Joel Fuhrman, M.D.2013-05-25T17:49:09-04:00Joel Fuhrman, M.D.http://www.huffingtonpost.com/author/index.php?author=joel-fuhrman-mdCopyright 2008, HuffingtonPost.com, Inc.HuffingtonPost Blogger Feed for Joel Fuhrman, M.D.Good old fashioned elbow grease.Cruciferous Vegetables Improve Survival in Women With Breast Cancertag:www.huffingtonpost.com,2012:/theblog//3.16249652012-07-16T13:00:43-04:002012-09-15T05:12:02-04:00Joel Fuhrman, M.D.http://www.huffingtonpost.com/joel-fuhrman-md/breast cancer protection.
The cruciferous vegetable family:
Arugula
Bok choy
Broccoli
Broccoli rabe
Broccolini
Brussels sprouts
Cabbage
Cauliflower
Collards
Horseradish
Kale
Kohlrabi
Mustard greens
Radish
Red cabbage
Rutabaga
Turnips
Turnip greens
Watercress
The cruciferous family is unique among vegetables because of their glucosinolate content -- glucosinolates give cruciferous vegetables their characteristic spicy or bitter tastes; when the plant cell walls are broken by blending, chopping, or chewing, an enzyme called myrosinase converts glucosinolates to isothiocyanates (ITCs) -- compounds with potent anti-cancer effects, including:1
Anti-inflammatory effects -- ITCs have been found to decrease the secretion of inflammatory molecules.
Anti-angiogenic effects -- isothiocyanates can inhibit the development of new blood vessels to limit tumor growth.
Detoxification of carcinogens -- Some carcinogens must be converted to their active form before they can bind DNA to cause carcinogenic changes -- isothiocyanates can block this transformation.
Preventing DNA damage -- Isothiocyanates also increase the production of our body's natural detoxification enzymes, which protect DNA against damage from carcinogens and free radicals.
Stopping cell division in cells whose DNA has been damaged
Promoting programmed cell death in cancerous cells
Anti-estrogenic activity -- Exposure to estrogen is known to increase breast cancer risk; estrogens can alter gene expression, promoting cell proliferation breast tissue. ITCs have been shown to inhibit the expression of estrogen-responsive genes.
Shifting hormone metabolism -- Eating cruciferous vegetables regularly helps the body to shift hormone metabolism, reducing the cancer-promoting potency of estrogen and other hormones.
Eating cruciferous vegetables produces measurable isothiocyanates in breast tissue,2 and observational studies show that women who eat more cruciferous vegetables are less likely to be diagnosed with breast cancer. In a recent Chinese study, women who regularly ate one serving per day of cruciferous vegetables had a 50 percent reduced risk of breast cancer.3 A 17 percent decrease in breast cancer risk was found in a European study for consuming cruciferous vegetables at least once a week.4
What about women who already have cancer? Is it too late for cruciferous vegetables to improve their prognosis? We know that childhood and adolescence are the most crucial times for environmental stimuli to affect breast cancer risk, but changes made during adulthood and even after diagnosis still have the potential to create positive changes in the body.
The new study kept track of cruciferous vegetable intake in Chinese women with breast cancer for the first three years after diagnosis, and followed the women for a total of five years. They found dose-response effects -- this means that the more cruciferous vegetables women ate, the less likely they were to experience breast cancer recurrence or to die from breast cancer. When the women were grouped into four quartiles of cruciferous vegetable consumption, in the highest quartile had a 62 percent decrease in risk of death and 35 percent reduced risk of recurrence compared to the lowest quartile.5
This new data supports a previous report from the Women's Healthy Eating and Living (WHEL) study. Breast cancer survivors who reported higher than median cruciferous vegetable intake and were in the top third of total vegetable intake had a 52 percent reduced risk of recurrence -- especially powerful since the average intakes were quite low, 3.1 and 0.5 servings/day of total and cruciferous vegetables, respectively.6
Don't forget: cruciferous vegetables must be chopped, crushed, or chewed well for maximum benefit! The myrosinase enzyme is physically separated from the glucosinolates in the intact vegetables, but when the plant cells are broken, the chemical reaction can occur and ITCs can be formed. The more you chop before cooking (or chew, if you are eating the vegetables raw), the better. Some ITC benefit may be lost with boiling or steaming, so we get the maximum benefit from eating cruciferous vegetables raw -- however, gut bacteria also have the myrosinase enzyme, so additional ITC production may occur in cooked cruciferous vegetables after we eat them. Also, we can increase ITC production from cooked cruciferous vegetables by having some shredded raw cruciferous vegetables such as cabbage, kale, collards or arugula in a salad in the same meal to supply the myrosinase enzyme, which the body can use during the digestive process.
Combine anti-cancer foods to maximize protection against all cancers: A number of plant foods are associated with lower risk of cancers, and substances contained in these foods display anti-cancer or immune-boosting properties. The cancer-fighting strategy I describe in my book Super Immunity involves eating these super-foods ("G-BOMBS": greens, beans, onions, mushrooms, berries and seeds) simultaneously and in significant quantities. The combination of cruciferous vegetables with the rest of these powerful anti-cancer foods -- the onion family, mushrooms, beans and seeds -- creates delicious, healthful, and powerfully protective meals.
1. Higdon J, Delage B, Williams D, et al. "Cruciferous vegetables and human cancer risk: epidemiologic evidence and mechanistic basis." Pharmacol Res 2007;55:224-236.
2. Cornblatt BS, Ye L, Dinkova-Kostova AT, et al. "Preclinical and clinical evaluation of sulforaphane for chemoprevention in the breast." Carcinogenesis 2007;28:1485-1490.
3. Zhang CX, Ho SC, Chen YM, et al. "Greater vegetable and fruit intake is associated with a lower risk of breast cancer among Chinese women." Int J Cancer 2009;125:181-188.
4. Bosetti C, Filomeno M, Riso P, et al. "Cruciferous vegetables and cancer risk in a network of case-control studies." Ann Oncol 2012.
5. Nechuta SJ, Lu W, Cai H, et al: "Cruciferous Vegetable Intake After Diagnosis of Breast Cancer and Survival: a Report From the Shanghai Breast Cancer Survival Study." Abstract #LB-322. In Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4. Chicago, Il; 2012.
6. Thomson CA, Rock CL, Thompson PA, et al. "Vegetable intake is associated with reduced breast cancer recurrence in tamoxifen users: a secondary analysis from the Women's Healthy Eating and Living Study." Breast Cancer Res Treat 2011;125:519-527.]]>GOMBBS: Greens, Onions, Mushrooms, Berries, Beans and Seedstag:www.huffingtonpost.com,2011:/theblog//3.9963522011-10-09T08:24:13-04:002011-12-09T05:12:01-05:00Joel Fuhrman, M.D.http://www.huffingtonpost.com/joel-fuhrman-md/"GOMBBS" is an acronym you can use to remember the most nutrient-dense, health-promoting foods on the planet. These are the foods you should eat every day, and they should make up a significant proportion of your diet -- these foods can be effective at preventing chronic disease and promoting health and longevity.
G -- Greens
Raw leafy greens contain only about 100 calories per pound and are packed with nutrients. Leafy greens contain substances that protect blood vessels and are associated with reduced risk of diabetes.1 Greens are an excellent tool for weight loss, since they can be consumed in virtually unlimited quantities. Leafy greens are also the most nutrient-dense of all foods, but unfortunately are only consumed in miniscule amounts in a typical American diet.
