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high-fiber-foods

How fiber-rich foods protect against breast cancer

Breast cancer —  two words that strike fear in every woman.  The good news is women can help lessen their risk.  One important defense is to consume a high-fiber diet.

A 2011 meta-analysis of 10 scientific studies found that higher fiber intake is associated with lower risk of breast cancer.1 In 2012, another meta-analysis of 16 studies came to the same conclusion.2 In the Nurses’ Health Study, higher fiber intake during childhood and adolescence was linked to a decrease in the risk of breast cancer in adulthood.3

How fiber impacts breast cancer risk

Given that animal products, refined grains, sugars and oils contain little or no fiber, fiber intake is a marker for greater intake of natural plant foods, many of which are known to have a variety of anti-cancer phytochemicals. Some breast cancer protective substances that have already been discovered include isothiocyanates from cruciferous vegetables4, organosulfur compounds from onions and garlic,5 aromatase inhibitors from mushrooms,6 flavonoids from berries,7,8 lignans from flax, chia and sesame seeds,9 and inositol pentakisphosphate (an angiogenesis inhibitor) from beans.10

Influence of fiber, glucose, insulin on breast cancer

High-fiber foods help to slow emptying of the stomach and absorption of sugars, which decreases the after-meal elevation in glucose. This is meaningful because elevated glucose levels lead to elevated insulin levels, which can send pro-cancer growth signals throughout the body, for example via insulin-like growth factor 1 (IGF-1).11 As such, high dietary glycemic index and glycemic load (characteristic of refined grains and processed foods) are associated with an increase in breast cancer risk.12-14  Accordingly, a study on Korean women found that higher white rice intake was associated with higher breast cancer risk.15

Fiber, estrogen, and breast cancer

Increased exposure to estrogen is known to increase breast cancer risk.16-18 A woman may be exposed to estrogen via her ovaries’ own production, estrogen production by excess fat tissue, or environmental sources such as endocrine-disrupting chemicals (like BPA, a chemical added to many consumer products). Fiber can reduce circulating estrogen levels, thereby reducing breast cancer risk, because it helps to remove excess estrogen from the body via the digestive tract. Fiber binds up estrogen in the digestive tract, accelerates its removal, and prevents it from being reabsorbed into the body.19-21

In addition, soluble fiber (as shown in studies using prunes and flaxseed) seems to alter estrogen metabolism so that a less dangerous form of estrogen is produced, whereas insoluble fiber (wheat bran) did not have the same effect. 22,23  For this reason, beans, oats, chia seeds and flaxseeds may provide some extra protection due to their high soluble fiber content.

Foods rich in fiber

Although most people probably just associate whole grains with fiber, beans contain more fiber than whole grains, and vegetables and fruits (and some seeds) contain comparable amounts – here are a few examples:

  • 1 cup cooked quinoa – 5 grams fiber
  • 1 cup cooked brown rice – 4 grams fiber
  • 1 cup cooked kidney beans – 11 grams fiber
  • 1 cup cooked broccoli – 6 grams fiber
  • 1 cup blueberries – 4 grams fiber
  • 1 tablespoon chia seeds – 6 grams fiber

Overall benefits of fiber: promotes weight loss and digestive health

Fiber, by definition, is resistant to digestion in the human small intestine. This means that during the digestive process, fiber arrives at the large intestine still intact. Fiber takes up space in the stomach but does not provide absorbable calories, and it also slows the emptying of the stomach.24 These properties of fiber make meals more satiating, slow the rise in blood glucose after eating and promote weight loss. In the colon, fiber adds bulk and accelerates movement, factors that are beneficial for colon health. Soluble fiber (primarily from legumes and oats) is effective at removing cholesterol via the digestive tract, resulting in lower blood cholesterol levels. Some types of fiber are fermented by intestinal bacteria. The fermentation products, short-chain fatty acids (SCFA) such as butyrate and propionate, have anti-cancer effects in the colon and also serve as energy sources for colonic cells. These SCFA are also thought to contribute to promoting insulin sensitivity and a healthy weight.25,26

Fermentable fiber also acts as a prebiotic in the colon, promoting the growth of beneficial bacteria. Fiber intake is associated with a multitude of health benefits, including healthy blood pressure levels and reduced risk of diabetes, heart disease and some cancers.24,27

Importance of choosing high-fiber and high-nutrient foods

Yes, fiber itself has some breast cancer-protective properties, like limiting glycemic effects of foods and assisting in estrogen removal, but we get optimal protection when we focus on foods that are both rich in fiber and rich in micronutrients and phytochemicals.

G-BOMBS contain fiber along with numerous anti-cancer phytochemicals, however, green (cruciferous) vegetables, mushrooms, flax and chia seeds in particular contain anti-estrogenic substances in addition to fiber, making them more effective breast cancer fighters than whole grains. Remember, beans are higher in fiber (and resistant starch) and lower in glycemic load than whole grains, making beans a better carbohydrate choice.

A Nutritarian diet is designed to include a full portfolio of the most protective foods to prevent cancer and slow the aging process.  Advances in nutritional science make winning the war against cancer a reality in our lifetime.

Originally printed on DrFuhrman.com. Reprinted with permission.

👉👉Get $10 off $150 or more on Dr. Fuhrman’s website. Use coupon LS10OFF150.


Joel Fuhrman, MD is a board-certified family physician specializing in nutritional medicine. He is President of the Nutritional Research Foundation and the author of 7 New York Times bestselling books, including his most recent book, “Eat to Live”. Visit his website, DrFuhrman.com.

 

