moderate and high intakes of vitamin K than in those with a low intake. (Am J Clin Nutr. 1999;69(1):74-79)

Researchers reporting in The American Journal of Clinical Nutrition in May 2000 found that men and women with the highest intake of dietary vitamin K had only 35% of the risk of a hip fracture as opposed to those with the lowest intake of vitamin K (approximately 250 mcg per day compared to 50 mcg per day). The study involved over 800 elderly men and women participating in the Framingham Heart Study. (Am J Clin Nutr. 2000;71(5):1201-1208).

There are three forms of vitamin K:

Vitamin K1, or phylloquinone, is found naturally in plants. Vitamin K2, or menaquinone, is made by the bacteria that line the gastrointestinal tract. Vitamin K3, or menadione, is a synthetic form that is man made.

Although vitamin K2 is made by bacteria lining the gastrointestinal tract, it is not clear how much of it is absorbed into the body. Therefore, it is important to eat a diet with adequate amounts of vitamin K.

Researchers in Japan reporting in the Journal of Bone and Mineral Metabolism noted that recent studies have reported that vitamin K reduces vertebral and hip fractures without increasing bone mass in patients with osteoporosis, suggesting that vitamin K could affect bone quality. (J Bone Miner Metab. 2001;19(3):146-9).

Japanese researchers reporting in the journal Nutrition in 2001 observed a large geographic difference in blood levels of vitamin K2 in postmenopausal women. They noted that Japanese women in Tokyo had significantly higher levels of vitamin K2 than Japanese women in Hiroshima and British women have much lower levels than both.

They also noted that natto, which contains a large amount of vitamin K2, is eaten frequently in Tokyo but seldom in Hiroshima. Analysing the relationship between the regional difference in natto intake and the incidence of fractures they found a significant association between the incidence of hip fractures in women and natto consumption in each region throughout Japan.

As previously noted, British women have significantly lower levels of vitamin K2, suggesting the possibility that higher vitamin K2 blood levels from natto consumption may contribute to the relatively lower fracture risk in Japanese women. (Nutrition. 2001 Apr;17(4):315-21).

Norwegian researchers noted that the level of vitamin K1 in the Norwegian diet appears to be lower than the recommended dietary allowance and that it is possible that the high incidence of osteoporosis in Norway may be due to the low dietary intake of vitamin K. (Tidsskr Nor Laegeforen. 2004 Jun 17;124(12):1650-4).

In April 2004, a Japanese researcher reporting in the journal Clinical Calcium, reviewed the literature up to that date and noted that vitamin K intake from the diet is reduced with aging and low vitamin K intakes are associated with an increased incidence of hip fractures and an increase of under carboxylated osteocalcin in elderly men and women. He concluded that Vitamin K2 treatment is effective for the prevention of fractures, but not for the increase of bone mineral density in osteoporosis.

Although he came to the conclusion that vitamin K2 did not increase bone mineral density, he stated that vitamin K2 administration could be a potential treatment to improve bone quality. (Clin Calcium. 2004 Apr;14(4):621-6).

Low vitamin K nutritional status is associated with increased fracture risk but is inconsistently related to bone mineral density (BMD), suggesting that vitamin K may affect components of bone strength not measured by BMD, such as microarchitecture. (Osteoporos Int. 2006 Jan 6:1-8).

Vitamin D and Vitamin K for increased bone mineral density.

The following demonstrates the importance of vitamin D for bone mineral density. Vitamin D is needed for the absorption of calcium and is essential for bone health.

Combined administration of vitamin D3 and vitamin K2 potentially stimulates bone formation (mineralization) in patients with primary osteoporosis, resulting in an increase in lumbar bone mineral density. (Clin Calcium. 2002 Jul;12(7):955-65).

As can be seen by the above studies and studies below, vitamin K improves bone quality and strength. The addition of vitamin D3 (with or without increased calcium intake) also helps increase bone mineral density.