We should follow the example of our closest living relatives -- chimpanzees and gorillas -- who consume tens of pounds of green leaves every day. The majority of calories in green vegetables, including leafy greens, come from protein, and this plant protein is packaged with beneficial phytochemicals: Green vegetables are rich in folate (the natural form of folic acid), calcium and contain small amounts of omega-3 fatty acids. Leafy greens are also rich in antioxidant pigments called carotenoids, specifically lutein and zeaxanthin, which are the carotenoids known to promote healthy vision.2
Also, several leafy greens and other green vegetables (such as bok choy, broccoli and kale) belong to the cruciferous family of vegetables. Vegetables contain protective micronutrients and phytochemicals, but cruciferous vegetables have a unique chemical composition. They contain glucosinolates, and when their cell walls are broken by blending, chopping or chewing, a chemical reaction converts glucosinolates to isothiocyanates (ITCs) -- compounds with a variety of potential anti-cancer effects. Because different ITCs can work in different locations in the cell and on different molecules, they can have combined additive effects, working synergistically to remove carcinogens, reduce inflammation, neutralize oxidative stress, inhibit angiogenesis (the process by which tumors acquire a blood supply) and help kill cancer cells.3
O -- Onions
Onions, along with leeks, garlic, shallots and scallions, make up the allium family of vegetables, which can have beneficial effects on the cardiovascular and immune systems, as well as posible anti-diabetic and anti-cancer effects. Allium vegetables are known for their characteristic organosulfur compounds. Similar to the ITCs in cruciferous vegetables, organosulfur compounds are released when onions are chopped, crushed or chewed. Epidemiological studies have suggested that increased consumption of allium vegetables is associated with lower risk of gastric and prostate cancers. It's been said these compounds prevent the development of cancers by detoxifying carcinogens, halting cancer cell growth and blocking angiogenesis.4
Onions also contain high concentrations of health-promoting flavonoid antioxidants, predominantly quercetin, and red onions also contain at least 25 different anthocyanins.5,6 Quercetin has been shown to slow tumor development, suppress growth and proliferation and induce cell death in colon cancer cells.7 Flavonoids also have anti-inflammatory effects that may contribute to cancer prevention.8
M -- Mushrooms
Consuming mushrooms regularly has been associated with decreased risk of breast, stomach and colorectal cancers. In one recent Chinese study, women who ate at least 10 grams of fresh mushrooms each day (about one mushroom per day) had a 64 percent decreased risk of breast cancer. Even more dramatic protection was gained by women who ate 10 grams of mushrooms and drank green tea daily -- an 89 percent decrease in risk for premenopausal women, and 82 percent for postmenopausal women.9,10
White, cremini, Portobello, oyster, shiitake, maitake and reishi mushrooms all have anti-cancer properties -- some have been shown to be anti-inflammatory, stimulate the immune system, prevent DNA damage, slow cancer cell growth, cause programmed cancer cell death and inhibit angiogenesis. In addition to these properties, mushrooms are unique in that they contain aromatase inhibitors -- compounds that can block the production of estrogen. These compounds are thought to be largely responsible for the preventive effects of mushrooms against breast cancer -- in fact, there are aromatase-inhibiting drugs on the market that are used to treat breast cancer. Regular consumption of dietary aromatase inhibitors is an excellent strategy for prevention, and it's been shown even the most commonly eaten mushrooms (white, cremini and Portobello) have a high anti-aromatase activity.11
B -- Berries
Blueberries, strawberries and blackberries are true super foods. Naturally sweet and juicy, berries are low in sugar and high in nutrients -- they are among the best foods you can eat. Their vibrant colors mean that they are full of antioxidants, including flavonoids and antioxidant vitamins -- berries are some of the highest antioxidant foods in existence. Berries' plentiful antioxidant content confers both cardioprotective and anti-cancer effects, such as reducing blood pressure, reducing inflammation, preventing DNA damage, inhibiting tumor angiogenesis and stimulating of the body's own antioxidant enzymes. Berry consumption has been linked to reduced risk of diabetes, cancers and cognitive decline.12 Berries are an excellent food for the brain -- berry consumption has been shown to improve both motor coordination and memory. 13
B -- Beans
Beans (and other legumes, as well) are a powerhouse of superior nutrition and the most nutrient-dense carbohydrate source. They can act as an anti-diabetes and weight-loss food because they are digested slowly, having a stabilizing effect on blood sugar, which promotes satiety and helps to prevent food cravings. Plus, they contain soluble fiber, which has been shown to lower cholesterol levels.14 Beans are unique foods because of their very high levels of fiber and resistant starch, carbohydrates that are not broken down by digestive enzymes. Fiber and resistant starch not only reduce total the number of calories absorbed from beans but are also fermented by intestinal bacteria into fatty acids that can help to prevent colon cancer.15 Eating beans, peas or lentils at least twice a week has been found to decrease colon cancer risk by 50 percent.16 Legume intake can also provide protection against oral, larynx, pharynx, stomach and kidney cancers.17
S -- Seeds
Nuts and seeds contain healthy fats and are rich in a spectrum of micronutrients including phytosterols, minerals and antioxidants. Countless studies have demonstrated the cardiovascular benefits of nuts, and including nuts in the diet can help aid in weight maintenance and diabetes prevention. 18,19
The nutritional profiles of seeds are similar to nuts when it comes to healthy fats, minerals and antioxidants, but seeds are also abundant in trace minerals, higher in protein than nuts, and each kind of seed is nutritionally unique. Flax, chia and hemp seeds are extremely rich sources of omega-3 fats. In addition to the omega-3s, flaxseeds are rich in fiber and lignans. Flaxseed consumption has been shown to protect against heart disease by a number of different mechanisms, and lignans, which are present in both flaxseeds and sesame seeds, can have anti-cancer effects.20
Sunflower seeds are especially rich in protein and minerals. Pumpkin seeds are rich in iron and calcium and are a good source of zinc. Sesame seeds have the greatest amount of calcium of any food in the world and provide abundant amounts of vitamin E. Also, black sesame seeds are extremely rich in antioxidants.21 The healthy fats in seeds and nuts also aid in the absorption of nutrients when eaten with vegetables.
You can learn more about the health benefits of GOMBBS in my new book "Super Immunity," a guide to naturally strengthening the immune system against everything from the common cold to cancer.
Dr. Fuhrman is a New York Times best-selling author, nutritional researcher and board certified family physician specializing in nutritional medicine. Learn more by visiting his informative website at DrFuhrman.com and his blog at Diseaseproof.com, and following Dr. Fuhrman on Facebook and Twitter.
21. Shahidi F, Liyana-Pathirana CM, Wall DS. Antioxidant activity of white and black sesame seeds and their hull fractions. Food Chemistry 2006;99(3): 478-483.]]>A Fast Metabolism Could Make You Age More Quicklytag:www.huffingtonpost.com,2011:/theblog//3.8708452011-06-15T18:33:57-04:002011-08-15T05:12:01-04:00Joel Fuhrman, M.D.http://www.huffingtonpost.com/joel-fuhrman-md/weight loss.
Toxic byproducts of metabolism and biological aging
The chemical reactions of normal, everyday physiology produces byproducts. In particular, cellular energy production produces reactive oxygen species as a byproduct, which can damage DNA, proteins and lipids. Although we have natural antioxidant defenses, oxidative damage can still occur, especially if we don't take in adequate antioxidants from our diet. (3) Oxidative damage accelerates aging.
Aging here refers to biological aging -- the progressive decline in the efficiency of the body's physiological functions over time. This leads to tissue and organ damage, and increased risk of chronic disease and death.
Why do our bodies age? It is a combination of factors. One, the accumulation of oxidative damage over time damages the body's tissues, leading to accelerated aging. (4,5) And two, just the rate of living slowly wears out our cellular machinery, so if we function at a faster rate -- i.e. a faster metabolism -- the body will "wear out" more quickly. In animals, energy expenditure is indeed inversely related to lifespan, supporting this. (6) Though both these mechanisms of aging are related, as a faster metabolic rate means faster energy turnover and greater production of free radicals, leading to increased oxidative damage.
Metabolic rate and lifespan
A study on thyroid function published last year further supported the idea that a slower metabolic rate could prolong lifespan. Now, a new study has measured resting metabolic rate directly and come to the same conclusion. Metabolic rate was measured by two different methods at the start of the study. Subjects were followed for 11 to 15 years, and deaths from natural causes were recorded. For each 100-calorie increase in 24-hour resting metabolic rate, the risk of natural mortality increased by 25 to 29 percent. These results strongly support the hypothesis that a slow metabolic rate promotes longevity. (7)
Do we have any control over our resting metabolic rate? How can we slow it down?
Resting metabolic rate is largely genetically determined, but our calorie intake has an effect as well. (8) Caloric restriction and negative energy balance have been shown to reduce resting metabolic rate, and in contrast overeating increases resting metabolic rate. (9-10) Furthermore, caloric restriction has been consistently shown to prolong maximal lifespan by up to 60 percent in animals. (11) My findings have demonstrated that an optimal micronutrient intake reduces the desire for calories and reduces body temperature and white blood cell counts. This means that if you follow a high-nutrient eating style that reduces calorie intake while meeting micronutrient demands, we can reduce our resting metabolic rate and potentially increase our longevity potential dramatically.
Keep in mind that although exercise raises total calorie expenditure, it does not raise the body's basal metabolism. Exercise is the only safe way to "raise metabolism" because it activates the peripheral tissues to utilize more calories and also increases muscle mass, which in turn increases total calorie expenditure. (12) Plus, exercise promotes longevity. (13)
The goal here is to eat so healthy that it reduces your desire to overeat and reduces your metabolism slowly, so you can comfortably desire less food, though not get too thin. Eating a high-nutrient diet actually makes you more satisfied with less food, and actually gives the ability to enjoy food more without overeating.
So, this new study suggests that having a fast metabolism does not mean that you are healthier -- in fact, it probably means that you are aging more quickly. Instead of trying to increase your metabolism with the goal of losing weight, try to slow your metabolism with a low-calorie, high-nutrient diet for a longer, healthier life.