References:
  1. Dong JY, He K, Wang P, et al. Dietary fiber intake and risk of breast cancer: a meta-analysis of prospective cohort studies. Am J Clin Nutr 2011.
  2. Aune D, Chan DS, Greenwood DC, et al. Dietary fiber and breast cancer risk: a systematic review and meta-analysis of prospective studies. Ann Oncol 2012.
  3. Farvid MS, Eliassen AH, Cho E, et al. Dietary Fiber Intake in Young Adults and Breast Cancer Risk. Pediatrics 2016, 137:1-11.
  4. Liu X, Lv K. Cruciferous vegetables intake is inversely associated with risk of breast cancer: A meta-analysis. Breast 2012.
  5. Powolny A, Singh S. Multitargeted prevention and therapy of cancer by diallyl trisulfide and related Allium vegetable-derived organosulfur compounds. Cancer Lett 2008, 269:305-314.
  6. Chen S, Oh SR, Phung S, et al. Anti-aromatase activity of phytochemicals in white button mushrooms (Agaricus bisporus). Cancer Res 2006, 66:12026-12034.
  7. Stoner GD. Foodstuffs for preventing cancer: the preclinical and clinical development of berries. Cancer Prev Res (Phila) 2009, 2:187-194.
  8. Kristo AS, Klimis-Zacas D, Sikalidis AK. Protective Role of Dietary Berries in Cancer. Antioxidants (Basel) 2016, 5.
  9. Bergman Jungestrom M, Thompson LU, Dabrosin C. Flaxseed and its lignans inhibit estradiol-induced growth, angiogenesis, and secretion of vascular endothelial growth factor in human breast cancer xenografts in vivo. Clin Cancer Res 2007, 13:1061-1067.
  10. Maffucci T, Piccolo E, Cumashi A, et al. Inhibition of the phosphatidylinositol 3-kinase/Akt pathway by inositol pentakisphosphate results in antiangiogenic and antitumor effects. Cancer Res 2005, 65:8339-8349.
  11. Gallagher EJ, LeRoith D. The proliferating role of insulin and insulin-like growth factors in cancer. Trends Endocrinol Metab 2010, 21:610-618.
  12. Dong JY, Qin LQ. Dietary glycemic index, glycemic load, and risk of breast cancer: meta-analysis of prospective cohort studies. Breast Cancer Res Treat 2011, 126:287-294.
  13. Romieu I, Ferrari P, Rinaldi S, et al. Dietary glycemic index and glycemic load and breast cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC). Am J Clin Nutr 2012, 96:345-355.
  14. Sieri S, Pala V, Brighenti F, et al. High glycemic diet and breast cancer occurrence in the Italian EPIC cohort. Nutrition, metabolism, and cardiovascular diseases : NMCD 2012.
  15. Yun SH, Kim K, Nam SJ, et al. The association of carbohydrate intake, glycemic load, glycemic index, and selected rice foods with breast cancer risk: a case-control study in South Korea. Asia Pac J Clin Nutr 2010, 19:383-392.
  16. Hankinson SE, Eliassen AH. Endogenous estrogen, testosterone and progesterone levels in relation to breast cancer risk. J Steroid Biochem Mol Biol 2007, 106:24-30.
  17. Pike MC, Pearce CL, Wu AH. Prevention of cancers of the breast, endometrium and ovary. Oncogene 2004, 23:6379-6391.
  18. Bernstein L, Ross RK. Endogenous hormones and breast cancer risk. Epidemiol Rev 1993, 15:48-65.
  19. Aubertin-Leheudre M, Gorbach S, Woods M, et al. Fat/fiber intakes and sex hormones in healthy premenopausal women in USA. J Steroid Biochem Mol Biol 2008, 112:32-39.
  20. Aubertin-Leheudre M, Hamalainen E, Adlercreutz H. Diets and hormonal levels in postmenopausal women with or without breast cancer. Nutr Cancer 2011, 63:514-524.
  21. Goldin BR, Adlercreutz H, Gorbach SL, et al. Estrogen excretion patterns and plasma levels in vegetarian and omnivorous women. N Engl J Med 1982, 307:1542-1547.
  22. Haggans CJ, Travelli EJ, Thomas W, et al. The effect of flaxseed and wheat bran consumption on urinary estrogen metabolites in premenopausal women. Cancer Epidemiol Biomarkers Prev 2000, 9:719-725.
  23. Kasim-Karakas SE, Almario RU, Gregory L, et al. Effects of prune consumption on the ratio of 2-hydroxyestrone to 16alpha-hydroxyestrone. Am J Clin Nutr 2002, 76:1422-1427.
  24. Higdon J, Drake VJ: Fiber. In An Evidence-based Approach to Phytochemicals and Other Dietary Factors New York: Thieme; 2013: 133-148
  25. Canfora EE, Jocken JW, Blaak EE. Short-chain fatty acids in control of body weight and insulin sensitivity. Nat Rev Endocrinol 2015, 11:577-591.
  26. Sonnenburg ED, Sonnenburg JL. Starving our microbial self: the deleterious consequences of a diet deficient in microbiota-accessible carbohydrates. Cell Metab 2014, 20:779-786.
  27. Carbohydrates. In Nutritional Sciences: From Fundamentals to Food. Edited by McGuire M, Beerman KA; 2013
omega3-sources

Want to live longer? Watch your omega-3 levels

A recent study spanning 11 years and more than 2,000 participants yielded a startling finding: When comparing omega-3 index to conventional cardiovascular risk factors in older adults, it showed that having a low blood omega-3 index was as strong a predictor of mortality as smoking.1

The average age of the participants at the beginning of the study was 65, when their blood fatty acids were measured, and they were followed for 11 years. There were 2240 participants and 384 deaths over that time.

Comparing omega-3s and smoking

Omega-3 index is a measurement of DHA and EPA as a percentage of the total fatty acids in red blood cell membranes.  The average omega-3 index in the study was 5.8%, the lowest fifth had omega-3 index less than 4.2%, and the highest fifth had levels greater than 6.8%.

Using mathematical modeling, the researchers estimated that participants who were in the highest fifth of omega-3 index at age 65 gained 4.74 years of life compared to those in the lowest fifth. This was similar to the difference between smokers and non-smokers at age 65; smokers lost 4.73 years of life, according to the model.

Over the 11-year follow-up, of participants in both of the low-risk categories – non-smokers who had a high omega-3 index – 85% survived. This is compared to only 47% of those in the high-risk categories – smokers with a low omega-3 index.1 The loss of life years was similar in low-omega-3 + non-smoking and high-omega-3 + smoking.

More evidence connecting omega-3 levels with longevity 

This research comes a few months after a meta-analysis of 17 prospective cohort studies that linked higher circulating omega-3 fatty acid levels to longevity. In a pooled analysis of the studies, participants in the highest fifth of combined blood DHA and EPA were 15-18% less likely to die from any cause over the follow-up period (median follow-up time was 16 years in these studies). Higher blood omega-3s were also associated with reduced risk for death from cardiovascular disease and cancer.2

The importance of DHA and EPA

DHA and EPA are important structural and functional components of brain and retinal cell membranes. They also have triglyceride-lowering, anti-inflammatory, anti-platelet, and anti-hypertensive properties, plus beneficial effects on cell membranes that may also contribute to better health and a longer life.2

Previous studies have linked low omega-3 index (below approximately 5%) with increased risk of cognitive decline in older adults.3,4  All the above studies corroborate the prior studies linking low omega index to brain shrinkage and cognitive impairment, and they reinforce how critical it is to properly address this issue.

The bottom line

DHA and EPA supplementation is important for anyone who doesn’t eat fatty fish frequently. Omega-3 index is low in vegans – approximately 4% when measured in studies, and the research suggests that adding ALA from flax seeds and walnuts does not significantly raise omega-3 index in most people. Most of the ALA in our diet is burned for energy, not converted to EPA and DHA. Consuming pre-formed DHA and EPA is the most reliable way to increase omega-3 levels in the blood.5-8 I recommend checking the omega-3 index with a blood test and assuring DHA and EPA adequacy using an algae-based supplement (refrigerated if possible) to avoid the pollutants, microplastics, and animal protein in fatty fish, and as a more sustainable option than fish oil.

Originally printed on drfuhrman.com. Reprinted with permission.


Joel Fuhrman, MD is a board-certified family physician specializing in nutritional medicine. He is President of the Nutritional Research Foundation and the author of 7 New York Times bestselling books, including his most recent book, “Eat to Live”. Visit his website, DrFuhrman.com.

👉👉Get $10 off $150 or more on Dr. Fuhrman’s website. Use coupon LS10OFF150.


