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The case against nutritional supplements
Todd Becker gettingstronger.org
Ancestral Health Symposium
August 17, 2013
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How did our ancestors thrive without supplements? Do we really need them?
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Main Thesis
• For most* people, routine supplementation with vitamins, minerals and essential fatty acids is unnecessary and may be counterproductive
• A paleo diet and lifestyle – enhanced by hormesis – reduces or eliminates the need for supplementation
* Caveat: Short term supplementation may be advisable in cases of malnutrition, infection, illness, pregnancy or special athletic goals.
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Outline
• The case for nutritional supplements
• General doubts and objections
• Four examples
– Antioxidants
– Vitamin D
– Calcium
– Omega-3 fatty acids
• The role of hormesis
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The “paleo” case for nutritional supplements
• Inability to synthesize (vitamin C)
• Inefficient synthesis (vitamin D, omega-3)
• Deficient soils and oceans (minerals, omega-3)
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General doubts and objections
1. You are not what you eat
You are what your body does with what you eat
This applies to macronutrients
• Excess glucose triglycerides
• Excess protein glucose
• Soluble fiber short chain fatty acids
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General doubts and objections
1. You are not what you eat
You are what your body does with what you eat
But it also applies to micronutrients
• Malabsorption / excretion (calcium)
• Oxidation (antioxidants, fatty acids)
• Hormone signaling (vitamin D)
• Gene expression (antioxidants, vitamin D)
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General doubts and objections
2. Nutrients are regulated homeostatically
Exogenous nutrients
can downregulate endogenous defenses
Examples
– Antioxidants – Vitamin D
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The case for antioxidants
• Reactive oxygen species (ROS)
• Can’t synthesize our own vitamin C
• Mega doses suggested for: – Common cold – Infections – Cancer
• Other antioxidants • Vitamin A • Vitamin E • Beta carotene • Co-Q10 • Alpha lipoic acid
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Fruits & vegetables
• Health benefits of fruits and vegetables “ associated” with antioxidant content
?
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Interventional studies show no benefit …or even positive harm
AMA (2004):
Meta-analysis 20 studies: C, E beta carotene > No reduction in CVD, stroke or mortality
Cochrane (2008):
Meta-analysis 67 studies: A, C, E, selenium > No reduction in mortality Antioxidants adversely impact exercise!
Ristow (2009): Vitamins C and E + exercise for 4 weeks > decreased insulin sensitivity improvement > reduced antioxidant enzyme levels
Before exercise
After exercise
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What could be going wrong?
• Oxidative “stress” by ROS is not always bad!
• ROS are essential for cell signaling, exercise regulation, and fighting infection
• Moderate ROS plays a hormetic role in improving mitochondrial function and upregulating endogenous antioxidant enzymes
• Antioxidant supplements indiscriminately suppress cell signaling and downregulate endogenous antioxidant enzymes
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Endogenous Antioxidants
• The xenobiotic metabolism produces Phase II antioxidant enzymes to catalytically neutralize chemical toxins: – Superoxide dismutase (SOD), glutathione reductase (GSH), etc.
• We have co-evolved with certain edible plants to tolerate modest amounts their polyphenolic “toxins”
• Exposure to these polyphenolic “hormetins” activate the Nrf2 pathway, which produces the endogenous antioxidants
• Hormetins are abundant in pigmented, bitter plants and herbs
• Resveratrol
• Sulforaphane
• Curcumin
• Green tea
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Supplements vs. Hormetins
Supplements: Antioxidants, minerals, vitamins and essential fatty acids taken to correct apparent deficiencies
Hormetins: Spices, herbs, phytonutrients that activate and strengthen the body’s endogenous processes of defense, repair, and tolerance and performance.
Typically hormetins work synergistically and at low dose
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Hormetins are agents of hormesis
• Dose-response effect
• Stressors we’ve evolved with
• Activate Defense & repair mechanisms
Edward Calabrese
Suresh Rattan
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Many examples of hormesis
• Chemicals
• Sunlight (UV)
• Ionizing radiation
• Exercise
• Barefoot running
• Fasting / Ketosis
• Cold exposure
• Immunotherapy
• Vision Improvement
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Vitamin C recycling
• Vitamin C (ascorbate) neutralizes oxidants 1-for 1
• Dehydroascorbate (oxidized vitamin C) is readily recycled thousands of times by endogenous glutathione reductase
• Elevated blood glucose inhibits reuptake and recycling of dehydroascorbate
ROS
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Vitamin C storage
• Advocates of mega dose vitamin C note that most primates (simians) consume 10-20X the RDA of vitamin C
• But humans can efficiently store 10-100X the blood levels of vitamin C in adrenal, thymus, pituitary and other glands – enough to ward of scurvy for 3-8 months
Antioxidants: Take home message
• Based upon adequate storage and catalytic recycling, a low glycemic diet rich in hormetic polyphenols greatly decreases the daily need for dietary and supplemental vitamin C
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The case for vitamin D
• From diet or action of UV on skin
• D3 itself is not biologically active
– Requires liver & kidney conversions
– Active form (1,25-D) binds VDR receptor
• Vitamin D has a dual function
– Low dose: calcium absorption
– Higher dose: immune function (VDR)
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Correlation and causation
• Low vitamin D3 levels correlate with higher heart disease, stroke, immune problems, infection & overall mortality
• But is low vitamin D3 a cause – or a consequence – of ill health?