In 2002 researchers at Osaka Medical College in Japan demonstrated this fact. Women with low vertebral bone mineral density (osteopenia and osteoporosis) were enrolled for the study. One group (43 participants) was given vitamin K2 supplementation. Another group (43 participants) were supplemented with vitamin K2 and vitamin D3 combined. The study lasted 2 years, and bone mineral density was measured prior to therapy and after.

The group supplemented with both vitamin K2 and vitamin D3 for 24 months showed significantly increased bone mineral density, while the group given vitamin K2 alone showed only a small increase. (Maturitas. 2002 Mar 25;41(3):211-21).

In July 2005, Japanese researchers reviewed the literature to date. Reporting in the journal Clinical Calcium, they noted that recent clinical studies have shown that the occurrence of new fractures does not always depend on bone mineral density. Therefore bone quality has become an important issue in osteoporosis research.

They carried out a study to investigate the effectiveness of treating rats with a low magnesium diet. Results revealed that the low magnesium diet resulted in reduced bone strength without decreasing bone mineral content. Vitamin K2 increased bone strength without influencing bone mineral content suggesting that the vitamin may improve bone quality. (Clin Calcium. 2005 Jul;15(7):49-55).

In August 2005 American researchers reported in a review that the results of two dose-response studies have indicated that the amount of vitamin K needed for optimal gamma-carboxylation of osteocalcin is significantly higher than what is provided through diet alone and that current dosage recommendations should be increased to optimize bone mineralization. (Am J Health Syst Pharm. 2005 Aug 1;62(15):1574-81. Review).

Evidence suggests that dietary phylloquinone (vitamin K1) intake of less than 100 micrograms daily might not be optimal for bone health. Low intake of vitamin K could contribute to osteoporosis and subsequent fracture due to the undercarboxylation of osteocalcin. (Canadian family physician. 2004 Jul;50:993-7).

The vitamin K that I recommend is vitamin K1, which is natural and not toxic at even 500 times the RDA. Vitamin K2, which is made in your body and also produced by fermented foods, is also a superior form of vitamin K. (Dr Mercola).

Vitamin K levels tend to decrease with age whilst the risk of fracture increases.

Family physicians need to be aware of the importance of encouraging adequate vitamin K intake, particularly among institutionalized elderly people, to prevent increased bone resorption. (Canadian family physician. 2004 Jul;50:993-7).

Does Hormone Replacement Therapy (HRT) increase bone mineral density?

Researchers at Toyama Medical and Pharmaceutical University, Japan, noted in 2002 that estrogen increases bone mineral density (BMD) for 2 or 3 years, and only maintains BMD thereafter.

They carried out a study involving 94 patients with postmenopausal osteoporosis. All patients were placed on HRT for more than 1 year. Ten patients whose bone mineral density had increased up to a plateau and showed a decreasing trend thereafter while they were receiving HRT were placed on HRT in combination with vitamin K2.

After supplementation with vitamin K2 for 12 months their bone mineral density increased significantly. They concluded that vitamin K2 is a good therapeutic option for patients with postmenopausal osteoporosis who are placed on HRT. (J Bone Miner Metab. 2002;20(4):235-9).

Astronauts suffer from osteoporosis, being in a weightless environment which results in a calcium, vitamin D, and vitamin K deficiency.

Japanese researchers wrote in a review that high calcium intake and vitamin D supplementation during space flight prevents an elevation of blood calcium levels through increased calcitriol levels, while vitamin K counteracts the decrease in bone formation. A note of importance here is that vitamin D supplementation increases calcium absorption thereby preventing the elevation of blood calcium levels. (Keio J Med. 2005 Jun;54(2):55-9. Review).

In a study done on Russian cosmonauts, levels of free osteocalcin skyrocketed within 4 days. This means it was not being utilized. During the 179 day Euromir 95 mission, investigators administered 10 mg of vitamin K from in-flight day 86 to day 136 to one astronaut. During and after supplementation, bone formation markers increased significantly during this part of the mission (his levels returned to normal). Therefore, vitamin K seems to play a significant role in bone turnover during space flight. (Nutrition. 2002 Oct;18(10):853-6. Review).