REFERENCES

  1. McBurney MI, Tintle NL, Vasan RS, et al. Using an erythrocyte fatty acid fingerprint to predict risk of all-cause mortality: the Framingham Offspring Cohort. Am J Clin Nutr 2021.
  2. Harris WS, Tintle NL, Imamura F, et al. Blood n-3 fatty acid levels and total and cause-specific mortality from 17 prospective studies. Nature Communications 2021, 12:2329.
  3. Coley N, Raman R, Donohue MC, et al. Defining the Optimal Target Population for Trials of Polyunsaturated Fatty Acid Supplementation Using the Erythrocyte Omega-3 Index: A Step Towards Personalized Prevention of Cognitive Decline? J Nutr Health Aging 2018, 22:982-998.
  4. Lukaschek K, von Schacky C, Kruse J, Ladwig KH. Cognitive Impairment Is Associated with a Low Omega-3 Index in the Elderly: Results from the KORA-Age Study. Dement Geriatr Cogn Disord 2016, 42:236-245.
  5. Craddock JC, Probst YC, Neale EP, Peoples GE. A Cross-Sectional Comparison of the Whole Blood Fatty Acid Profile and Omega-3 Index of Male Vegan and Omnivorous Endurance Athletes. J Am Coll Nutr 2021:1-9.
  6. Sarter B, Kelsey KS, Schwartz TA, Harris WS. Blood docosahexaenoic acid and eicosapentaenoic acid in vegans: Associations with age and gender and effects of an algal-derived omega-3 fatty acid supplement. Clin Nutr 2014.
  7. Office of Dietary Supplements, National Institutes of Health. Omega-3 Fatty Acids. Fact Sheet for Health Professionals [https://ods.od.nih.gov/factsheets/Omega3FattyAcids-HealthProfessional/]
  8. Arterburn LM, Hall EB, Oken H. Distribution, interconversion, and dose response of n-3 fatty acids in humans. Am J Clin Nutr 2006, 83:1467S-1476S.
plant-protein

Eat Plant Protein to Live Longer

Scientific research continues to show consuming red and processed meats or a high-animal protein diet has a profoundly damaging effect on overall health and longevity. It is vitally important that red meat in our diet should be replaced (or at least greatly limited) in favor of foods that are proven to offer protection against cancer – such as green vegetables, berries, beans, nuts and seeds. This should not be seen as controversial and is supported by an overwhelming amount of data. 

Long-term studies

Large, long-term studies investigating intakes of animal and plant protein with regard to mortality have consistently concluded that more plant protein and less animal protein is linked to a longer life. (1-4) Studies consistently link greater red meat consumption to a greater risk of premature death. (5-7)

Here’s an example:

A 2016 study published in JAMA Internal Medicine investigated the relationship between animal vs. plant protein sources and mortality risk from almost 30 years of follow-up from the Nurses’ Health Study and Health Professionals Follow-up Study. Together, these two studies included over 170,000 participants.

Interesting findings came out of one particular question the researchers asked: What would happen if the participants replaced some of their animal protein with plant protein?

They analyzed the data to estimate how participants’ risk of death from all causes over the follow-up period would change if some of the animal protein sources (equivalent to 3 percent of total daily calories) were replaced with plant protein sources:

  • Replace processed red meat: 34 percent decrease in risk
  • Replace unprocessed red meat: 12 percent decrease in risk
  • Replace poultry: 6 percent decrease in risk
  • Replace fish: 6 percent decrease in risk
  • Replace eggs: 19 percent decrease in risk
  • Replace dairy: 8 percent decrease in risk3

Higher intake of plant protein sources is associated with better health: for example, seeds and nuts reduce the risk of cardiovascular disease and are linked to longevity, and micronutrient and fiber-rich beans are linked to improved blood pressure, LDL cholesterol, body weight, insulin sensitivity and enhanced lifespan. (4, 8-13)

Prospective cohort studies are observational and cannot prove causality, but these studies are crucial to our understanding of health and longevity, because heart disease and cancer – our two biggest killers – develop over the course of multiple decades, not just a few months. Studies that follow tens of thousands of people for 10 or 20 years or more, and evaluate hard endpoints (death, heart attack, stroke, cancer, etc.) provide valuable insights into the habits that may promote or prevent these diseases. The significance of findings from observational studies is supported by laboratory studies showing there are plausible mechanisms for the association – good reasons why it’s not just a random correlation, but likely a causal relationship.

Many meat-centered diet proponents dismiss these important studies out of hand, ignoring the careful collection of data and complex mathematical analysis by skilled epidemiologists that control for potential confounding factors and detect potentially significant associations. 

The correlations between animal protein intake and all-cause mortality in long-term prospective studies are consistent with other observational studies on specific diseases, and are backed up by laboratory studies that have uncovered the plausible cellular and molecular mechanisms behind the correlations:

  • High animal protein intake excessively elevates insulin-like growth factor 1 (IGF-1), which promotes cancer development. (14-18) 
  • Research on nutrient-sensing pathways that respond to protein intake suggests reducing essential amino acid intake (i.e. reducing animal protein) promotes longevity. (19) (Note that the elderly require more protein than younger adults. (20, 21))
  • The pro-inflammatory effects of dietary saturated animal fats. (22-25)
  • The pro-oxidant and pro-inflammatory properties of excess heme iron. (26, 27)
  • Cooking-produced carcinogens in meats, such as heterocyclic amines and polycyclic aromatic hydrocarbons. (28-31)
  • Genotoxic N-nitroso compounds produced from processed meats. (30-33)
  • Detrimental effects of carnitine and choline on the gut microbiome that promote inflammation. (34-37)

Although eating a keto or carnivores’ diet can lower blood sugar and promote weight loss in the short term, the long-term effects of a diet so high in animal products (according to the preponderance of evidence) is damaging over the long term. That is why I reiterated that it is important to see the long-term studies with hard endpoints. Looking at short-term weight loss studies will lead you on a path to damage your potential for optimal longevity.

Although the disease-promoting effects take many years to build up, several short-term studies point to the beginnings of the damage of a high-animal product diet:

  • Measured after a single meal, butter impaired vascular function compared to nuts and other predominantly unsaturated plant fats. (38)
  • A study comparing Atkins, South Beach, and Ornish weight maintenance diets (all with the same calorie counts) assigned participants to each diet for four weeks each. At the end of the Atkins diet phase, LDL cholesterol was higher and vascular function lower compared to the other diets. (39) 
  • Participants (who lived at the study site during the study) were fed 420 g red meat or a vegetarian meal daily for 15 days, with the rest of their diets kept exactly the same. Stool samples and colon cells collected after 10 days on each diet showed an increase in production of carcinogenic N-nitroso compounds during the red meat diet compared to the vegetarian diet, and an increase in N-nitroso compounds binding to DNA in colon cells (which leads to DNA damage and colon cancer). (40)
  • A study comparing about two servings daily of fiber-rich whole grains to red meat for three weeks each suggested the whole grain diet improved gut microbiome diversity compared to the red meat diet. Body fat mass was also lower after the whole grain intervention. (41)
  • After four weeks, a diet containing red meat increased production of the pro-inflammatory compound TMAO, compared to white meat and vegetarian diets. (36)

Meat-heavy diets get one important thing right: They cut out weight gain-promoting, disease-promoting high-glycemic refined carbohydrates. But large amounts of animal products are unquestionably disease-promoting, too.  The Nutritarian diet does more than just restrict one type of harmful food. It limits or completely avoids all other disease-promoting foods and focuses heavily on foods that are richest in protective nutrients and are linked in scientific studies most consistently to a lower risk of cardiovascular disease, cancer, and other chronic diseases.