– Healthy people may get more sun and exercise, elevating D3
– People with low D3 often have elevated 1,25-D
• Could 25-D be a mere “biomarker” for health status?
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Vitamin D risks & questions
• Interventional studies show no benefit, possible harm:
– AMA(2010): Supplements for 5 years in women over 70 produced 15% more falls and 26% more fractures
– NCI (2012): Elevated 25-D linked to aggressive prostate cancer
• Vitamin D is a secosteroid – binds the VDR receptor
– VDR activation dampens the innate immune response
– Provides short term control of infection and autoimmunity
– Long term supplementation with the inactive 25-D might inhibit 1,25-D action and/or down-regulate VDR function
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An alternative to vitamin D?
• Can we get the benefits of Vitamin D without the risks of daily supplementation or sun exposure?
• Hoyer-Hansen studied the pathways activated by the VDR receptor and noted that
“Autophagy could be a general mediator of the health-promoting effects of 1,25-(OH)2 (D3). Accordingly, there is a striking overlap among the diseases promoted by VD deficiency and defective autophagy.”
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Autophagy
• A cellular housecleaning process – Recycles damaged cytoplasmic matter – Activated by calorie restriction and exercise
• Regulates the same pathways as vitamin D receptor – Inhibits mTOR, bcl-1, bcl-2 – Inhibition of carcinogenesis and tuberculosis
Take home message – Vitamin D • Be wary of supplementing , especially at high doses • Consider that intermittent fasting and exercise might
activate the same metabolic benefits
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The case for calcium supplements
• Strong bone formation requires an adequate supply of calcium
• Deficiencies of calcium (and vitamin D) lead to rickets and osteoporosis
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What do interventional studies show?
• Harvard study of 77,761 nurses for 12 years showed no protection from bone fractures at any dose of calcium (from dairy or supplements)
• Confirmed by similar studies in Australia and the UK
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Is calcium getting to where it is needed?
• Blood levels of calcium are tightly regulated
• High levels of vitamin D deplete vitamin K2 and promote calcification of vascular tissue
• On a standard diet high in grains, phytates bind calcium, leading to poor absorption
• High blood glucose and insulin levels “leach” calcium from bones
• In short, taking calcium supplements doesn’t ensure it will get into bones
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A better way to build bones
• The solution is not supplementation, but a whole food diet of “available” calcium, with vits. D, A, K2
• Weight bearing exercise is the most practical way to stimulate uptake of calcium into bones
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The case for omega-3 supplements
• EPA and DHA are long chain essential N-3 fatty acids (EFAs), critical to brain, eye and heart function
• A low n-3/n-6 ratio has been linked to CVD, Alzheimer’s, depression, autoimmune disorders
• Most Westerner’s show poor enzymatic conversion of shorter chain n-3s to the EFAs
• EFAs from consumption of fatty fish is inadequate
Hence, dietary supplementation is recommended
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Stillwell, William. “The role of polyunsaturated lipids in membrane raft function”, Scandinavian Journal of Food and Nutrition, 2006; 50 (S2): 107 -113.
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However EFA supplements have a downside
• A 2013 JAMA study of 2000 men found that men with the highest blood levels of EPA and DHA had
– 71% higher risk of aggressive prostate cancer
– 44% higher risk of low-grade prostate cancer
• These results replicate earlier findings from a 2011 study
• Under-reported: The increased risk appears associated only with the more easily oxidized DHA, not EPA (Nina Bailey)
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Diet impact on DHA “survival”
• Low carbohydrate diets dramatically increase “end product” DHA in muscle membranes – This improves insulin sensitivity and
inhibits lipogenesis
• This happens despite reduced enzymatic synthesis of DHA under carbohydrate restriction
• Low carb diets appear to help “preserve” DHA by suppressing ROS-driven lipid peroxidation
From Volek and Phinney, “The Art and Science of Low Carbohydrate Living” (2011)
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Diet controls fate of EFAs
• DHA is less stable than EPA to lipid peroxidation. The higher association of DHA with cancer may reflect this fact.