Vitamin K2 (menatetrenone, MK-4) has been clinically used in the treatment of patients with osteoporosis in Japan, Korea and Thailand. (Clin Calcium. 2005 Apr;15(4):605-10. Review).

Excellent sources of vitamin K include: spinach, Brussels sprouts, Swiss chard, carrots, green string beans, asparagus, red bell peppers, strawberries and eggs. Very good sources include tomatoes, and green peas. Freezing food can decrease its vitamin K content. (World’s Healthiest Foods).

Vitamin K levels tend to decrease with age whilst the risk of fracture increases. Therefore, it is important for older individuals to include foods containing vitamin K in their diet. Leafy green vegetables are also rich sources of calcium and boron which are important for bone health.

Anticoagulant medications, such as Coumadin, are designed to decrease clotting by interfering with vitamin K.

Vitamin K participates in bone metabolism and, since oral anticoagulants antagonize vitamin K, their use may increase the risk of osteoporosis. Long-term exposure to oral anticoagulation is associated with an increased risk of vertebral and rib fractures. (Arch Intern Med. 1999 Aug 9-23;159(15):1750-6).

References

Feskanich D, Weber P, Willett WC, Rockett H, Booth SL, Colditz GA. Vitamin K intake and hip fractures in women: a prospective study. Am J Clin Nutr. 1999;69(1):74-79.

Booth SL, Tucker KL, Chen H, et al. Dietary vitamin K intakes are associated with hip fracture but not with bone mineral density in elderly men and women. Am J Clin Nutr. 2000;71(5):1201-1208.

Kaneki M. [Vitamin K2 as a protector of bone health and beyond] Clin Calcium. 2005 Apr;15(4):605-10. Review. Japanese.

Kaneki M, Hedges SJ, Hosoi T, Fujiwara S, Lyons A, et al. Japanese fermented soybean food as the major determinant of the large geographic difference in circulating levels of vitamin K2: possible implications for hip-fracture risk. Nutrition. 2001 Apr;17(4):315-21.

Drevon CA, Henriksen HB, Sanderud M, Gundersen TE, Blomhoff R. [Biological effects of vitamin K and concentration of vitamin K in Norwegian food] Tidsskr Nor Laegeforen. 2004 Jun 17;124(12):1650-4.

Sugiyama T, Kawai S. Carboxylation of osteocalcin may be related to bone quality: a possible mechanism of bone fracture prevention by vitamin K. J Bone Miner Metab. 2001;19(3):146-9.

Kishimoto H. [Vitamin K and bone quality] Clin Calcium. 2004 Apr;14(4):621-6.

Kobayashi M, Hara K, Akiyama Y. [Vitamin K2 and bone quality] Clin Calcium. 2005 Jul;15(7):49-55.

Iwamoto J. [Efficacy of combined administration of vitamin D3 and vitamin K2 for primary osteoporosis] Clin Calcium. 2002 Jul;12(7):955-65. Japanese.

Adams J, Pepping J. Vitamin K in the treatment and prevention of osteoporosis and arterial calcification. Am J Health Syst Pharm. 2005 Aug 1;62(15):1574-81. Review.

Iwamoto J, Takeda T, Sato Y. Interventions to prevent bone loss in astronauts during space flight. Keio J Med. 2005 Jun;54(2):55-9. Review.

Heer M. Nutritional interventions related to bone turnover in European space missions and simulation models. Nutrition. 2002 Oct;18(10):853-6. Review.

Ryan-Harshman M, Aldoori W. Bone health. New role for vitamin K? Can Fam Physician. 2004 Jul;50:993-7. Review.

Hidaka T, Hasegawa T, Fujimura M, Sakai M, Saito S. Treatment for patients with postmenopausal osteoporosis who have been placed on HRT and show a decrease in bone mineral density: effects of concomitant administration of vitamin K(2). J Bone Miner Metab. 2002;20(4):235-9.