 


Joel Fuhrman, MD is a board-certified family physician specializing in nutritional medicine. He is President of the Nutritional Research Foundation and the author of 7 New York Times bestselling books, including his most recent book, “Eat to Live”. Visit his website, DrFuhrman.com.

👉👉Get $10 off $150 or more on Dr. Fuhrman’s website. Use coupon LS10OFF150.

Originally posted on DrFuhrman.com. Reprinted with permission.

References

  1. Budhathoki S, Sawada N, Iwasaki M, et al. Association of Animal and Plant Protein Intake With All-Cause and Cause-Specific Mortality. JAMA Intern Med 2019. doi: 10.1001/jamainternmed.2019.2806
  2. Huang J, Liao LM, Weinstein SJ, et al. Association Between Plant and Animal Protein Intake and Overall and Cause-Specific Mortality. JAMA Intern Med 2020. doi: 10.1001/jamainternmed.2020.2790
  3. Song M, Fung TT, Hu FB, et al. Association of Animal and Plant Protein Intake With All-Cause and Cause-Specific Mortality. JAMA Intern Med 2016, 176:1453-1463. doi: 10.1001/jamainternmed.2016.4182
  4. Tharrey M, Mariotti F, Mashchak A, et al. Patterns of plant and animal protein intake are strongly associated with cardiovascular mortality: the Adventist Health Study-2 cohort. Int J Epidemiol 2018. doi: 10.1093/ije/dyy030
  5. Wang X, Lin X, Ouyang YY, et al. Red and processed meat consumption and mortality: dose-response meta-analysis of prospective cohort studies. Public Health Nutr 2016, 19:893-905. doi: 10.1017/S1368980015002062
  6. Pan A, Sun Q, Bernstein AM, et al. Red Meat Consumption and Mortality: Results From 2 Prospective Cohort Studies. Arch Intern Med 2012. doi: 10.1001/archinternmed.2011.2287
  7. Sinha R, Cross AJ, Graubard BI, et al. Meat intake and mortality: a prospective study of over half a million people. Arch Intern Med 2009, 169:562-571. doi: 169/6/562 [pii] 10.1001/archinternmed.2009.6
  8. Grosso G, Yang J, Marventano S, et al. Nut consumption on all-cause, cardiovascular, and cancer mortality risk: a systematic review and meta-analysis of epidemiologic studies. Am J Clin Nutr 2015, 101:783-793. doi: 10.3945/ajcn.114.099515
  9. Jenkins DJ, Kendall CW, Augustin LS, et al. Effect of legumes as part of a low glycemic index diet on glycemic control and cardiovascular risk factors in type 2 diabetes mellitus: a randomized controlled trial. Arch Intern Med 2012, 172:1653-1660. doi: 10.1001/2013.jamainternmed.70
  10. Bazzano LA, Thompson AM, Tees MT, et al. Non-soy legume consumption lowers cholesterol levels: a meta-analysis of randomized controlled trials. Nutrition, metabolism, and cardiovascular diseases : NMCD 2011, 21:94-103. doi: 10.1016/j.numecd.2009.08.012
  11. Papanikolaou Y, Fulgoni VL, 3rd. Bean consumption is associated with greater nutrient intake, reduced systolic blood pressure, lower body weight, and a smaller waist circumference in adults: results from the National Health and Nutrition Examination Survey 1999-2002. J Am Coll Nutr 2008, 27:569-576. doi:
  12. Darmadi-Blackberry I, Wahlqvist ML, Kouris-Blazos A, et al. Legumes: the most important dietary predictor of survival in older people of different ethnicities. Asia Pac J Clin Nutr 2004, 13:217-220. doi:
  13. Li SS, Blanco Mejia S, Lytvyn L, et al. Effect of Plant Protein on Blood Lipids: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. J Am Heart Assoc 2017, 6. doi: 10.1161/JAHA.117.006659
  14. Travis RC, Appleby PN, Martin RM, et al. A Meta-analysis of Individual Participant Data Reveals an Association between Circulating Levels of IGF-I and Prostate Cancer Risk. Cancer Res 2016, 76:2288-2300. doi: 10.1158/0008-5472.CAN-15-1551
  15. Vigneri PG, Tirro E, Pennisi MS, et al. The Insulin/IGF System in Colorectal Cancer Development and Resistance to Therapy. Front Oncol 2015, 5:230. doi: 10.3389/fonc.2015.00230
  16. Anisimov VN, Bartke A. The key role of growth hormone-insulin-IGF-1 signaling in aging and cancer. Crit Rev Oncol Hematol 2013, 87:201-223. doi: 10.1016/j.critrevonc.2013.01.005
  17. Key TJ, Appleby PN, Reeves GK, Roddam AW. Insulin-like growth factor 1 (IGF1), IGF binding protein 3 (IGFBP3), and breast cancer risk: pooled individual data analysis of 17 prospective studies. Lancet Oncol 2010, 11:530-542. doi: 10.1016/S1470-2045(10)70095-4
  18. Kaaks R. Nutrition, insulin, IGF-1 metabolism and cancer risk: a summary of epidemiological evidence. Novartis Found Symp 2004, 262:247-260; discussion 260-268. doi:
  19. Mirzaei H, Raynes R, Longo VD. The conserved role of protein restriction in aging and disease. Curr Opin Clin Nutr Metab Care 2016, 19:74-79. doi: 10.1097/MCO.0000000000000239
  20. Bauer J, Biolo G, Cederholm T, et al. Evidence-based recommendations for optimal dietary protein intake in older people: a position paper from the PROT-AGE Study Group. J Am Med Dir Assoc 2013, 14:542-559. doi: 10.1016/j.jamda.2013.05.021
  21. Volpi E, Campbell WW, Dwyer JT, et al. Is the optimal level of protein intake for older adults greater than the recommended dietary allowance? J Gerontol A Biol Sci Med Sci 2013, 68:677-681. doi: 10.1093/gerona/gls229
  22. Erridge C. The capacity of foodstuffs to induce innate immune activation of human monocytes in vitro is dependent on food content of stimulants of Toll-like receptors 2 and 4. Br J Nutr 2011, 105:15-23. doi: 10.1017/S0007114510003004
  23. Erridge C, Attina T, Spickett CM, Webb DJ. A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation. Am J Clin Nutr 2007, 86:1286-1292. doi: 10.1093/ajcn/86.5.1286
  24. Masson CJ, Mensink RP. Exchanging saturated fatty acids for (n-6) polyunsaturated fatty acids in a mixed meal may decrease postprandial lipemia and markers of inflammation and endothelial activity in overweight men. J Nutr 2011, 141:816-821. doi: 10.3945/jn.110.136432
  25. Fritsche KL. The science of fatty acids and inflammation. Adv Nutr 2015, 6:293S-301S. doi: 10.3945/an.114.006940
  26. Cornelissen A, Guo L, Sakamoto A, et al. New insights into the role of iron in inflammation and atherosclerosis. EBioMedicine 2019, 47:598-606. doi: 10.1016/j.ebiom.2019.08.014
  27. Brewer GJ. Risks of copper and iron toxicity during aging in humans. Chemical research in toxicology 2010, 23:319-326. doi: 10.1021/tx900338d
  28. Zheng W, Lee S-A. Well-Done Meat Intake, Heterocyclic Amine Exposure, and Cancer Risk. Nutrition and Cancer 2009, 61:437-446. doi: 10.1080/01635580802710741
  29. National Cancer Institute. Chemicals in Meat Cooked at High Temperatures and Cancer Risk.
  30. International Agency for Research on Cancer, World Health Organization. Press Relsease No. 240. IARC Monographs evaluate consumption of red meat and processed meat. 2015.
  31. Turesky RJ. Mechanistic Evidence for Red Meat and Processed Meat Intake and Cancer Risk: A Follow-up on the International Agency for Research on Cancer Evaluation of 2015. Chimia (Aarau) 2018, 72:718-724. doi: 10.2533/chimia.2018.718
  32. Lunn JC, Kuhnle G, Mai V, et al. The effect of haem in red and processed meat on the endogenous formation of N-nitroso compounds in the upper gastrointestinal tract. Carcinogenesis 2007, 28:685-690. doi: 10.1093/carcin/bgl192
  33. Herrmann SS, Granby K, Duedahl-Olesen L. Formation and mitigation of N-nitrosamines in nitrite preserved cooked sausages. Food Chem 2015, 174:516-526. doi: 10.1016/j.foodchem.2014.11.101
  34. Koeth RA, Wang Z, Levison BS, et al. Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis. Nat Med 2013, 19:576-585. doi: 10.1038/nm.3145
  35. Tang WH, Wang Z, Levison BS, et al. Intestinal microbial metabolism of phosphatidylcholine and cardiovascular risk. N Engl J Med 2013, 368:1575-1584. doi: 10.1056/NEJMoa1109400
  36. Wang Z, Bergeron N, Levison BS, et al. Impact of chronic dietary red meat, white meat, or non-meat protein on trimethylamine N-oxide metabolism and renal excretion in healthy men and women. Eur Heart J 2019, 40:583-594. doi: 10.1093/eurheartj/ehy799
  37. Wang Z, Klipfell E, Bennett BJ, et al. Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature 2011, 472:57-63. doi: 10.1038/nature09922
  38. Keogh JB, Grieger JA, Noakes M, Clifton PM. Flow-mediated dilatation is impaired by a high-saturated fat diet but not by a high-carbohydrate diet. Arterioscler Thromb Vasc Biol 2005, 25:1274-1279. doi: 10.1161/01.ATV.0000163185.28245.a1
  39. Miller M, Beach V, Sorkin JD, et al. Comparative effects of three popular diets on lipids, endothelial function, and C-reactive protein during weight maintenance. J Am Diet Assoc 2009, 109:713-717. doi: 10.1016/j.jada.2008.12.023
  40. Lewin MH, Bailey N, Bandaletova T, et al. Red meat enhances the colonic formation of the DNA adduct O6-carboxymethyl guanine: implications for colorectal cancer risk. Cancer Res 2006, 66:1859-1865. doi: 10.1158/0008-5472.CAN-05-2237
  41. Foerster J, Maskarinec G, Reichardt N, et al. The influence of whole grain products and red meat on intestinal microbiota composition in normal weight adults: a randomized crossover intervention trial. PLoS One 2014, 9:e109606. doi: 10.1371/journal.pone.0109606
fruits veggies colorful

