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Research Article

The Preventable Causes of Death in the United States: Comparative Risk Assessment of Dietary, Lifestyle, and Metabolic Risk Factors

  • Goodarz Danaei,

    Affiliations: Harvard School of Public Health, Boston, Massachusetts, United States of America, Initiative for Global Health, Harvard University, Cambridge, Massachusetts, United States of America

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  • Eric L. Ding,

    Affiliation: Harvard School of Public Health, Boston, Massachusetts, United States of America

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  • Dariush Mozaffarian,

    Affiliations: Harvard School of Public Health, Boston, Massachusetts, United States of America, Harvard Medical School, Boston, Massachusetts, United States of America

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  • Ben Taylor,

    Affiliations: Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada, Public Health Sciences, University of Toronto, Toronto, Canada

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  • Jürgen Rehm,

    Affiliations: Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada, Public Health Sciences, University of Toronto, Toronto, Canada, Clinical Psychology and Psychotherapy, Technische Universität Dresden, Dresden, Germany

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  • Christopher J. L. Murray,

    Affiliation: Institute for Health Metrics and Evaluation, The University of Washington, Seattle, Washington, United States of America

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  • Majid Ezzati mail

    majid_ezzati@harvard.edu

    Affiliations: Harvard School of Public Health, Boston, Massachusetts, United States of America, Initiative for Global Health, Harvard University, Cambridge, Massachusetts, United States of America

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  • Published: April 28, 2009
  • DOI: 10.1371/journal.pmed.1000058

Reader Comments (3)

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Modifiable risk factors, PUFAs, w3s, trans, health care reform

Posted by optimalpolicies on 21 May 2009 at 15:20 GMT

Although the substantive message of the study, that behavioral or modifiable factors account for more preventable deaths than any likely improvements in health care via health care reform (Health IT, best evidence, good intentions, comparative effectiveness, more disease management via drugs, etc.), some specific recommendations are likely flawed because they are based on flawed etiological effects of risk factors on disease-specific mortality from systematic reviews and meta-analyses of epidemiological studies (authors statement). This is because epidemiological studies usually have very low predictive value (Rsquare under .3, indicating that major predictive factors are unaccounted).
The authors focused on “the following 12 modifiable dietary, lifestyle, and metabolic risk factors in the United States (US) using consistent and comparable methods: high blood glucose, low-density lipoprotein (LDL) cholesterol, and blood pressure; overweight–obesity; high dietary trans fatty acids and salt; low dietary polyunsaturated fatty acids, omega-3 fatty acids (seafood), and fruits and vegetables; physical inactivity; alcohol use; and tobacco smoking.”
I invented the technology to accurately measure fatty acids in human tissue. Based on my review the literature and laboratories I visited or spoke to, I believe I was the first researchers to accurately separate and measure over 100 fatty acids in human tissue, including w3s, w6s, isomers and trans. I reported data at conferences and meetings in Boston and elsewhere early in 1980s.
My analysis of cis and trans FA in Framingham Heart disease data found that trans FA account for about 10% of the variability of TC/HDL while PUFAs account for far more. Due to limited space and time, I cannot describe the complexities of my analysis (see references). The role of FAs is very complex. There are over 50 critical FAs. In general, about 30% of adult US have inadequate levels of w6s, about 75% have inadequate levels of w3s (with a wide range depending on the measures used). Overweight (not just obese) people have imbalances or relative deficiencies caused by excessive saturated FAs. Almost everyone with elevated total cholesterol or triglycerides (over 90% of US adults, using reference levels of healthy people, not the artificial level of TC < 200 mg/dl) have abnormal FA profiles. Although the ideal reference levels for total cholesterol are in dispute, individuals with no known disease have cholesterol levels below 200 mg/dl.
Based on my research, the critical factors are excessive caloric intake, affecting about 70+% of the US adult population. Next are imbalances of the intake of w3s and w6s. This usually means not eating enough w3s of the appropriate kind (not all w3s are equal, and I dispute suggestions that adequate intake of linolenic acid is not enough, see my references).
A substantial number of individuals also have selected nutritional abnormalities (deficiencies, imbalances, excesses) of specific nutrients.
Together (excessive caloric intake, imbalance of essential fats, nutrient imbalance), they probably account for overweight, abnormal lipids, high blood pressure, diabetes type 2.
In contrast, salt intake is probably far below the list in terms of importance, if individuals had optimal caloric and nutrient intake (data not found to answer this issue).
I revise the risk factors as follows:
Direct risk factors (individuals can modify them):
excessive calorie, imbalance of essential fats (low dietary intake PUFAs, particularly w3s), nutrient imbalance, eating too many processed fats high in isomers and trans (not just trans FAs!), physical inactivity; alcohol use; and tobacco smoking.
Risk markers, but not really etiological causes (likely the consequence of above factors):
high blood glucose, low-density lipoprotein (LDL) cholesterol, and blood pressure; overweight–obesity
Correctable actions
Eat fewer calories.
Limited drinking
Eat more foods in their natural state with more membranes, PUFAs, w3s, nutrients. This approach provides more nutrients, more PUFAs, limits intake of isomers and trans.
No smoking.
No drug abuse.
Avoid risky sports (prevents accidents).
Eat more fruits and vegetables.
Exercise more.
(in no specific order except eat less, not smoke are at the top).
My differences with the authors is not substantial, and with further research we would probably agree.
These findings also agree with recent studies in the Br. Medical Journal.