Caraballo PJ, Heit JA, Atkinson EJ, Silverstein MD, O'Fallon WM, Castro MR, Melton LJ 3rd. Long-term use of oral anticoagulants and the risk of fracture. Arch Intern Med. 1999 Aug 9-23;159(15):1750-6.

McLean RR, Booth SL, Kiel DP, Broe KE, Gagnon DR, Tucker KL, Cupples LA, Hannan MT. Association of dietary and biochemical measures of vitamin K with quantitative ultrasound of the heel in men and women. Osteoporos Int. 2006 Jan 6;:1-8.

Ushiroyama T, Ikeda A, Ueki M. Effect of continuous combined therapy with vitamin K(2) and vitamin D(3) on bone mineral density and coagulofibrinolysis function in postmenopausal women. Maturitas. 2002 Mar 25;41(3):211-21.

Copyright 2007 Kevin Flatt. Disclaimer: The information contained in this article is presented for information purposes only and is in no way intended to replace professional medical care or attention by a qualified practitioner. It cannot and should not be used as a basis for diagnosis or choice of treatment.

Breast Cancer Risk and Adolescent Diet

The evidence that adolescent diet may affect the risk of breast cancer derives from several lines of evidence. Rates of breast cancer among Asian immigrants to the United States do not approach those of US white women until the second or third generation, suggesting that exposures during childhood and adolescence are important in establishing a higher risk of breast cancer. (J Natl Cancer Inst 1973, 51:1479-1483, J Natl Cancer Inst 1993, 85:1819-1827).

Norwegian women who were adolescents during World War II, when average caloric intake decreased by 22%, have a reduced incidence of breast cancer, suggesting that energy restriction might affect risk. (Cancer Causes Control 1996, 7:507-512).

A nested case-control study was conducted among participants in the Nurses’ Health Study who completed a 24-item questionnaire about diet during high school. There were 843 eligible cases diagnosed [with breast cancer] between onset of study (1976) and before the return of the high school diet questionnaire (1986), who were matched 10:1 with controls on the basis of age.

Participants who had completed the high school diet assessment section of the 1986 follow-up questionnaire and who also had reported current diet in 1980 were eligible for the study.

Breast cancer cases reported lower vitamin A intake and higher alcohol intake in 1980 than did controls.

Increased consumption of eggs was inversely associated with risk of breast cancer. Eggs are rich sources of essential amino acids, minerals and vitamins. For instance, one egg contains 11.5% of the recommended daily allowance for folate and 6.5% of that for vitamin D.

Conversely, increased consumption of butter was associated with a slight increase in risk. Neither animal fat, total fat, nor unsaturated fat was associated with increased risk on nutrient analysis; however, another nutrient in butter might confer increased risk, or the consumption of butter might be a proxy for another risk factor.

When specific nutrients were examined, increased consumption of both vegetable fat and dietary fiber was associated with a decreased risk of breast cancer. Fiber might affect the risk of breast cancer by decreasing estrogen levels; fiber binds estrogen excreted into the gastrointestinal tract and reduces enterohepatic circulation. (J Steroid Biochem Mol Biol 1991, 39:193-202, J Steroid Biochem Mol Biol 1991, 38:621-628).

In addition, higher dietary fiber intake has been associated with higher plasma levels of sex-hormone-binding globulin, which can reduce the bioavailability of estrogens. (Cancer 1994, 74:1125-1131).

The potential mechanism of a protective effect of vegetable fat is more speculative: vegetable fat is a composite of multiple forms of fatty acids, some of which have been proposed to increase risk - such as C18:2n-6, whereas other specific fatty acids have been proposed to decrease risk - such as C18:1, the primary fatty acid in olive oil. (Am J Clin Nutr 1997, 66(Suppl):1557S-1563S).

More detail on the type and composition of the vegetable oil used is necessary to pursue this relation with greater precision.