5 Ways to Amp Up Your Nutrient Intake

Thanks to fad diets, everyone has their own idea of what constitutes a healthy diet – and has a mental list of which foods will never touch their lips again. We’ve all been there: Low-Carb, No-Carb, Paleo, South Beach, Atkins, Gluten-Free, Foods That Match Your Eye Color – you name it. But these diet trends simply cherry-pick a few nutritional facts, served up alongside lots of disinformation.

The simple truth is that a healthful, nutritionally favorable diet means consuming a variety of vegetables, fruits, legumes, nuts, seeds and herbs. Fun fact: each and every plant food has its own distinct nutritional profile. More importantly: there are over 100,000 biologically active chemicals found in plants, agents that offer anticancer, antimicrobial, antioxidant, analgesic, and wound healing effects.

So how do you get those active chemicals to up our chances of living a long and healthy life? Let’s break it down:

1. Eat “the rainbow,” using a variety of natural plant foods.

Ensure that you consume a wide range of phytonutrients, many of which are antioxidants that offer a range of health benefits, from helping you lose excess weight and preventing disease, to slowing brain degeneration. The red in tomatoes comes from lycopene, the orange in carrots and sweet potatoes from alpha- and beta-carotene, the blues and reds of berries from anthocyanins, and the green in spinach and kale from lutein and chlorophylls. A variety of colors means a variety of health-promoting nutrients. 

2. The next time you load up at the grocery store, be sure your cart has these Superfoods.

Greens, Beans, Onions, Mushrooms, Berries and Seeds, known collectively to Nutritarians as G-Bombs. The planet’s best foods should be a part of everyone’s diet every day. Why? According to Dr. Fuhrman, these six magical foods benefit the immune system, can make you slim and healthy, and keep you that way while protecting you from cancer. Here’s just a taste of the power they possess and a simple recipe to help you reap some of their amazing benefits:

  • Greens, cruciferous vegetables in particular provide unique phytochemicals (ITCs) with a variety of cancer-fighting effects. Greater consumption of these vegetables is linked to reduced risk of cancer and cardiovascular disease and a longer life.1-3
  • Beans and other legumes  are rich in fiber and resistant starch, which help keep blood glucose, blood pressure, and LDL cholesterol down, promote weight loss, promote colon health, and nourish the microbiome.4-7
  • Onions and garlic are linked to a reduction in the risk of several cancers, and their distinctive sulfur-containing phytochemicals have a number of actions that benefit the cardiovascular system.8-11
  • Mushroom phytochemicals are unique in their promotion of immune system function and their abiity to inhibit of estrogen production; mushroom consumption is associated with a reduced risk of breast cancer.12-15
  • Berry phytochemicals have anti-cancer and blood pressure-lowering effects, and are linked to a reduced risk of heart attack.  Blueberries in particular have also shown promise for improving brain health, in studies on memory and cognitive function.16-22
  • Seeds and nuts: Eating nuts regularly is associated with longevity, reduced risk of cardiovascular disease, and a healthy body weight. Different seeds have different nutritional benefits; flax and chia, for example, are rich in omega-3 ALA and lignans, anti-estrogenic phytochemicals linked to a reduction in breast and prostate cancer risk.23-27

3. Focus on the nutrient-density of your diet.

A standard weight loss “diet” is one that focuses on controlling portion size and cutting down on junk food. The absolute best diet is one that concentrates on the amount of nutrients that food can provide and their phytonutrient power to protect against cancer. Natural foods with a high nutrient-density contain a significant amount of vitamins, minerals and other healthful substances with respect to their calories. This way of eating, called a Nutritarian Diet, has surged in popularity just as interest in the health benefits of various ingredients – kale, turmeric, berries – has spiked. Superfoods describe not only G-Bombs, but many others, too. For the list of some of Dr. Fuhrman’s must-eat foods, download his infographic 10 Best and 10 Worst Foods. Or for a deeper dive into the foods that benefit health and longevity, read Dr. Fuhrman’s magazine to learn his choices for the planet’s 100 Best Foods.