References:
1. Astrup A, Gotzsche PC, van de Werken K, et al: Meta-analysis of resting metabolic rate in formerly obese subjects. Am J Clin Nutr 1999;69:1117-1122.
2. Ravussin E, Lillioja S, Knowler WC, et al: Reduced rate of energy expenditure as a risk factor for body-weight gain. N Engl J Med 1988;318:467-472.
3. Joseph JA, Denisova N, Fisher D, et al: Age-related neurodegeneration and oxidative stress: putative nutritional intervention. Neurol Clin 1998;16:747-755.
4. Hulbert AJ, Pamplona R, Buffenstein R, et al: Life and death: metabolic rate, membrane composition, and life span of animals. Physiol Rev 2007;87:1175-1213.
5. Farooqui T, Farooqui AA: Aging: an important factor for the pathogenesis of neurodegenerative diseases. Mech Ageing Dev 2009;130:203-215.
6. Speakman JR, Selman C, McLaren JS, et al: Living fast, dying when? The link between aging and energetics. J Nutr 2002;132:1583S-1597S.
7. Jumpertz R, Hanson RL, Sievers ML, et al: Higher Energy Expenditure in Humans Predicts Natural Mortality. J Clin Endocrinol Metab 2011.
8. Bouchard C, Tremblay A, Nadeau A, et al: Genetic effect in resting and exercise metabolic rates. Metabolism 1989;38:364-370.
9. Martin CK, Heilbronn LK, de Jonge L, et al: Effect of calorie restriction on resting metabolic rate and spontaneous physical activity. Obesity 2007;15:2964-2973.
10. Roberts SB, Fuss P, Evans WJ, et al: Energy expenditure, aging and body composition. J Nutr 1993;123:474-480.
11. Fontana L: The scientific basis of caloric restriction leading to longer life. Curr Opin Gastroenterol 2009;25:144-150.
12. Broeder CE, Burrhus KA, Svanevik LS, et al: The effects of aerobic fitness on resting metabolic rate. Am J Clin Nutr 1992;55:795-801.
13. Manini TM, Everhart JE, Patel KV, et al: Daily activity energy expenditure and mortality among older adults. JAMA 2006;296:171-179.]]>Girls' Early Puberty: What Causes It, And How To Avoid Ittag:www.huffingtonpost.com,2011:/theblog//3.8571672011-05-06T08:40:26-04:002011-07-06T05:12:01-04:00Joel Fuhrman, M.D.http://www.huffingtonpost.com/joel-fuhrman-md/study determined that the number of girls entering puberty (defined by breast development) at these early ages has increased markedly between 1997 and 2010.[1]
Trends in Age at Menarche
The average age at menarche in Western countries began declining during the early part of the 20th century due to increased consumption of animal products and increasing calorie intake; the decline slowed in the 1960s, and now in the U.S. there has been a more recent surge in early puberty starting in the mid-1990s.[2]
In Europe, in 1830, the average age at menarche was 17. Similarly in the 1980s in rural China, the average age at menarche was 17.3 In the U.S. in 1900, the average was 14.2. By the 1920s, average age at menarche in the U.S. had fallen to 13.3 and by 2002, it had reached 12.34.[4] Similar trends are occurring in other Western nations.[5,6] For example, age at menarche in Ireland has declined from 13.52 in 1986 to 12.53 in 2006.[7] In Italy, a recent study showed that girls' age at menarche was on average 3 months earlier than their mothers'.[8]
Taking all this data together, we can estimate that the normal, healthy age at menarche under conditions of excellent nutrition without caloric excess would probably fall somewhere between 15 and 18. But today in the U.S., about half of girls begin developing breasts before age 10, and the average age at menarche is less than 12 ½ and still declining.
Why Is this happening?
The neurological and hormonal systems that regulate pubertal timing are complex, but research has identified a number of environmental factors that may be contributing to the decline in age at puberty:
Increasing rates of childhood overweight and obesity
Several studies have found associations between higher childhood BMI and earlier puberty in girls.[4,9-11] Excess body fat alters the levels of the hormones insulin, leptin, and estrogen, and these factors are believed to be responsible for the acceleration of pubertal timing by obesity. Also, physical inactivity may decrease melatonin levels, which can also affect signals in the brain that trigger pubertal development.[4, 12]
Increased animal protein intake
Higher total protein, animal protein, and meat intake in children age 3-7 have been associated with earlier menarche in multiple studies.[13-15] In contrast, higher vegetable protein intake at age 5-6 is associated with later menarche.[15] High protein intake elevates IGF-1 levels and promotes growth, which could accelerate the onset of puberty - IGF-1 contributes to pubertal development on its own and in part by its involvement in estradiol signaling.[4,16] Meat and dairy consumption in children may also reflect ingestion of environmental endocrine-disrupting chemicals (EDCs) that have accumulated in animal tissues (see EDCs below).
Other dietary factors:
High dairy consumption is associated with earlier than average menarche.[17] Soft drink consumption is associated with early menarche.[18]
Children with lower nutrient diets (based on analysis of macronutrients, vitamins, minerals, and certain whole foods) tend to enter puberty earlier.[19] Overall our modern diet rich in processed foods, dairy, processed meats and fast food is disruptive to normal development and aging. Early puberty is an early sign of premature aging.
Exposure to endocrine-disrupting chemicals (EDCs)
EDCs are hormonally active synthetic chemicals that either mimic, inhibit, or alter the action of natural hormones. These chemicals are ubiquitous in our environment, and are considered by scientists to be a significant public health concern. Although EDCs are thought to pose a threat to adults as well, children's bodies are more sensitive to exposure to exogenous hormones.[20]
Chemicals are not currently tested for their endocrine disruption potential before they are approved for use and enter our environment, and there are endocrine disruptors in a vast array of products we come into contact with every day, including organochlorine pesticides, plastics, fuels, and other industrial chemicals.[21]
The substances of most concern currently are BPA and phthalates. BPA is one of the highest volume chemicals produced in the world. It is used in the manufacture of polycarbonate plastics, such as rigid cups, water bottles and food storage containers; BPA is also found in the linings of food cans and dental sealants. BPA can leach from containers into food and beverages, especially during heating and washing.[4] BPA exposure is associated with early puberty in girls.[22]
Phthalates are chemicals used to make PVC plastics more flexible, and are found in a variety of products including toys, food packaging, hoses, raincoats, shower curtains, vinyl flooring, wall coverings, lubricants, adhesives, detergents, nail polish, hair spray, and shampoo. Phthalates are associated with early breast development in girls.[22, 23] They are considered chemicals of concern to the EPA and may be phased out -- some phthalates have already been removed from children's toys and cosmetics. [24]
Additional EDCs that have been associated with dysregulation of pubertal timing include industrial chemicals such as PCBs, pesticides such as DDT and endosulfan, the flame retardant PBB, and dioxins and furans, which are formed during incineration of waste, chlorine bleaching of paper, and chemical manufacturing. [22,23,25,26]
It is important to note that EDCs break down very slowly and accumulate in the fatty tissues of animals, so animal foods contain higher levels of these chemicals than plant foods.
Why is this troublesome?
The most significant and alarming consequence of early maturation is an increased risk for breast cancer in adulthood. Early menarche is an established risk factor for breast cancer, and this is believed to be due to the extended lifetime exposure to ovarian hormones.[10,27,28] Similarly, exposure to EDCs during childhood is associated with hormonal cancers, such as breast and testicular cancers.[29-31]
Girls of 7, 8 or 9 years old are not emotionally or psychologically equipped to handle puberty. As such, earlier puberty is also associated with a higher risk of psychological problems during adolescence such as anxiety, depression, and eating disorders. Girls who mature earlier are also more likely to take part in risky behaviors like smoking and alcohol use.[4,12]
What can parents do to protect their children?
Children's diets should focus on whole plant foods rather than animal foods -- this will keep protein intake in a safe range and reduce their consumption of EDCs.
Minimize dairy products in children's diets -- use almond and hemp milks instead of cows' milk
Encourage children to exercise and exercise with them.
Minimize processed foods -- these are calorie-dense and nutrient-poor, and they promote obesity and other diseases.
Children's diets should include a wide variety of natural plant foods as possible including, green vegetables, squashes, corn, carrots, tomatoes, onions, mushrooms, nuts, seeds, avocados, beans, fruits and whole grains. This means that healthy eating is a lifetime event.
Buy organic produce when possible to avoid synthetic pesticides.