References

Adolescent diet and risk of breast cancer. Frazier AL, Ryan CT, Rockett H, Willett WC, Colditz GA. Breast Cancer Res 2003, 5:R59-R64 (21 February 2003). This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL. http://breast-cancer-research.com/content/5/3/R59

Buell P: Changing incidence of breast cancer in Japanese-American women. J Natl Cancer Inst 1973, 51:1479-1483.

Ziegler RG, Hoover RN, Pike MC, Hildesheim A, Nomura AM, West DW, Wu-Williams AH, Kolonel LN, Horn-Ross PL, Rosenthal JF: Migration patterns and breast cancer risk in Asian-American women. J Natl Cancer Inst 1993, 85:1819-1827.

Tretli S, Gaard M: Lifestyle changes during adolescence and risk of breast cancer: an ecologic study of the effect of World War II in Norway. Cancer Causes Control 1996, 7:507-512.

Arts CJ, de Bie AT, van den Berg H, van't Veer P, Bunnik GS, Thijssen JH: Influence of wheat bran on NMU-induced mammary tumor development, plasma estrogen levels and estrogen excretion in female rats. J Steroid Biochem Mol Biol 1991, 39:193-202.

Arts CJ, Govers CA, van den Berg H, Wolters MG, van Leeuwen P, Thijssen JH: In vitro binding of estrogens by dietary fiber and the in vivo apparent digestibility tested in pigs. J Steroid Biochem Mol Biol 1991, 38:621-628.

Goldin BR, Woods MN, Spiegelman DL, Longcope C, Morrill-LaBrode A, Dwyer JT, Gualtieri LJ, Hertzmark E, Gorbach SL: The effect of dietary fat and fiber on serum estrogen concentrations in premenopausal women under controlled dietary conditions. Cancer 1994, 74:1125-1131.

Willett WC: Specific fatty acids and risks of breast and prostate cancer: dietary intake. Am J Clin Nutr 1997, 66(Suppl):1557S-1563S.

Type 1 Diabetes - Gymnema significantly lowers insulin usage

Gymnema is a well-proven treatment for diabetes. It has been used for this purpose for over 2,000 years and has proved to be very effective in the treatment of type 1 diabetes.

“Gurmar” translates in English as “sugar destroyer”. The translation is literal: When Gymnema is applied to the mouth, it prevents the taste buds from perceiving sweet tastes.

"In my own clinical experience, I have found Gymnema to be the best herb available for treating this condition [diabetes] and controlling excessive blood sugar levels. (Kerry Bone, FNIMH, FNHAA, Nutrition and Healing Newsletter, January 2002).

Gymnema (Gymnema sylvestre) is a climbing plant that grows in open woods and bushland at an altitude of 100-1000 m in India, China, Indonesia, Japan, Malaysia, Sri Lanka, Vietnam and South Africa. Gymnema is also known as gurmar, gurmabooti, periploca of the woods, and meshasringi (ram’s horn). The Hindu word gurmar best describes the primary use of gymnema.

It is best known for its apparent ability to lower blood sugar levels. Results from case reports and studies in humans and animals suggest that it may work in several ways to help control both type 1 and type 2 diabetes. First, the acids contained in gymnema sylvestre seem to decrease the amounts of sugar that are absorbed from foods. As a result, blood sugar levels may not increase as much as usual after meals. Secondly, gymnema sylvestre may promote the production of insulin by the body. It is possible that gymnema sylvestre may even prompt the pancreas to develop more beta cells - the source of insulin. It may also make body cells more responsive to the insulin that is available. (DrugDigest).

In a 1990 study carried out by researchers at the University of Madras, India, 27 participants with insulin-dependent type 1 diabetes, ages from 10 to 50 years and with varying disease duration, were supplemented with 400 milligrams of Gymnema extract daily in two divided doses.

All were using daily insulin injections. After 6 to 8 months of treatment with the Gymnema extract the average insulin requirements were decreased from 60 to 45 units per day and fasting blood glucose levels were lowered.