4. 
Break the junk food habit.

Processed junk foods are incredibly harmful to our health. They lead to obesity and illness, and cause detrimental chemical changes in the brain, affecting our emotional well being and drive cravings for more junk food. Eating junk food is a learned habit. These foods need to be eliminated entirely from your diet.

Kick start your transformation by cleaning out your refrigerator and pantry so you won’t be tempted with unhealthy foods. Here’s some easy ways to start:

  1. Sauté with water or low-sodium vegetable broth instead of oil
  2. Switch from cow’s milk to unsweetened soy, hemp, or almond milk
  3. Switch from sugar-sweetened breakfast cereal to steel cut oats topped with flax or chia seeds and berries
  4. Add tofu into a veggie scramble instead of eggs
  5. Say no to cheese
  6. Finish your meals with fresh fruit rather than sugary desserts

5. Don’t snack on healthy foods, either.

Learn to eat only at mealtimes, and only when you are hungry. If you are hungry between meals, it means you didn’t eat enough during the meal, so adjust your portions accordingly. Refraining from snacking might be hard to do at first, but it will become second nature after a while.  It is especially important not to eat after dinner before bedtime.


Article originally printed on DrFuhrman.com. Reprinted with permission from Dr. Fuhrman.

Joel Fuhrman, MD is a board-certified family physician specializing in nutritional medicine. He is President of the Nutritional Research Foundation and the author of 7 New York Times bestselling books, including his most recent book, “Eat to Live”. Visit his website, DrFuhrman.com.

 

References:

  1. Zhang X, Shu XO, Xiang YB, et al. Cruciferous vegetable consumption is associated with a reduced risk of total and cardiovascular disease mortality. Am J Clin Nutr 2011, 94:240-246
  2. Pollock RL. The effect of green leafy and cruciferous vegetable intake on the incidence of cardiovascular disease: A meta-analysis. JRSM Cardiovasc Dis 2016, 5:2048004016661435.
  3. Higdon J, Delage B, Williams D, Dashwood R. Cruciferous vegetables and human cancer risk: epidemiologic evidence and mechanistic basis. Pharmacol Res 2007, 55:224-236.
  4. Papanikolaou Y, Fulgoni VL, 3rd. Bean consumption is associated with greater nutrient intake, reduced systolic blood pressure, lower body weight, and a smaller waist circumference in adults: results from the National Health and Nutrition Examination Survey 1999-2002. J Am Coll Nutr 2008, 27:569-576.
  5. Jayalath VH, de Souza RJ, Sievenpiper JL, et al. Effect of dietary pulses on blood pressure: a systematic review and meta-analysis of controlled feeding trials. Am J Hypertens 2014, 27:56-64.
  6. Bazzano LA, Thompson AM, Tees MT, et al. Non-soy legume consumption lowers cholesterol levels: a meta-analysis of randomized controlled trials. Nutrition, metabolism, and cardiovascular diseases : NMCD 2011, 21:94-103.
  7. Sievenpiper JL, Kendall CW, Esfahani A, et al. Effect of non-oil-seed pulses on glycaemic control: a systematic review and meta-analysis of randomised controlled experimental trials in people with and without diabetes. Diab tologia 2009, 52:1479-1495.
  8. Rahman K, Lowe GM. Garlic and cardiovascular disease: a critical review. J Nutr 2006, 136:736S-740S.
  9. Powolny A, Singh S. Multitargeted prevention and therapy of cancer by diallyl trisulfide and related Allium vegetable-derived organosulfur compounds. Cancer Lett 2008, 269:305-314.
  10. Bradley JM, Organ CL, Lefer DJ. Garlic-Derived Organic Polysulfides and Myocardial Protection. J Nutr 2016, 146:403S-409S.
  11. Galeone C, Pelucchi C, Levi F, et al. Onion and garlic use and human cancer. Am J Clin Nutr 2006, 84:1027-1032.
  12. Borchers AT, Krishnamurthy A, Keen CL, et al. The Immunobiology of Mushrooms. Exp Biol Med 2008, 233:259-276.
  13. Jeong SC, Koyyalamudi SR, Pang G. Dietary intake of Agaricus bisporus white button mushroom accelerates salivary immunoglobulin A secretion in healthy volunteers. Nutrition 2012, 28:527-531.
  14. Li J, Zou L, Chen W, et al. Dietary mushroom intake may reduce the risk of breast cancer: evidence from a meta-analysis of observational studies. PLoS One 2014, 9:e93437.
  15. Chen S, Oh SR, Phung S, et al. Anti-aromatase activity of phytochemicals in white button mushrooms (Agaricus bisporus). Cancer Res 2006, 66:12026-12034.
  16. Krikorian R, Shidler MD, Nash TA, et al. Blueberry supplementation improves memory in older adults. Journal of agricultural and food chemistry 2010, 58:3996-4000.
  17. Bowtell JL, Aboo-Bakkar Z, Conway M, et al. Enhanced task related brain activation and resting perfusion in healthy older adults after chronic blueberry supplementation. Appl Physiol Nutr Metab 2017.
  18. Stoner GD, Wang LS, Casto BC. Laboratory and clinical studies of cancer chemoprevention by antioxidants in berries. Carcinogenesis 2008, 29:1665-1674.
  19. Cassidy A, Mukamal KJ, Liu L, et al. High anthocyanin intake is associated with a reduced risk of myocardial infarction in young and middle-aged women. Circulation 2013, 127:188-196.
  20. Cassidy A, O’Reilly EJ, Kay C, et al. Habitual intake of flavonoid subclasses and incident hypertension in adults. Am J Clin Nutr 2011, 93:338-347.
  21. Johnson SA, Figueroa A, Navaei N, et al. Daily blueberry consumption improves blood pressure and arterial stiffness in postmenopausal women with pre- and stage 1-hypertension: a randomized, double-blind, placebo-controlled clinical trial. J Acad Nutr Diet 2015, 115:369-377.
  22. Whyte AR, Schafer G, Williams CM. Cognitive effects following acute wild blueberry supplementation in 7- to 10-year-old children. Eur J Nutr 2016, 55:2151-2162.
  23. Mattes RD, Dreher ML. Nuts and healthy body weight maintenance mechanisms. Asia Pac J Clin Nutr 2010, 19:137-141.
  24. Grosso G, Yang J, Marventano S, et al. Nut consumption on all-cause, cardiovascular, and cancer mortality risk: a systematic review and meta-analysis of epidemiologic studies. Am J Clin Nutr 2015, 101:783-793.
  25. Kris-Etherton PM, Hu FB, Ros E, Sabate J. The role of tree nuts and peanuts in the prevention of coronary heart disease: multiple potential mechanisms. J Nutr 2008, 138:1746S-1751S.
  26. Buck K, Zaineddin AK, Vrieling A, et al. Meta-analyses of lignans and enterolignans in relation to breast cancer risk. Am J Clin Nutr 2010, 92:141-153.
  27. Thompson LU, Chen JM, Li T, et al. Dietary flaxseed alters tumor biological markers in postmenopausal breast cancer. Clin Cancer Res 2005, 11:3828-3835.
heart-stethoscope