Minimize children's exposure to BPA: Avoid using of rigid polycarbonate plastics (recycling label #7) whenever possible; Do not use plastic water bottles if they are old or scratched; Do not microwave in plastic containers; Minimize the use of canned foods and avoid canned infant formulas.32
Minimize children's exposure to phthalates:Avoid plastics marked with recycling label #3 (PVC) whenever possible; Check ingredient lists on personal care products for phthalates. Also be aware that "fragrance" listed as an ingredient often means that the products contains phthalates. For more information, visit the Environmental Working Group's guide to children's personal care products.
To conclude, the earlier occurrence of puberty is an ominous event that we can stop. We can even win the war on breast cancer in America and prevent millions of young females from developing it. The answer however, must begin in the way we feed ourselves and our children. The most effective type of health care is vigilant and excellent self care.
References:
1. Biro FM, Galvez MP, Greenspan LC, et al: Pubertal Assessment Method and Baseline Characteristics in a Mixed Longitudinal Study of Girls. Pediatrics 2010.
2. Biro FM, Khoury P, Morrison JA: Influence of obesity on timing of puberty. Int J Androl 2006;29:272-277; discussion 286-290.
3. Gates JR, Parpia B, Campbell TC, et al: Association of dietary factors and selected plasma variables with sex hormone-binding globulin in rural Chinese women. Am J Clin Nutr 1996;63:22-31.
4. Steingraber S: Tha Falling Age of Puberty in U.S. Girls: What We Know, What We Need To Know. In Breast Cancer Fund; 2007.
5. McDowell MA, Brody DJ, Hughes JP: Has age at menarche changed? Results from the National Health and Nutrition Examination Survey (NHANES) 1999-2004. J Adolesc Health 2007;40:227-231.
6. Anderson SE, Must A: Interpreting the continued decline in the average age at menarche: results from two nationally representative surveys of U.S. girls studied 10 years apart. J Pediatr 2005;147:753-760.
7. O'Connell A, Gavin A, Kelly C, et al: The mean age at menarche of Irish girls in 2006. Ir Med J 2009;102:76-79.
8. Rigon F, Bianchin L, Bernasconi S, et al: Update on age at menarche in Italy: toward the leveling off of the secular trend. J Adolesc Health 2010;46:238-244.
9. Aksglaede L, Juul A, Olsen LW, et al: Age at puberty and the emerging obesity epidemic. PloS one 2009;4:e8450.
10. Vandeloo MJ, Bruckers LM, Janssens JP: Effects of lifestyle on the onset of puberty as determinant for breast cancer. Eur J Cancer Prev 2007;16:17-25.
11. Kaplowitz PB: Link between body fat and the timing of puberty. Pediatrics 2008;121 Suppl 3:S208-217.
12. Burt Solorzano CM, McCartney CR: Obesity and the pubertal transition in girls and boys. Reproduction 2010;140:399-410.
13. Berkey CS, Gardner JD, Frazier AL, et al: Relation of childhood diet and body size to menarche and adolescent growth in girls. Am J Epidemiol 2000;152:446-452.
14. Rogers IS, Northstone K, Dunger DB, et al: Diet throughout childhood and age at menarche in a contemporary cohort of British girls. Public Health Nutr 2010:1-12.
15. Gunther AL, Karaolis-Danckert N, Kroke A, et al: Dietary protein intake throughout childhood is associated with the timing of puberty. J Nutr 2010;140:565-571.
16. Veldhuis JD, Roemmich JN, Richmond EJ, et al: Endocrine control of body composition in infancy, childhood, and puberty. Endocr Rev 2005;26:114-146.
17. Wiley AS: Milk intake and total dairy consumption: associations with early menarche in NHANES 1999-2004. PloS one 2011;6:e14685.
18. Vandeloo MJ, Bruckers LM, Janssens JP: Effects of lifestyle on the onset of puberty as determinant for breast cancer. Eur J Cancer Prev 2007;16:17-25.
19. Cheng G, Gerlach S, Libuda L, et al: Diet quality in childhood is prospectively associated with the timing of puberty but not with body composition at puberty onset. J Nutr 2010;140:95-102.
20. Aksglaede L, Juul A, Leffers H, et al: The sensitivity of the child to sex steroids: possible impact of exogenous estrogens. Hum Reprod Update 2006;12:341-349.
21. Diamanti-Kandarakis E, Bourguignon JP, Giudice LC, et al: Endocrine-disrupting chemicals: an Endocrine Society scientific statement. Endocr Rev 2009;30:293-342.
22. Roy JR, Chakraborty S, Chakraborty TR: Estrogen-like endocrine disrupting chemicals affecting puberty in humans--a review. Med Sci Monit 2009;15:RA137-145.
23. Den Hond E, Schoeters G: Endocrine disrupters and human puberty. Int J Androl 2006;29:264-271; discussion 286-290.
24. Chemical Families: Phthalates. In Environmental Working Group.
25. Schell LM, Gallo MV: Relationships of putative endocrine disruptors to human sexual maturation and thyroid activity in youth. Physiol Behav 2010;99:246-253.
26. Massart F, Parrino R, Seppia P, et al: How do environmental estrogen disruptors induce precocious puberty? Minerva Pediatr 2006;58:247-254.
27. Leung AW, Mak J, Cheung PS, et al: Evidence for a programming effect of early menarche on the rise of breast cancer incidence in Hong Kong. Cancer Detect Prev 2008;32:156-161.
28. Pike MC, Pearce CL, Wu AH: Prevention of cancers of the breast, endometrium and ovary. Oncogene 2004;23:6379-6391.
29. Cohn BA, Cirillo PM, Christianson RE: Prenatal DDT exposure and testicular cancer: a nested case-control study. Arch Environ Occup Health 2010;65:127-134.
30. Cohn BA, Wolff MS, Cirillo PM, et al: DDT and breast cancer in young women: new data on the significance of age at exposure. Environ Health Perspect 2007;115:1406-1414.
31. Maffini MV, Rubin BS, Sonnenschein C, et al: Endocrine disruptors and reproductive health: the case of bisphenol-A. Mol Cell Endocrinol 2006;254-255:179-186.
32. Consumer tips to avoid BPA exposure. In Environmental Working Group.
]]>High Salt Diet Is Risky, Even if Your Blood Pressure Is Normaltag:www.huffingtonpost.com,2011:/theblog//3.8213232011-02-15T08:48:07-05:002011-05-25T18:30:24-04:00Joel Fuhrman, M.D.http://www.huffingtonpost.com/joel-fuhrman-md/natural foods, adding up to only about 1000 mg sodium per day. The dietary intake of sodium in the U.S. today is about 3500 mg/day. [2]
Excess dietary salt is most notorious for increasing blood pressure. Americans have a 90 percent lifetime probability of developing high blood pressure -- so even if your blood pressure is normal now, if you continue to eat the typical American diet, you will be at risk. Elevated blood pressure accounts for 62 percent of strokes and 49 percent of coronary heart disease. [3] Notably, the risk for heart attack and stroke begins climbing with systolic pressures (first number in the blood pressure reading) above 115 mm Hg -- considered "normal" by most standards.[4] Even if you eat an otherwise healthy diet, and your arteries are free of plaque, hypertension late in life damages the delicate blood vessels of the brain, increasing the risk of hemorrhagic stroke.
The American Heart Association, recognizing the significant risks of high blood pressure, has recently dropped their recommended maximum sodium intake from 2300 mg to 1500 mg.[5]
But did you know that salt has additional dangerous effects that are not related to blood pressure?
Cardiovascular disease.
In the 1990s, it was found that the relationship between salt intake and stroke mortality was stronger than the relationship between blood pressure and stroke mortality; this result suggested that salt may have deleterious effects on the cardiovascular system that are not related to blood pressure. [6] Further research determined that long-term excess dietary sodium promotes excessive cell growth leading to thickening of the vessel wall and altered production of structural proteins leading to arterial stiffening. [7-10]
Dietary salt has also been associated with endothelial dysfunction (the inability of endothelial cells to properly regulate blood pressure), which is one of the initiating events of atherosclerosis. [12] In fact, endothelial function is suppressed within a mere 30 minutes following a high salt meal. [13]
Kidney disease.
Hypertension is an important risk factor for kidney disease, but dietary sodium has other damaging effects on the kidneys. High salt intake drives the production of oxygen radicals, leading to oxidative stress in kidney tissue. [10] In the Nurses' Health Study, high dietary sodium was associated with a decline in kidney function over an 11-year follow-up period. [14] In patients who already have kidney disease, high salt intake promotes fibrosis of kidney tissue, contributing to kidney injury. [15]
Osteoporosis.