In fact, one patient with a disease duration of 10 years and another with a lesser duration were able to discontinue insulin usage completely. These improvements continued through out the trial till its completion.

One has to find it remarkable that, compared to conventional treatment, patients with type 1 diabetes for 25 years responded equally as well as those who had been diagnosed for only one year when given the Gymnema extract supplement. So, there appears to be no time limitation on Gymnema use to still receive benefits.

This contrasts significantly to the diabetic group not taking Gymnema and receiving insulin alone for a year. Their insulin requirements either remained the same or increased and their average insulin usage was almost double that of the Gymnema group. Also, the drop in fasting blood glucose was statistically insignificant in this group.

In addition, cholesterol levels also returned to near normal levels and triglycerides were lowered in the group taking Gymnema. (J. Ethnopharmacol. 1990 Oct; 30(3): 281-94).

References

Shanmugasundaram, E R : Rajeswari, G : Baskaran, K : Rajesh Kumar, B R : Radha Shanmugasundaram, K : Kizar Ahmath, B. Use of Gymnema sylvestre leaf extract in the control of blood glucose in insulin-dependent diabetes mellitus. J. Ethnopharmacol. 1990 Oct; 30(3): 281-94.


Copyright 2007 Kevin Flatt. Disclaimer: The information contained in this article is presented for information purposes only and is in no way intended to replace professional medical care or attention by a qualified practitioner. It cannot and should not be used as a basis for diagnosis or choice of treatment.

Obesity and Erectile Dysfunction: Another Sad Story, Same Happy Ending

Written by Caroline Cederquist, M.D.

In the pantheon of contemporary culture, neither Adonis nor Aphrodite has love handles.

But two thirds of Americans do. Yet, contrary to conventional stereotypes, their excess weight hasn't hampered their interest in having a healthy sex life. In fact, research shows that overweight men are just as interested in sex as the next guy; they just may not be as able to perform.

Now, when it comes to performance anxiety, low self-esteem about body image can be a real impediment to confidence, so that may account for some of the problem.

But experts say that 90 percent of erectile dysfunction is physical in origin, not psychological. In large-scale studies, nearly 80 percent of men who reported having erectile dysfunction were also overweight or obese.



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So perhaps it won't be a surprise that a recent study published in the Journal of the American Medical Association has yielded some promising news about resolving this sensitive problem, and it doesn't have anything to do with little blue pills you hear advertised during major sporting events.

The research in question was a two-year study conducted at the Second University of Naples, Italy. The subjects were recruited from a campus weight-loss clinic. They were all obese men between the ages of 35 and 55. All reported some degree of erectile dysfunction, but they were otherwise healthy, without the complications of diabetes, hypertension or heart disease that are so common with obesity.

Half the subjects were supervised by medical professionals in individualized weight-loss treatment programs. They were educated about diet, fitness and personal behavioral adjustments in visits with a nutritional counselor and a personal trainer, every month for the first year, and then bi-monthly during the second year of the study.

The other half—the control group—just got general information about exercise and healthy dietary choices during visits every other month during the two-year study period.

By the end of the study, all the men in the supervised group had lost weight and experienced various health and sexual function improvements. In fact, by the time they'd achieved a weight loss of just 10 percent, erectile dysfunction was completely alleviated for one out of three men in that group.

But there was no change in weight for the control group, and even by the end of the study, only three of the 55 men in the control group had recovered normal erectile function.

Perhaps the most important finding of this study is one the researchers weren't even trying to prove: regardless of the objective, the weight loss effort is more effective with professional supervision. Remember that these men were all what you would call "motivated" subjects; they were recruited from among people who had already shown up at a weight-loss clinic, so they wanted to lose some weight. But even at that, the subjects who didn't have any particular guidance just couldn't do it.

The men did not know that the study was specifically examining the potential improvement in sexual function. Had they known this was a possible outcome of their effort, even the unsupervised group might have been more "motivated." When a healthy sex life is at stake—and for most overweight men, it is—men shouldn't just try to handle the problem on their own, because the right support seems to make all the difference.