Body Fat Promotes Heart Disease

Risk factors for heart disease – elevated LDL cholesterol, hypertension, elevated triglycerides, inflammation, and blood glucose – are all exacerbated by excess body fat, and overweight/obesity itself is considered a risk factor.1-3

Is it beneficial to be a little overweight?

However, there has been controversy about a potential “obesity paradox” in heart disease: the idea that some amount of excess weight either does not pose any risk or is even protective. Unfortunately, the studies that suggest there may be a protective effect of body fat are often the ones that get more news coverage; but this does a disservice to an already overweight and nutritionally misguided public, allowing them to believe that excess body fat won’t harm their health.

Is there really an obesity paradox? Or is it just that BMI is not a good measure of body fat?

Many of these studies have used body mass index (BMI), however BMI, which only takes into account height and weight, is not an accurate indicator of body fatness. BMI does not distinguish between fat mass and lean mass, nor does it take into account fat distribution (visceral fat vs. subcutaneous fat). Many people whose weights are within the “normal” BMI range are still carrying excess fat.

There has been no evidence providing a convincing explanation of how excess fat could possibly provide a cardiovascular advantage.  Plus, there are numerous medical conditions may cause unintentional weight loss, including depression, anxiety, autoimmune diseases, cancers, and digestive disorders. In the elderly especially, a low BMI may be an indicator of muscle loss and frailty rather than an indicator of a healthy low level of body fat. In short, people who are thinner are not necessarily healthier.

Relationship between body fat and heart disease: using better measures than BMI

A new study  is helping to clear this issue up,4 in a cohort of almost 300,000 people in the UK (age 40-69) who were followed for an average of 5 years. Their first analysis puts the optimal range of BMI for heart disease prevention at 22-23 kg/m2. It was a “J-shaped” association, meaning risk rose both above and below the 22-23 range. But the researchers went further. They used multiple measures of body fatness to get a more accurate picture: waist circumference, waist-to-hip ratio, waist-to-height ratio, and percent body fat.

Ultimately, what the researchers found was that using BMI produces different results than the other indicators. BMI was the only one that showed an increase in risk at the low end (<18.5 kg/m2). When they excluded smokers and participants with pre-existing diseases, the increase in risk associated with low BMI almost disappeared.  The more accurate measures of body fatness – body fat percentage, waist circumference, waist-to-hip-ratio, and waist-to-height ratio – showed a clear trend: more body fat, greater risk.4


More body fat, greater cardiovascular risk

The researchers concluded that the obesity paradox observation mainly occurs due to confounding effects of disease and other factors on BMI, and that the “public misconception of a potential ‘protective’ effect of fat on CVD risk should be challenged.”4

As discussed above, a low BMI is often an indicator of disease, rather than an indicator of a healthy weight resulting from healthful eating. The standard American diet (SAD) is fattening. If someone is eating the SAD and is not overweight, there is likely something wrong.

Lose weight permanently on a Nutritarian diet

The dramatic weight loss-promoting effect of the Nutritarian diet contributes to cardiovascular protection. A 2015 study published in the American Journal of Lifestyle Medicine analyzed and reported weight loss results provided by 75 obese patients who had switched to a Nutritiarian diet. The average weight loss was 55 pounds, and very importantly, they kept the weight off. None of these respondents had gained back the lost weight after three years.5

Reprinted with permission from Dr. Fuhrman.


Dr. Fuhrman is a board-certified family physician specializing in nutritional medicine. He is President of the Nutritional Research Foundation and the author of 6 NY Times bestselling books, including The End of Heart Disease.  Visit him at DrFuhrman.com

 

References

  1. Coelho M, Oliveira T, Fernandes R. Biochemistry of adipose tissue: an endocrine organ. Arch Med Sci 2013, 9:191-200.
  2. Tchernof A, Despres JP. Pathophysiology of human visceral obesity: an update. Physiol Rev 2013, 93:359-404.
  3. Benjamin EJ, Blaha MJ, Chiuve SE, et al. Heart Disease and Stroke Statistics-2017 Update: A Report From the American Heart Association. Circulation 2017, 135:e146-e603.
  4. Iliodromiti S, Celis-Morales CA, Lyall DM, et al. The impact of confounding on the associations of different adiposity measures with the incidence of cardiovascular disease: a cohort study of 296 535 adults of white European descent. Eur Heart J 2018:ehy057-ehy057.
  5. Fuhrman J, Singer M. Improved Cardiovascular Parameter With a Nutrient-Dense, Plant-Rich Diet-Style: A Patient Survey With Illustrative Cases. Am J Lifestyle Med 2015.
scale

The Dangers of Weight Cycling (Yo-Yo Dieting)

Regaining weight after losing it on a diet is much more common than keeping the weight off. Often dieters gain back more than they lost, and it’s a common experience to have an even harder time losing weight the next time. “Weight cycling” is the term for these repeating episodes of intentional weight loss followed by unintentional regain, also often called “yo-yo dieting.”

Research reveals health dangers of weight cycling

In addition to making the next attempt at weight loss more difficult, repeated cycles of weight loss and gain have damaging effects on the body.

A study presented at the American Heart Association’s March 2019 Scientific Sessions reported that weight cycling was associated with poorer cardiovascular health parameters. Women were assigned a cardiovascular risk score based on 7 factors: smoking, diet, physical activity, BMI, blood pressure, cholesterol, and blood glucose. Women with a history of weight cycling were less likely to have a favorable BMI and less likely to have a favorable overall cardiovascular health score.1 Previous research also linked bouts of weight cycling to a greater risk of endometrial cancer.2 It is also worth noting that in the cardiovascular study, over 70% of the 485 women reported having a history of weight cycling (at least one instance of weight loss and regain), highlighting how common this issue is.1

One of the most important messages about weight loss is this: change your diet, lose the weight and keep your new, healthier way of eating forever.