High salt intake is a risk factor for osteoporosis because excess dietary sodium promotes urinary calcium loss, leading to calcium loss from bone and therefore decreased bone density. Daily sodium intakes characteristic of Americans have been associated with increased bone loss at the hip, and sodium restriction reduces markers of bone breakdown. [16] Even in the presence of a high calcium diet, high salt intake results in net calcium loss from bone. [17]
Although postmenopausal women are most vulnerable to these calcium losses [18], high salt intake in young girls may prevent the attainment of peak bone mass during puberty, putting these girls at risk for osteoporosis later in life. [10]
Ulcers & gastric cancer.
Salt is the strongest factor relating to stomach cancer -- sodium intake data from 24 different countries were significantly correlated to stomach cancer mortality rates. [19] Additional studies have found positive correlations between salt consumption and gastric cancer incidence. [20] A high salt diet increases growth of the ulcer-promoting bacteria H. pylori in the stomach, which is also a risk factor for gastric cancer.[10]
Asthma.
In asthma patients, high dietary sodium may increase severity of the disease. [10]
Avoid added salt!
Reducing dietary salt is not only important for those who already have elevated blood pressure -- limiting added salt is essential for all of us to remain in good health. It is also important to note that expensive and exotic sea salts are still salt. All salt originates from the sea -- it contains over 98 percent sodium chloride, and it is not health-promoting. Sea salts may contain small amounts of trace minerals, the amounts are insignificant compared to those in natural plant foods. A high-nutrient, vegetable-based diet with little or no added salt is ideal.
Salt also deadens the taste buds -- this means that when you avoid highly salted and processed foods, you will regain your ability to detect and enjoy the subtle flavors in natural foods and actually experience heightened pleasure from natural, unsalted foods.
Dr. Fuhrman is a best-selling author, nutritional researcher and board certified family physician specializing in nutritional medicine. Visit his informative website at DrFuhrman.com, and his blog at DiseaseProof.com.
References:
1. Jacobson, M.F. Salt: The Forgotten Killer. Center for Science in the Public Interest, 2005.
2. Bernstein, A.M. and W.C. Willett, Trends in 24-h urinary sodium excretion in the United States, 1957-2003: a systematic review. The American journal of clinical nutrition, 2010. 92(5): p. 1172-80.
3. He, F.J. and G.A. MacGregor, A comprehensive review on salt and health and current experience of worldwide salt reduction programmes. J Hum Hypertens, 2009. 23(6): p. 363-84.
4. Lewington, S., et al., Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet, 2002. 360(9349): p. 1903-13.
5. Appel, L.J., et al., The Importance of Population-Wide Sodium Reduction as a Means to Prevent Cardiovascular Disease and Stroke: A Call to Action From the American Heart Association. Circulation, 2011.
6. Perry, I.J. and D.G. Beevers, Salt intake and stroke: a possible direct effect. J Hum Hypertens, 1992. 6(1): p. 23-5.
7. Simon, G., Experimental evidence for blood pressure-independent vascular effects of high sodium diet. Am J Hypertens, 2003. 16(12): p. 1074-8.
8. Sanders, P.W., Vascular consequences of dietary salt intake. Am J Physiol Renal Physiol, 2009. 297(2): p. F237-43.
9. Safar, M.E., et al., Pressure-independent contribution of sodium to large artery structure and function in hypertension. Cardiovasc Res, 2000. 46(2): p. 269-76.
10. de Wardener, H.E. and G.A. MacGregor, Harmful effects of dietary salt in addition to hypertension. Journal of human hypertension, 2002. 16(4): p. 213-23.
11. Lorenz, M.W., et al., Prediction of clinical cardiovascular events with carotid intima-media thickness: a systematic review and meta-analysis. Circulation, 2007. 115(4): p. 459-67.
12. Dickinson, K.M., J.B. Keogh, and P.M. Clifton, Effects of a low-salt diet on flow-mediated dilatation in humans. Am J Clin Nutr, 2009. 89(2): p. 485-90.
13. Dickinson, K.M., P.M. Clifton, and J.B. Keogh, Endothelial function is impaired after a high-salt meal in healthy subjects. The American journal of clinical nutrition, 2011.
14. Diets High In Sodium And Artificially Sweetened Soda Linked To Kidney Function Decline. ScienceDaily, 2009.
15. Jones-Burton, C., et al., An in-depth review of the evidence linking dietary salt intake and progression of chronic kidney disease. American journal of nephrology, 2006. 26(3): p. 268-75.
16. Devine, A., et al., A longitudinal study of the effect of sodium and calcium intakes on regional bone density in postmenopausal women. The American journal of clinical nutrition, 1995. 62(4): p. 740-5.
17. Teucher, B., et al., Sodium and bone health: impact of moderately high and low salt intakes on calcium metabolism in postmenopausal women. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2008. 23(9): p. 1477-85.
18. Heaney, R.P., Role of dietary sodium in osteoporosis. Journal of the American College of Nutrition, 2006. 25(3 Suppl): p. 271S-276S.
19. Sonnenberg, A., Dietary salt and gastric ulcer. Gut, 1986. 27(10): p. 1138-42.
20. Tsugane, S. and S. Sasazuki, Diet and the risk of gastric cancer: review of epidemiological evidence. Gastric Cancer, 2007. 10(2): p. 75-83.
]]>How Much Vitamin D? Why Many Experts Take Issue With The IOM's New Recommendationstag:www.huffingtonpost.com,2010:/theblog//3.8004682010-12-25T09:33:43-05:002011-05-25T18:20:30-04:00Joel Fuhrman, M.D.http://www.huffingtonpost.com/joel-fuhrman-md/Institute of Medicine (IOM) surprised many of us when it announced its new dietary reference intake (DRI) for vitamin D. The consensus of the scientific community was that the previous DRI of 400 IU was insufficient, and that supplementation with at least 1,000 IU would be necessary for most people to achieve vitamin D sufficiency. The IOM disagreed.
The IOM's new recommendations call for 600 IU per day for children and adults under age 70 (formerly 400 IU; for adults over age 70, the new recommendation is 800 IU), and the tolerable upper limit (amount not to be exceeded in one day) has been raised to 4,000 IU from 2,000 IU. Their definition of vitamin D sufficiency is a 25(OH)D level of 20 ng/ml.
There has been a great deal of research in recent years on vitamin D's role in a variety of human diseases. Low vitamin D status has been associated with cardiovascular disease, certain cancers, cognitive decline, depression, diabetes, pregnancy complications, autoimmune diseases and even a 78 percent increase in all-cause mortality risk (<17.8 ng/ml 25(OH)D compared to >32.1 ng/ml).[1] However, because there are not yet enough randomized controlled trials to clearly and conclusively confirm the benefits of vitamin D supplementation for conditions unrelated to bone health [2], the IOM did not find the existing evidence for non-skeletal conditions sufficient enough to raise the daily recommendations any higher than 600 IU. The 600 IU figure is based solely on bone health -- they did not take into account whether a greater quantity of vitamin D might be necessary to prevent non-skeletal diseases, even though there are vitamin D receptors in almost every cell of the human body.
Many experts are weighing in on -- and disagreeing with -- the IOM's report, and there is general agreement among the experts on these points:
The increase of the tolerable upper limit to 4,000 IU is a positive change.
The IOM's definition of 20 ng/ml as a sufficient 25(OH)D is potentially low, and this could be dangerous for some people
The lack of randomized controlled trials does not mean that we should ignore the epidemiological evidence showing vitamin D's importance for preventing non-skeletal diseases.
I agree with those who have brought up these issues, including Dr. John Cannell of the Vitamin D Council, respected public health researcher Dr. Walter Willett and prominent vitamin D scientist Dr. Heike Bischoff-Ferrari. Cannell also stressed the importance of vitamin D during fetal development, advising pregnant women especially to confirm sufficient 25(OH)D levels. Walter Willett of the Harvard School of Public Health, together with Heike Bischoff-Ferrari published an online commentary stating that there is ample evidence that 20 ng/ml (the IOM's definition of sufficiency) is not even sufficient for bone health, according to recent meta-analyses. [3] A new meta-analysis of randomized controlled trials by Bischoff-Ferrari found that supplementation with a mean of approximately 1,400 IU (range 792-2,000 IU) allowed adults age 65 and older to achieve a significant reduction in fracture rate. Taking this into account, increasing from 600 to 800 IU as recommended by the IOM at age 70 may still be sub-optimal. [4, 5]
My recommendations have not changed as a result of the IOM's updated recommendations. I agree with the experts mentioned above that we cannot discount the epidemiologically suggested benefits of supplementation with more than 600 IU vitamin D because of a lack of randomized controlled trials existing at this time. Especially since the risk of toxicity is so low: the minimum dose known to produce toxicity when taken for an extended period of time is 10,000 IU/day or even 50,000 IU according to some reports, resulting in blood 25(OH)D of 140 ng/ml or greater. [6] According to the Vitamin D council, a single 30 minute dose of sunshine has the potential to stimulate the production of up to 10,000 IU vitamin D, so it is extremely unlikely that doses below 10,000 IU will cause harm. [7]
Comparison of my recommendations to those of the IOM and the Vitamin D Council:
Recommendations for 25(OH)D and Vitamin D supplementation (for adults)
Institute of Medicine: >20 ng/ml; 600 IU
Dr. Fuhrman: 35-55 ng/ml; 2000 IU*
Vitamin D Council: 50-80 ng/ml; 5000 IU*
*also recommends to adjust supplementation according to 25(OH)D level
A chart showing IOM's revised recommendations for Calcium and Vitamin D intake: from the IOM website
As you can see, the IOM is on the low extreme, the Vitamin D council on the high extreme, and my recommendations are more moderate.