• Low carb/paleo/non-inflammatory diets result in a reduced dietary requirement for EFAs because they are better “preserved” against oxidative damage and inter-conversion is optimized
• Thus, a non-inflammatory diet may be critical to getting EFA benefits without the risks posed by unstable and “damaged” DHA
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Parting thoughts
• Recommended Daily Allowances for supplements came from studies of people eating Western diets
• Those diets oxidize nutrients, impair absorption and recycling, and downregulate endogenous defenses
• A low insulinogenic, non-inflammatory, whole food diet greatly improves micronutrient utilization
• Phytonutrients and hormesis can boost endogenous antioxidants and other defenses
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For further reading
Related articles on my blog
gettingstronger.org
“The case against antioxidants”
“Why I don’t take vitamin D supplements”
“An alternative to vitamin D supplements”
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References Antioxidants
1. Kris-Etherton, Penny M. et al, “Antioxidant vitamin supplements and cardiovascular disease” Circulation 2004, 110: 637-641.
2. Bjelakovic, Goran et al, “Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases”. Cochrane Database of Systematic Reviews 3: John Wiley & Sons, 2008 and updated 2012.
3. Cheung, M.C. et al, “Antioxidant supplements block the response of HDL to simvastatin-niacin therapy in patients with coronary artery disease and low HDL” Arterioscler Thromb Vasc Biol, 2001, Aug; 21 (8) 1320-6,
4. Ristow, Michael et al., “Antioxidants prevent health-promoting effects of physical exercise in humans” PNAS 2009 ; published ahead of print May 11, 2009, doi:10.1073/pnas.0903485106
5. Mendriatta, S. et al. “Erythrocyte ascorbate recycling: antioxidant effects in blood”, Free Radic Biol Med. 1998, 24 (5): 789-97.
6. Wang, Yaohui et al. “Ascorbate recycling in human neutrophils: Induction by bacteria” Proc. Nat Acad Sci of U.S.A., 1997, 94 (25) 13816-9.
7. Li, Guolin, “The Positive and Negative Aspects of Reactive Oxygen Species in Sports Performance”, Ch. 6 in Michael Hamlin et al., ed, Current Issues in Sports and Exercise Medicine, ISBN 978-953-51, 2013, -1031-6,, 2013
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References 8. Rountree, Robert, “Beyond Antioxidants: Nutrigenomic Regulation of the Adaptive Stress
Response.” Integrative Practitioner, 2010. http://www.integrativepractitioner.com/article.aspx?id=17183
Vitamin D
9. Sanders, K.M. et al., “Annual High-Dose Oral Vitamin D and Falls and Fractures in Older Women: A Randomized Controlled Trial. JAMA 2010, 303 (18) , 1815-1822.
10. Masterjohn, C. “Vitamin D toxicity redefined: vitamin K and the molecular mechanisms” Med Hypotheses 2007, 8 (5): 1026-34.
11. Agus, David B., The End of Illness. New York: Simon & Schuster, 2011.
12. Hoyer-Hansen, M.D. “Autophagy as a basis for the health-promoting effects of vitamin D”. Trends in Molecular Medicine (2010) 16:7, 295-302
Calcium
13. Feskanich, D. et al. “Milk, dietary calcium and bone fractures in women: a 12-year prospective study” Am J Public Health, 1997, 87 (6) 992-7.
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References Omega-3 fatty acids
14. Stillwell, William. “The role of polyunsaturated lipids in membrane raft function”, Scandinavian Journal of Food and Nutrition, 2006; 50 (S2): 107 -113.
15. Brasky, T. M. et al. “Plasma Phospholipid Fatty Acids and Prostate Cancer Risk in the SELECT Trial” Journal of the National Cancer Institute, Aug 7; 105 (15) 1132-1141, 2013
16. Bailey, Nina. “DHA, not EPA, responsible for omega-3 prostate cancer risk. Igennus Healthcare Nutrition blog, http://www.igennus-hn.com/dha-not-epa-responsible-for-omega-3-prostate-cancer-risk-by-dr-nina-bailey/
17. Volek, Jeff S. and Stephen D. Phinney. The Art and Science of Low Carbohydrate Performance: A Revolutionary Program to Extend your Physical and Mental Performance Envelope. Createspace.com, Chapter 9 and references, 2012
Hormesis
18. Calabrese, Edward J., and Linda A. Baldwin. "Hormesis: The Dose-Response Revolution." Annu. Rev. Pharmacol. Toxicol. 43: 175-97, 2003.
19. Rattan, Suresh I and Dino Demirovic. “Hormesis Can and Does Work in Humans.” Dose-Response. 8(1): 58-63, 2010.