The consequences are substantial for health care reform.
We can improve outcomes and lower expenses by more than 30% (100s of billions per year) AND implement comprehensive health care reform.
To do so we should change best evidence, and health care coverage to focus on behavior modification. Make people more responsible for the consequences of their actions. Basic coverage should not cover for obvious consequences of improper behavior. Such coverage should be available at higher prices for those who want it. People do have the right to lower their life expectancy in exchange for pleasures, and exercise that right every day in the way they drive, eat, smoke, travel, exercise, practice sports, etc. Except for some behaviors, like smoking or drunk driving, that harm others, governments should not regulate by demanding changes but let people pay for their choices (a free market for choices and consequences).
Eduardo Siguel, MD, PhD
References
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Siguel E, Maclure, M. Relative Activity of Unsaturated Fatty Acid Metabolic Pathways in Humans. Metabolism, 1987; 36: 664-69.
Siguel E, Chee, KM, Gong J, Schaefer, EJ. Criteria for Essential Fatty Acid Deficiency in Plasma as Assessed by Capillary Column Gas-Liquid Chromatography. Clin.Chem, 1987; 33:1869-73.
Siguel, E. Method and Apparatus for Diagnosis of Fatty Acid or Lipid Abnormalities. U.S. Patent No. 5075101, Issue date 12/24/91.
Siguel E, Lerman, RH. Trans Fatty Acid Patterns in Patients with Angiographically Documented Coronary Artery Disease. Am. J. Cardiology, 1993; 71:916-20.
Siguel E, Lerman, RH. Altered Fatty Acid Metabolism in Patients With Angiographically Documented Coronary Artery Disease. Metabolism 1994; 43:982-93.
Siguel E. Essential and Trans Fatty Acid Metabolism in Health and Disease. Nutrition Issue. Comprehensive Therapy, 1994; 20(9):500-10 (Review).
Siguel E. Essential Fatty Acids in Health and Disease. 1994, P.O. Box 10187, Dept F, Gaithersburg, MD 20898 (book, see amazon.com).
Siguel E, Lerman RH. The Role of Essential Fatty Acids: Dangers in the USDA Dietary Recommendations ("Pyramid") and in Low Fat Diets. Am. J. Clin. Nutrition, 1994; 60:973-79 (let).
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Siguel E, Lerman RH. The Effects of Low-Fat Diet on Lipid Levels. JAMA, 1996; 275:759-60 (let).
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Siguel, E. Issues and Problems in the Design of Foods Rich in Essential Fatty Acids. Lipid Technology, 1996; 8(4):81-86 (July).
Siguel E. EFA Status in Patients. J Parent.Ent.Nutr. 1997 Jul-Aug; 21(4):243 (let).
Siguel, E. Dietary Fat: How Low Can or Should You Go? Abstracts, Am. Oil. Chemistry Society Annual Meeting 1997; INFORM, 1997:8(7):714-17.
Siguel, E. The Essential Fat Revolution: Part I, Nutrition and Essential Fatty Acids. Decision Resources, Waltham, MA. December 12, 1997: 81-1 - 81-12.
Siguel, E. The Essential Fat Revolution Part II, Implications for Food Design and Marketing. Decision Resources, Waltham, MA. December 12, 1997:82-1 - 82-10.
Siguel E. Diagnosing Essential Fatty Acid Deficiency. Circulation. 1998; 97(25):2580-83 (let).
Siguel, E. Identification and Quantification of Fatty Acids. J.Parent.Ent.Nutr. 1998; 22(6):401-02.
Siguel, E. Deficiencies and Abnormalities of Essential Fats in Gastrointestinal and Coronary Artery Disease. Journal of Clinical Ligand Assay 2000; 23:104–11.
Siguel, E. Clinical Impact of Methodological Issues in the Diagnosis of Deficiencies and Abnormalities of Essential Fats. Journal of Clinical Ligand Assay 2000; 23:112–21.
Siguel, E. n-3 Fatty Acids and the Risk of Sudden Death. N.Engl.J.Med. 2002; 347(7):531-33 (let).
Siguel, E. Some Thoughts to Ponder Before Condemning Trans Fatty Acids. Viewpoint. Inform, (Am. Oil Chem Society), 2002; 13:339 (April).

For more articles and discussion, see www.essentialfats.com

Competing interests declared: Patent (listed in comment).
Research in fatty acids. See www.essentialfats.com
Write articles, see healthnewsreview.com