What I recommend is a safe, conservative amount of vitamin D which is supported by the literature. Recent reviews by prominent vitamin D researchers taking into account several studies on hypertension and colorectal cancer (for which evidence for a beneficial effect of vitamin D is quite strong) in addition to bone health concluded that 30 ng/ml should be the minimum sufficient level, and that a desirable range was approximately 36-48 ng/ml. I agree with this.
About 50 percent of North Americans have blood levels lower than 30 ng/ml. They further estimated that supplementation of at least 1000 IU would be necessary for most people to reach this desirable range. [8-10] The IOM's recommendation falls short of these figures. The IOM claims to be conservative, citing potential risks of over-supplementation, but I believe it is safer and more conservative to take the studies on non-skeletal conditions into account. The IOM with their still low recommended level of D may be taking risks with our lives here; my guidelines and D recommendations are more conservative and sensible given the strong possibility that 25(OH)D levels in the 20s may not be ideally protective, and certainly blood levels in the 30s and 40s could not be dangerous, since exposure to sunshine brings levels even higher than that.
It has been my experience that most people can reach sufficiency (defined by 35 ng/ml) with a 1,500-3,000 IU dose of vitamin D. We want to assure optimal levels, not just prevent deficiencies, and supplementing with 1,500-3,000 IU still falls well below the new tolerable upper limit of 4,000 IU.
The Vitamin D Council bases their higher recommendations on a body of research demonstrating the importance of vitamin D for fetal development, and vitamin D deficiency of millions of pregnant women (and their infants). They have concluded that 5,000 IU is an appropriate dose for pregnant women, and recommend that as a starting dose for all adults. Their recommended 25(OH)D level is at least 50 ng/ml for healthy people and higher for people with chronic diseases. As mentioned above, reviews of the literature have found that 36-48 ng/ml is likely the optimal range for disease prevention. [8, 9] The study on vitamin D levels and mortality agrees with this conclusion: 25(OH)D of 30-49 ng/ml was associated with the lowest mortality risk, and there was a significant (though slight) increase in risk above 50 ng/ml in women. [1]
Skin color, geographical location, time spent outside, sunscreen use, age etc., are all factors in how much vitamin D is produced by the skin (and therefore how much vitamin D is present and active in the body) before we take any supplements. People can differ greatly in the amount of Vitamin D required. So the supplemented dose is best determined by blood test, not by a predetermined amount set by the IOM or anyone else. Even then, the supplements we take may have varying potencies - some studies have found D2 to be less active, while others disagree.[11] In my practice, and vast experience monitoring Vitamin D levels over the last ten years or more, I have noticed that those taking D2 need a greater number of IUs compared to D3 to reach similar 25(OH)D levels.
A note on Calcium recommendations. Along with these new vitamin D recommendations by the IOM came revisions of their calcium recommendations, as shown in the chart above. Much of the scientific community has also been in agreement that calcium recommendations for Americans have been too high. For example, the World Health Organization advises an intake of 500 mg, whereas the IOM recommends 1000 mg. When making calcium recommendations, the interplay with vitamin D is important. As was found in the meta-analysis by Bischoff-Ferrari and Willett, vitamin D supplements in the range of 792-2000 IU were required to protect against osteoporosis-related fracture, demonstrating the inadequacy of the IOM's recent pronouncement. However, the most interesting finding here was related to calcium: low dose calcium supplementation (500 mg) combined with vitamin D supplementation reduced osteoporosis fracture rates, but high dose calcium supplements (1000 mg or more) combined with vitamin D supplementation did not. [3-5] These results suggest that high dose calcium blunts the beneficial effects of vitamin D. Furthermore, a recent meta-analysis has revealed that there is potential for cardiovascular harm from taking high dose calcium supplements. [12] I advise caution here - conventional (high) levels of calcium supplementation (above 1000 mg) are not only unnecessary, but may even be counter-productive.
Adjust supplementation accordingly to remain in the range of 35-55 ng/ml
If you do not yet know your 25(OH)D levels, approximately 2000 IU is a reasonable dose of vitamin D to take until you can get your levels tested.
References:
1. Melamed, M.L., et al., 25-Hydroxyvitamin D Levels and the Risk of Mortality in the General Population. Archives of Internal Medicine, 2008. 168(15): p. 1629-1637.
2. Zhang, R. and D.P. Naughton, Vitamin D in health and disease: Current perspectives. Nutr J, 2010. 9(65).
3. Bischoff-Ferrari, H.A. and W. Willett Comment on the IOM Vitamin D and Calcium Recommendations. Harvard School of Public Health: The Nutrition Source, 2010.
4. Zoler, M.L., High Vitamin D Intake Linked to Reduced Fractures. Family Practice News, 2010(November 16, 2010).
5. Bischoff-Ferrari, H.A., Orav, E.J., Willett, W. et al., A Higher Dose of Vitamin D is Required for Hip and Non-vertebral Fracture Prevention: A Pooled Participant-based Meta-analysis of 11 Double-blind RCTs, in The American Society for Bone and Mineral Research 2010 Annual Meeting2010: Toronto, Ontario, Canada.
6. Vieth, R., Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety. Am J Clin Nutr, 1999. 69(5): p. 842-56.
7. Cannel, J.J. Vitamin D Council Statement on FNB Vitamin D Report. 2010.
8. Bischoff-Ferrari, H.A., Optimal serum 25-hydroxyvitamin D levels for multiple health outcomes. Adv Exp Med Biol, 2008. 624: p. 55-71.
9. Bischoff-Ferrari, H.A., et al., Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr, 2006. 84(1): p. 18-28.
10. University of California - Riverside (2010, July 19). More than half the world's population gets insufficient vitamin D, says biochemist. ScienceDaily July 28, 2010]; Available from: http://www.sciencedaily.com/releases/2010/07/100715172042.htm.
11. Holick, M.F., et al., Vitamin D2 Is as Effective as Vitamin D3 in Maintaining Circulating Concentrations of 25-Hydroxyvitamin D. Journal of Clinical Endocrinology & Metabolism, 2007. 93(3): p. 677-681.
12. Bolland, M.J., et al., Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. Bmj, 2010. 341: p. c3691.
]]>Redefining Hunger Can Kick Start Weight Losstag:www.huffingtonpost.com,2010:/theblog//3.7899802010-12-05T11:00:47-05:002011-05-25T18:15:22-04:00Joel Fuhrman, M.D.http://www.huffingtonpost.com/joel-fuhrman-md/uncomfortable symptoms are the undoing of all of their attempts to lose weight by eating less food. Since eating removes the symptoms, these common symptoms are mistakenly believed to be hunger. People are led by these symptoms to consume more calories than they require, and this widespread overeating behavior has led to an epidemic of obesity, and a continual rise in preventable chronic diseases. Understanding the science behind overeating behaviors could be a key factor in reversing these trends.
Are these sensations truly signs of hunger? Conventional wisdom, and even medical textbooks, would suggest that they are. I disagree.
In my experience treating thousands of patients and guiding them through transitioning to a high nutrient density diet, I have observed that my patients' perceptions of hunger change. As their diet improves -- feelings of hunger become less frequent, less uncomfortable, and are mainly felt in the mouth and throat ("true hunger") rather than the head and stomach. I have now documented and published these results in the article "Changing perceptions of hunger on a high nutrient density diet" in Nutrition Journal, a peer-reviewed publication that encourages scientists and physicians to publish results that challenge current models, tenets or dogmas. This data collected on 768 participants does just that -- these results argue for a complete re-evaluation of our definition of human hunger.
The following are the five key results from my study:
1. "Hunger pains" were experienced less often and less intensely on a high nutrient density diet.
2. Discomfort between meals or upon a skipped meal was experienced less often on a high nutrient density diet.
3. Eighty percent of respondents reported that their experience of hunger had changed upon following a high nutrient density diet. The changed perception of hunger was proportional with the degree of dietary compliance.