Dump the Dieting Mentality

The human body responds to weight loss the same way it would respond to starvation – by conserving energy. The brain uses information about calorie intake and the body’s amount of stored energy to determine whether to release appetite-enhancing or appetite-suppressing hormones. One way the body adapts to weight loss is by altering the production of appetite-regulating hormones such as ghrelin and leptin, favoring weight regain by increasing appetite and promoting fat storage. Another way is by decreasing resting energy expenditure.1

These compensatory systems make going back to one’s old unhealthy diet even more weight gain-promoting. The highly palatable low nutrient foods, which stimulate cravings via the dopamine reward system, are even more dangerous for someone whose calorie expenditure has fallen. Also, when you lose weight, some loss of muscle is unavoidable, and strength exercise helps to limit muscle loss. However, when someone gains weight back after dieting, that weight is fat, potentially leaving the dieter with a greater body fat percentage than before.

Studies have linked weight cycling to a greater risk of diabetes, hypertension, gallbladder stones, and shorter telomere length.2-6 Shorter telomeres mean rapid aging. Weight cycling women were also found to have a greater waist circumference, and seem to gain more weight over time than “non-cyclers” who start off at the same BMI.7,8

The bottom line is that making changes to your diet to improve your health and your weight need to be permanent changes, not temporary.

Body fat is not just stored energy

Why is gaining back body fat harmful? Adipose (fat) tissue is more than a vessel for storing excess energy. In addition to storing fat, adipose tissue acts as an endocrine organ: it contains macrophages (a type of white blood cell) in addition to adipocytes; it produces and secretes compounds that affect the function of other types of cells. Obesity is accompanied by a systemic low-grade inflammation.9,10 Adipose releases compounds that can induce negative consequences such as insulin resistance, higher triglycerides, and reduced immune function, and even growth promoters that can increase risk of cancer. As fat tissue grows, more of these pro-inflammatory compounds are produced, leading to chronic inflammation, which increases the risk of cardiovascular disease, diabetes, and cancer.11

How to avoid weight cycling

The key to losing weight and keeping it off forever is changing your diet forever. Stay away from extreme fad diets; they are not sustainable long-term. About 80 percent of dieters are unable to keep 10 percent of their original body weight off for more than one year.12 Feeling deprived and going back to your old diet is almost inevitable. However, if you use high-nutrient foods to resolve toxic hunger and achieve greater meal satisfaction with a smaller number of calories, it will be much easier to stick with your new way of eating and prevent future weight regain.

A recent study published in the American Journal of Lifestyle Medicine analyzed and reported weight loss results provided by 75 obese patients who had switched to a Nutritiarian diet. The average weight loss was 55 pounds after three years, which means they kept the weight off long-term. Compare these results to most weight loss intervention studies, which report average losses of only 6-13 pounds maintained after two years.13 One reason for the remarkable effects on permanent weight reduction with a Nutritarian diet is that the users are more fully educated regarding the long-term health and longevity benefits and it is adopted not merely for its weight loss benefits. Additionally, it has been demonstrated that this nutrient dense, plant-rich diet can suppress appetite and resolve food cravings and food addictions.14

My book The End of Dieting explains exactly how to break out of the cycle of physical and emotional addiction and overeating – how to keep the weight off permanently.

Originally printed on DrFuhrman.com. Reprinted with permission.


Joel Fuhrman, M.D. is a board-certified family physician, six-time New York Times bestselling author and internationally recognized expert on nutrition and natural healing, who specializes in preventing and reversing disease through nutritional methods. Dr. Fuhrman coined the term “Nutritarian” to describe his longevity-promoting, nutrient dense, plant-rich eating style.
 
For over 25 years, Dr. Fuhrman has shown that it is possible to achieve sustainable weight loss and reverse heart disease, diabetes and many other illnesses using smart nutrition. In his medical practice, and through his books and PBS television specials, he continues to bring this life-saving message to hundreds of thousands of people around the world.

References

  1. Byun SS, Bello NA, Liao M, Makarem N, Aggarwal B: Weight Cycling is Associated With Poorer Cardiovascular Health Assessed Using AHA’s Life’s Simple 7 in a Diverse Sample of Women Encompassing Different Life Stages. In American Heart Association’s Epidemiology and Prevention Lifestyle and Cardiometabolic Health Scientific Sessions 2019.
  2. Welti LM, Beavers DP, Caan BJ, Sangi-Haghpeykar H, Vitolins MZ, Beavers KM. Weight Fluctuation and Cancer Risk in Postmenopausal Women: The Women’s Health Initiative. Cancer Epidemiol Biomarkers Prev 2017, 26:779-786.
  3. Greenway FL. Physiological adaptations to weight loss and factors favouring weight regain. Int J Obes (Lond) 2015, 39:1188-1196.
  4. Delahanty LM, Pan Q, Jablonski KA, et al. Effects of weight loss, weight cycling, and weight loss maintenance on diabetes incidence and change in cardiometabolic traits in the Diabetes Prevention Program. Diabetes Care 2014, 37:2738-2745.
  5.  Guagnano MT, Ballone E, Pace-Palitti V, et al. Risk factors for hypertension in obese women. The role of weight cycling. Eur J Clin Nutr 2000, 54:356-360.
  6.   Tsai CJ, Leitzmann MF, Willett WC, Giovannucci EL. Weight cycling and risk of gallstone disease in men. Arch Intern Med 2006, 166:2369-2374.
  7. Syngal S, Coakley EH, Willett WC, et al. Long-term weight patterns and risk for cholecystectomy in women. Ann Intern Med 1999, 130:471-477.
  8. Mehta T, Smith DL, Jr., Muhammad J, Casazza K. Impact of weight cycling on risk of morbidity and mortality. Obes Rev 2014, 15:870-881.
  9. Field AE, Manson JE, Taylor CB, et al. Association of weight change, weight control practices, and weight cycling among women in the Nurses’ Health Study II. Int J Obes Relat Metab Disord 2004, 28:1134-1142.
  10. Strychar I, Lavoie ME, Messier L, et al. Anthropometric, metabolic, psychosocial, and dietary characteristics of overweight/obese postmenopausal women with a history of weight cycling: a MONET (Montreal Ottawa New Emerging Team) study. J Am Diet Assoc 2009, 109:718-724.
  11.  Coelho M, Oliveira T, Fernandes R. Biochemistry of adipose tissue: an endocrine organ. Arch Med Sci 2013, 9:191-200.
  12.  Strohacker K, Carpenter KC, McFarlin BK. Consequences of Weight Cycling: An Increase in Disease Risk? Int J Exerc Sci 2009, 2:191-201.
  13.  Strohacker K, McFarlin BK. Influence of obesity, physical inactivity, and weight cycling on chronic inflammation. Front Biosci (Elite Ed) 2010, 2:98-104.
  14.  Wing RR, Phelan S. Long-term weight loss maintenance. Am J Clin Nutr 2005, 82:222S-225S.
  15.  Franz MJ, VanWormer JJ, Crain AL, et al. Weight-loss outcomes: a systematic review and meta-analysis of weight-loss clinical trials with a minimum 1-year follow-up. J Am Diet Assoc 2007, 107:1755-1767.
  16.   Fuhrman J, Sarter B, Glaser D, Acocella S. Changing perceptions of hunger on a high nutrient density diet. Nutr J 2010, 9:51.