That said, consider some of the other outcomes: In the supervised group, overall blood pressure was lowered, but not in the control group. In the supervised group, overall cholesterol levels dropped, but the subjects had an increase in their good HDL cholesterol levels. The control group's overall cholesterol went up, but with no increase in their good HDL levels.

Triglyceride levels and C-reactive protein counts also dropped for the supervised group, but not the control.You probably recognize these things as factors in heart health and diabetes, and so you can understand how the supervised subjects' also reduced their disease risk.

The researchers also tested endothelial function —the performance of cells lining the blood vessels— which has an impact on both cardiovascular health and erectile function. The chronic oxidative stress and inflammation caused by obesity impairs endothelial function. Here again, the men in the intervention group showed improvement, while the control group did not.

We already knew from previous research that overweight men who initiate weight loss in mid-life have 70 percent less risk of ever having erectile dysfunction than those who remain sedentary. The current study was meant to determine if weight loss could also reverse erectile dysfunction that had already set in, and it seems clear that it can.

If sales of Viagra, Levitra and Cialis are any indication, the pursuit of vigorous sexual function is a strong motivator for men of any age. Hundreds of millions of dollars have been invested in promoting the take-a-pill approach to that pursuit, and millions of men have responded, in spite of potential side effects and other health risks involved.

Imagine if even a few million dollars were invested in a public education campaign letting men know that just losing weight and improving their fitness could be the answer to their personal distress.

It's true that recently, there have been more public health efforts to promote weight-loss and fitness in general, especially given the epidemic of obesity and associated increases in diabetes and heart disease. But imagine the impact of a campaign that gave men the concrete goal of a healthy sex life. Most would agree that seems more tangible to the average fellow than say, lowering his triglycerides.

There's likely to be some personal cost involved in pursuing comprehensive weight loss treatment. But how do those costs compare to the expense of prescription approaches? And consider how much overall health care costs would go down if men tried to recover their lost virility by losing weight and getting healthy, instead of popping a pill.

No matter how medically appropriate and cost-effective, this is one treatment that—as a JAMA editorial put it—will never be "accompanied by free pens, free notepads and its own Superbowl commercial."

That means it's up to public health advocates and doctors to carry this message of hope without any big-budget hype.

THROUGH THICK & THIN: Erectile Dysfunction

Erectile dysfunction affects more than half of American males between age 40 and 70, and nearly 80 percent of men with the problem are overweight. Research shows that just walking a couple miles a day can significantly help a man's chances of avoiding—or even reversing—erectile dysfunction, and it's a lot cheaper and less risky than certain pills we hear a lot about.

About The Author:

Caroline J. Cederquist, M.D. is a board certified Family Physician and a board certified Bariatric Physicians (the medical specialty of weight management). Dr. Cederquist is the founder of Bistro MD formerly Diet To Your Door, a home diet delivery program that specializes in low calorie gourmet food that is delivered to your home or office. Bistro MD serves as culmination of Dr. Cederquist's expertise and experience in the world of medical weight loss.

Article Source: http://www.articleblast.com/

The Glycemic Index: Good Carb, Bad Carb

Written by Caroline Cederquist, M.D.

If you're one of those people who can't stand all the counting and tracking and adding and charting that some diets require, you could find a refuge in one simple numerical scale: the glycemic index. On the other hand, you might find it another maddening way to complicate the simple act of eating.

The glycemic index is a measure of the quality of carbohydrate foods. It's kind of a good carbs/bad carbs thing, based on how they affect your blood sugar. Though it's not new, it did start getting a lot of press when the anti-carb movement took hold.

It works like this: in the glycemic index, pure glucose is arbitrarily assigned the score of 100; it doesn't mean anything in particular; it's just a set reference point for how it has affected the blood sugar by about two hours after eating. Then all other foods in the index are given a number relative to glucose and its affect on the blood sugar.