4. Irritability and decline in mood were experienced less often on a high nutrient density diet
5. A high nutrient density diet was associated with more feelings of hunger in the mouth and throat and less in the head and stomach.
Conclusion: Enhancing the micronutrient quality of the diet leads to changes in the experience of hunger and a reduction in uncomfortable symptoms associated with hunger despite a lower caloric intake [1].
So if stomach grumbling, headaches and light-headedness a few hours after a meal disappear on a diet rich in micronutrients and are not really hunger, what are they?
The typical Western diet is characterized by high calorie processed foods: oils, sweeteners and animal products; a diet that is low in phytochemicals and other micronutrients. There is evidence that such a diet, low in phytochemicals, results in inflammation, oxidative stress and accumulation of toxic metabolites [2-4].
When digestion is complete, the body begins to mobilize and eliminate waste products, causing uncomfortable symptoms. If we allow waste metabolites to build up by eating unhealthy foods, we will feel discomfort when the body attempts to mobilize and remove these wastes. I propose that these sensations are actually symptoms of detoxification and withdrawal from an unhealthy diet, lacking in crucial micronutrients. I call this "Toxic Hunger". Scientists now know that unhealthy food has effects on the brain similar to those of addictive drugs. Natural plant foods, rich in micronutrients, do not produce withdrawal symptoms -- because inflammatory compounds and excess free radicals do not accumulate.
This is why so many diets fail. Simply restricting portions of the same disease-causing foods does not resolve the symptoms of toxic hunger. In addition to being effective for weight loss, a high nutrient diet has now been scientifically shown to change the perception of hunger, getting people in touch with "true hunger" (throat hunger).
Thousands of obese individuals who have failed one diet after another in the past have now lost dramatic amounts of weight. A high nutrient diet, if widely adopted, could bring millions of people in touch with true hunger, and stop the proliferation of obesity and preventable chronic disease.
You can read the free full-text with complete references of my study here.
References
1. Fuhrman, J., et al., Changing perceptions of hunger on a high nutrient density diet. Nutr J, 2010. 9: p. 51.
2. Egger, G. and J. Dixon, Inflammatory effects of nutritional stimuli: further support for the need for a big picture approach to tackling obesity and chronic disease. Obes Rev, 2010. 11(2): p. 137-49.
3. Devaraj, S., et al., High-fat, energy-dense, fast-food-style breakfast results in an increase in oxidative stress in metabolic syndrome. Metabolism, 2008. 57(6): p. 867-70.
4. Bhosale, P., B. Serban, and P.S. Bernstein, Retinal carotenoids can attenuate formation of A2E in the retinal pigment epithelium. Arch Biochem Biophys, 2009. 483(2): p. 175-81.
]]>Heart Health: How You Can Prevent and Reverse Heart Diseasetag:www.huffingtonpost.com,2010:/theblog//3.7835652010-11-17T08:14:47-05:002011-05-25T18:10:25-04:00Joel Fuhrman, M.D.http://www.huffingtonpost.com/joel-fuhrman-md/heart disease. But there are other options. When it comes to treating heart disease, most doctors promote drugs, expensive, invasive testing, high-tech medical procedures and heart surgery as the standard options. A significant number of research studies have documented that heart disease is easily and almost completely preventable through a diet rich in plant produce and lower in processed foods and animal products.
In a recent CNN interview, Bill Clinton reminded Americans of these other options. When asked about his recent weight loss, he explained that his heart disease had progressed after bypass surgery, requiring his recent additional surgery to place stents. This experience led him to learn about the successes of lifestyle changes at reversing heart disease. He is now following a plant-based diet, similar to those described by Dean Ornish, M.D. and Caldwell Esselstyn, M.D. -- Clinton has cut out all meat (except for occasional fish) and dairy from his diet -- he says that he lives on "beans, legumes, vegetables, fruit." Drs. Ornish and Esselstyn then also appeared on CNN where they explained that removing the foods that cause blood vessel damage and providing the body with copious phytonutrients can facilitate the body's natural healing processes to reverse existing heart disease and restore quality of life.
This was an excellent reminder to Americans that cholesterol-lowering drugs, stents and bypass surgery are not magic bullets to cure heart disease. Some studies suggest that cholesterol-lowering drugs carry serious side effects, and there is no evidence that statin use reduces risk of death in individuals with elevated cholesterol when used as primary prevention. (1-3) Most patients who undergo stent and bypass procedures have not removed the cause of their disease, and so they continue to experience progressive disability and most often die a premature death as a result of their heart disease. (4) Nevertheless, drugs and surgical procedures are still the standard care for treatment of elevated cholesterol and coronary artery disease.
Some studies show that atherosclerotic plaque can be reversed, and cholesterol lowered without drugs or surgery. Making significant dietary and lifestyle changes allow many people who suffer with coronary heart disease, high cholesterol, obesity and/or high blood pressure to reduce or even eliminate their dependence on medications and avoid invasive surgical procedures.
But what is the optimal diet for heart disease prevention and reversal?
Certainly not the small dietary changes recommended by government agencies and other organizations -- these are only modest changes to the average American's diet, and the average American starts developing heart disease during childhood. (5) Unfortunately, these widely voiced recommendations have made many people think by eating reduced-fat, processed foods and replacing red meat with egg whites, fish and chicken, they will be protected. They will not. These changes are simply not rigorous enough to assure predictable reversal.
Low-fat vegetarian diets are a vast improvement. The low-fat, vegetarian diet devised by Dean Ornish, M.D. provided the first hard evidence that heart disease could be reversed -- that atherosclerotic plaques could regress -- with diet and lifestyle changes alone. (6) Similar results were found by Caldwell Esselstyn, M.D. (7)
I propose that a high-nutrient, vegetable-based diet can be even more effective. According to a study published in the American Journal of Cardiology, comparing the effects of dietary interventions on LDL cholesterol levels, a low-fat vegetarian diet reduces LDL by 16 percent, but a high-nutrient, vegetable-based diet including daily nuts and seeds reduces LDL cholesterol by 33 percent. (8, 9) This result suggests that if we improve the low-fat, vegetarian diet by making it more nutrient-dense, and include more greens, beans, seeds and nuts we may reverse heart disease even faster, and reduce heart disease risk even more.
What is a high-nutrient, vegetable-based diet? I call this a nutritarian diet, because it is guided by the ratio of micronutrients to calories in foods. 90 percent of calories come from nutrient-rich plant foods: vegetables, beans, fruits, nuts and seeds.
Not just vegetarian, nutritarian: vegetable-based and nutrient-dense. We need to take vegetables out of the role of side dish, even in low-fat, vegetarian diets, whose calories are generally derived mainly from grains and other starches. To provide optimal levels of protective micronutrients, a diet must be vegetable-based, not grain-based. Vegetables and beans are far superior to grains and white potato when it comes to nutrient density. Furthermore, low-fat, high carbohydrate diets tend to increase triglyceride levels, a risk factor for heart disease. In contrast, a high-nutrient, vegetable-based diet with beans as the preferred carbohydrate source decreased triglycerides, lower blood glucose and accelerate fat loss. (8, 10)
Not low-fat: include healthy fats from nuts and seeds. Seeds and nuts are indispensable for cardiovascular health. The protective properties of nuts against coronary heart disease were first recognized in the early 1990s, and a strong body of literature has followed, confirming these original findings. (11) In spite of this wealth of data and all of the press on healthy fats, a "low-fat" diet is still viewed in a positive light. Certainly adding fats in the form of oils is fattening and unhealthy, but naturally fat-rich foods like nuts and seeds have profound cardiovascular benefits. Moderate use of nuts also encourages weight loss, not weight gain. (12) By avoiding nuts and seeds you may be missing out on these benefits. A recent meta-analysis of 25 clinical studies that compared a nut-eating group to a control group solidified the LDL-lowering effects of nuts. (13) According to a study published in The Journal of Nutrition, nut consumption reduces coronary heart disease risk far more than can be explained by cholesterol lowering alone -- 35 percent reduction in risk for five or more servings of nuts per week. (14)
These additional effects are only beginning to be discovered -- recent data has shed light on the protective properties of almonds and walnuts on vascular health. (15, 16) The Physicians Health Study demonstrated that eating nuts and seeds regularly protects against sudden cardiac death caused by arrhythmia. The data suggests that following a low-fat diet for a long period of time, though effective at reducing atherosclerotic plaque, could actually increase the risk of sudden cardiac death. (17)
I have seen a nutritarian diet produce astounding results in my practice. Hundreds of my patients, readers of my books and members of my website have dropped their cholesterol levels into the favorable range and reversed their existing heart disease -- without drugs -- using high nutrient eating, which places vegetables -- not meat, and not grains -- at the base of our food pyramid.