Foods with a low index typically break down slowly and don't cause drastic fluctuations in blood sugar. Foods with a high index typically do. For instance, green peas have an index of 39, while corn flakes have an index of 92.

Originally developed to help folks—particularly diabetics—control their blood sugar, the index includes mainly carbohydrate foods, because protein and fat don't have much immediate effect on blood sugar.

But assigning numbers to different foods based on their glycemic effect just happens to create a scaled list of foods that ends up being a very useful tool for people dealing with obesity and other health issues, as well. That's because simply maintaining a low-glycemic index diet tends to guide people toward healthier eating and weight loss, even when that is not their specific goal.

Consider: Type II diabetes, as well as various cancers and cardiovascular disease, are all highly correlated with high index diets. There's abundant research that shows that reducing the overall glycemic index also reduces the risks of those problems.

That's because almost by default, a low-index diet will include more fresh fruits and vegetables, more fiber, more dairy, all foods that offer essential nutrients, that are more likely to be lower in calories and which tend to keep the body sated longer, holding off the next hunger spell. All that usually adds up to weight loss, no matter what the program.

Proponents of the index say it's more helpful than counting calories or grams of fats or carbs, and actually offers a simplified approach to learning to eat better, but some experts caution that people shouldn't get too wrapped up in worrying about the precise numbers. Instead, they urge that people pay attention to whether the foods they're eating have a low, medium or high index.

That's because, as with any rule, there are exceptions to the fairly consistent physiological rules that underlie the index. For instance, watermelon has a pretty high glycemic index, about 75, which is even higher than table sugar. Does that make it bad for you? No. Because in spite of its high index, watermelon actually has a pretty low glycemic load. That's a measure based on the amount of food you'd actually consume, not just an arbitrary quantity used in testing, as with the index.

The glycemic load of a food can be determined using the glycemic index number for a food, divided by 100 and multiplied times the available carbohydrate you'd eat. With most foods, low index is consistent with low load, but there are the quirky exceptions. Of course, to find them, you'd be back to doing a bunch of math again, and that's just not the way people normally eat.

That's why doctors and nutritional experts encourage people who are trying to develop a healthy diet to avoid getting caught up in the numbers game and look more generally at the foods in the index, leaning toward those at the low end. Anything over 70 is considered high index, 55 through 69 is medium and below 55 are foods with a low glycemic index.

And look what's in those groups: high index foods include most breakfast cereals, white breads and other processed baked goods, most potatoes, ice cream, candies and table sugar, your veritable Atkins nightmare.

Lower index foods include cherries, grapefruit, broccoli, legumes like lentils and beans, most whole grain baked goods and most dairy foods. So even without counting calories or keeping track of specific index numbers, you can see that steering your diet toward the low end of the index is bound to do you good.

We like to encourage patients to think of glycemic index and glycemic load as just two more tools that can be helpful in developing healthier thinking and planning about dietary habits.

A final thing to remember: there's not one standardizedglycemic index list and most indexes include brand-name items that people buy on a typical shopping trip, as well as the more generic items like vegetables and fruits. This is one of the more helpful aspects of the lists, but only if you get one that relates to where you live.

If your average Southwest Florida resident looked at an index created in Australia, it wouldn't be much help, because really, when's the last time you had a couple Golden Pikelets with a nice glass of Milo?

THROUGH THICK & THIN

Fruits tend to have a high glycemic index, so I recommend that people take their fruits with a meal, or with some protein like cottage cheese or regular cheese. These protein sources help mitigate the fruits glycemic effect. Don't let a high index number keep you away from your apple a day.

About The Author:

Caroline J. Cederquist, M.D. is a board certified Family Physician and a board certified Bariatric Physicians (the medical specialty of weight management). Dr. Cederquist is the founder of Bistro MD formerly Diet To Your Door, a home diet delivery program that specializes in low calorie gourmet food that is delivered to your home or office. Bistro MD serves as culmination of Dr. Cederquist's expertise and experience in the world of medical weight loss.

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