In this video, Ronnie Valentine tells his remarkable story of using a high-nutrient diet to reverse his heart disease and restore his health. After having quadruple bypass surgery, and then three stents and an angioplasty, he went to the internet for answers and decided to try a nutritarian diet. Ronnie has undergone a remarkable transformation.
The main point is not just the wonderful numbers he earned; it is that even after an angioplasty and with a medicine cabinet full of pills, he could not walk one block because of severe chest pain due to significant atherosclerosis and restenosis. Yet, in less than a year he became free of heart disease; he now runs, plays sports, and has a full, healthy, active life and needs no medications.
With the help of the Nutritional Research Project, I am in the planning stages of a scientific study that will document the extent of atherosclerotic plaque regression on the nutritarain diet.
References:
1. Ray, K.K., et al., Statins and all-cause mortality in high-risk primary prevention: a meta-analysis of 11 randomized controlled trials involving 65,229 participants. Arch Intern Med, 2010. 170(12): p. 1024-31.
2. Hippisley-Cox, J. and C. Coupland, Unintended effects of statins in men and women in England and Wales: population based cohort study using the QResearch database. Bmj, 2010. 340: p. c2197.
3. Sattar, N., et al., Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials. Lancet, 2010. 375(9716): p. 735-42.
4. Esselstyn, C.B., Jr., Resolving the Coronary Artery Disease Epidemic Through Plant-Based Nutrition. Prev Cardiol, 2001. 4(4): p. 171-177.
5. Berenson, G.S., et al., Atherosclerosis of the aorta and coronary arteries and cardiovascular risk factors in persons aged 6 to 30 years and studied at necropsy (The Bogalusa Heart Study). Am J Cardiol, 1992. 70(9): p. 851-8.
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8. Barnard, N.D., et al., Effectiveness of a low-fat vegetarian diet in altering serum lipids in healthy premenopausal women. Am J Cardiol, 2000. 85(8): p. 969-72.
9. Jenkins, D.J., et al., Effect of a very-high-fiber vegetable, fruit, and nut diet on serum lipids and colonic function. Metabolism, 2001. 50(4): p. 494-503.
10. Sarter, B., T.C. Campbell, and J. Fuhrman, Effect of a high nutrient density diet on long-term weight loss: a retrospective chart review. Altern Ther Health Med, 2008. 14(3): p. 48-53.
11. Fraser, G.E., et al., A possible protective effect of nut consumption on risk of coronary heart disease. The Adventist Health Study. Arch Intern Med, 1992. 152(7): p. 1416-24.
12. Mattes, R.D., P.M. Kris-Etherton, and G.D. Foster, Impact of peanuts and tree nuts on body weight and healthy weight loss in adults. J Nutr, 2008. 138(9): p. 1741S-1745S.
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]]>The Cure for the American Diet: Nutrient Densitytag:www.huffingtonpost.com,2010:/theblog//3.6954742010-09-09T07:00:00-04:002011-11-17T09:02:45-05:00Joel Fuhrman, M.D.http://www.huffingtonpost.com/joel-fuhrman-md/
The key to excellent health and longevity is to eat a high ratio of micronutrients to macronutrients. Macronutrients contain calories -- fat, carbohydrate and protein -- thereby supplying us with energy. Micronutrients -- vitamins, minerals, and phytochemicals -- don't contain calories, but have other essential roles. Thousands of these compounds work synergistically to detoxify carcinogens, deactivate free radicals, enable DNA repair, and maintain immune defenses. Lack of phytochemicals due to a low-micronutrient diet has an inevitable consequence: chronic disease. Low-nutrient foods also stimulate overeating. Low-nutrient, high-calorie food is known to be physiologically addictive, having effects on the brain similar to those of illegal drugs.(2) Dieting by portion control doesn't work because one is constantly fighting addictive drives. However, the drive to over-consume calories is blunted by high-micronutrient food.
I describe the basic principle of nutritional science with my Health Equation:
Health = Nutrients / Calories (H = N / C)
Your future health can be predicted by the nutrient density of your diet
The human body is a miraculous self-healing machine, but those self-repair systems require a nutrient-dense diet. It is normal for my diabetic patients to become un-diabetic, and for my patients with heart disease to have the plaque in their arteries shrink and slowly disappear -- these high-nutrient foods are powerful medicine:
Green vegetables contain potent anti-cancer compounds called isothiocyanates (3), and are the most nutrient-dense of all foods.
The Onion family contains cancer-protective organosulfur compounds (4), and consuming mushrooms regularly decreases the risk of breast cancer. (5)
Fruits, especially berries and pomegranate. Berries are full of antioxidants and are linked to reduced risk of diabetes, cancers and cognitive decline. (6) Pomegranate has multiple cardiovascular health benefits, for example reducing LDL cholesterol and blood pressure, and accelerating atherosclerotic plaque regression. (7)
Beans are a nutrient-dense weight-loss food -- they stabilize blood sugar, promoting satiety and preventing food cravings. Regular bean consumption helps to reduce cholesterol and is associated with decreased cancer risk. (8)
Nuts contain a spectrum of beneficial nutrients including healthy fats , LDL-lowering phytosterols, circulation-promoting arginine, minerals and antioxidants; they have significant cardiovascular benefits and promote weight control. (9) Seeds are abundant in trace minerals, and each kind is nutritionally unique. Flaxseeds provide abundant omega-3s, pumpkin seeds are rich in zinc and iron, and sesame seeds are high in calcium and multiple vitamin E fractions.
Doesn't every American have the right to know they don't have to suffer a heart attack or a stroke? They can protect themselves. They could choose otherwise, but shouldn't they be informed of the most effective lifestyle to protect against cancer? Should they just be given drugs for diabetes, cholesterol, blood pressure and more or should they know they have the opportunity for a complete non-drug recovery? I believe the time is now to take action and improve the health of our country. If we mobilize our resources to educate people of all ages, we can win this critical war against heart disease and cancer, which we are presently losing. We don't need to find the cure, it has already been found and it is sitting there on the shelves of our grocery stores.
Dr. Fuhrman is a best-selling author, nutritional researcher and board certified family physician specializing in nutritional medicine. Visit his informative website at DrFuhrman.com.
2. Johnson PM, Kenny PJ. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nat Neurosci. 2010 Mar 28. [Epub ahead of print]
Scripps Research Institute (2010, March 29). Compulsive eating shares addictive biochemical mechanism with cocaine, heroin abuse, study shows. ScienceDaily. Retrieved April 16, 2010, from http://www.sciencedaily.com/releases/2010/03/100328170243.htm
3. Higdon JV et al. Cruciferous Vegetables and Human Cancer Risk: Epidemiologic
Evidence and Mechanistic Basis. Pharmacol Res. 2007 March ; 55(3): 224-236
4. Powolny AA, Singh SV. Multitargeted prevention and therapy of cancer by
diallyl trisulfide and related Allium vegetable-derived organosulfur compounds.
Cancer Lett. 2008 Oct 8;269(2):305-14.
5. Zhang M, et al. Dietary intakes of mushrooms and green tea combine to reduce the risk of breast cancer in Chinese women. Int J Cancer. 2009;124:1404-1408
6. Bazzano LA, Li TY, Joshipura KJ, Hu FB. Intake of fruit, vegetables, and fruit juices and risk of diabetes in women. Diabetes Care. 2008 Jul;31(7):1311-7.
Hannum SM. Potential impact of strawberries on human health: a review of the science. Crit Rev Food Sci Nutr. 2004;44(1):1-17.
Joseph JA, Shukitt-Hale B, Willis LM. Grape juice, berries, and walnuts affect brain aging and behavior. J Nutr. 2009 Sep;139(9):1813S-7S.
Stoner GD, Wang LS, Casto BC. Laboratory and clinical studies of cancer chemoprevention by antioxidants in berries. Carcinogenesis. 2008 Sep;29(9):1665-74.
7. Aviram M, Rosenblat M, Gaitini D, et al. Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation. Clin Nutr 2004;23(3):423-33.
8. Bazzano LA, Thompson AM, Tees MT, et al. Non-soy legume consumption lowers cholesterol levels: A meta-analysis of randomized controlled trials. Nutr Metab Cardiovasc Dis. 2009 Nov 23. [Epub ahead of print]
Aune D, De Stefani E, Ronco A, et al. Legume intake and the risk of cancer: a multisite case-control study in Uruguay. Cancer Causes Control. 2009 Nov;20(9):1605-15.
9. Sabaté J, Ang Y. Nuts and health outcomes: new epidemiologic evidence. Am J Clin Nutr. 2009 May;89(5):1643S-1648S. Epub 2009 Mar 25.
Mattes RD et al. Impact of peanuts and tree nuts on body weight and healthy weight loss in adults. J Nutr. 2008 Sep;138(9):1741S-1745S.]]>
