Heart Disease andPrevention and Treatment of Heart Disease with the Same Nutrition Protocol Its Larger Context

Main Article Content

T Colin Campbell, PhD

Abstract

Addressing the effect of nutrition on heart disease requires a dialogue somewhat different from contemporary practice.


Heart disease is used here as a generic name for at least a dozen or more cardiovascular disease subtypes. Each subtype has its own identity, its own causes, its own pathology, its own biochemistry, and its own treatment protocols. Although disease specification certainly has advantages, it also has a shortcoming that is commonly overlooked. The more detailed this information is, the more difficult it is to comprehend prevention and treatment protocols that may benefit all heart disease subtypes.


Questions arise, for example, whether information specific for one disease subtype applies to other subtypes. This likely requires additional research, regulatory development, and health claims oversight. However effective this information may be, increasing disease fragmentation and specification nonetheless increases opportunities for confusion, both for the public and the practitioner.


Relying on specialized information, however, presents a serious dilemma for understanding nutrition, unless it is characterized by specific nutrients in food, specific mechanisms of action for each nutrient, and specific heart disease subtypes. This is reductionism, which is the popular but incorrect perspective on nutrition.


In contrast, wholist interpretation of nutrition refers to the combined biologic activities of countless nutrients when consumed as food, and countless metabolic activities for each nutrient, working in unison when the proper food is consumed. At the tissue level during metabolism, this dynamic is highly sensitive to change, and it does so very rapidly. Change simultaneously occurs with changing supply of nutrient substrate and changing demand of the tissues. The default position for nutrition, by definition, is that which optimizes health, prevents, and even reverses (treats) disease development. Numerous enzymatic and hormonal mechanisms, acting like transistor switches, are available to manage this extraordinary dynamic.


Oft cited evidence shows that nutrition, when properly understood and used, can control as much as 70-85% of the premature mortality caused by cardiovascular disease. This nutrition is ideally powered by whole foods from the plant kingdom, with nutrients acting wholistically in the body in a way to benefit all disease subtypes, even though effect size and outcome responses for each heart disease subtype may differ.

Article Details

How to Cite
CAMPBELL, T Colin. Heart Disease andPrevention and Treatment of Heart Disease with the Same Nutrition Protocol Its Larger Context. Medical Research Archives, [S.l.], v. 10, n. 9, sep. 2022. ISSN 2375-1924. Available at: <https://esmed.org/MRA/mra/article/view/3032>. Date accessed: 24 may 2024. doi: https://doi.org/10.18103/mra.v10i9.3032.
Section
Research Articles

References

1. T. C. Campbell, A plant based diet and animal protein: questioning dietary fat and considering animal protein as the main cause of heart disease. J. Geriatric Cardiol. 14, 331-337 (2017).
2. D. Giedrimiene, R. King, Burden of cardiovascular disease (CVD) on economic cost, comparison of outcomes in US and Europe. Circulation 10:A207, (2017).
3. S. E. Fleischhacker et al., Strengthening national nutrition research: rationale and options for a new coordinated federal research effort and authority. American Journal of Clinical Nutrition 112, 721-769 (2020).
4. T. O. Cheng, Ancel Keys, seven countries study, China connections, and K rations. J. Am. Diet Assoc. 105, 349 (2005).
5. A. Keys, J. T. Anderson, F. Grande, Serum cholesterol in man: diet fat and intrinsic responsiveness. Circulation 19, 201-214 (1959).
6. D. A. Pratt, K. A. Tallman, N. A. Porter, Free radical oxidation of polyunsaturated lipids: New mechanistic insights and the development of peroxyl radical clocks. Acc Chem Res 44, 458-467 (2011).
7. A. Keys, Mediterranean diet and public health: personal reflections. Am J Clin Nutr 61 (suppl), 1321S-1323S (1995).
8. R. B. Shekelle, W. J. Raynor Jr., Dietary vitamin A and risk of cancer in the Western Electric Study. Lancet 2, 1185-1190 (1981).
9. The Alpha-Tocopherol Beta Carotene Cancer Prevention Study Group, The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. New Engl. J. Med. 330, 1029-1035 (1994).
10. T. C. Campbell, Nutrition renaissance and public health policy. J. Nutr. Biology 3, 124-138 (2017).
11. C. B. Esselstyn, Jr., Updating a 12-year experience with arrest and reversal therapy for coronary heart disease (an overdue requiem for palliative cardiology). Am. J. Cardiol. 84, 339-341 (1999).
12. D. Ornish et al., Can lifestyle changes reverse coronary heart disease? Lancet 336, 129-133 (1990).
13. B. S. Appleton, T. C. Campbell, Effect of high and low dietary protein on the dosing and postdosing periods of aflatoxin B1-induced hepatic preneoplastic lesion development in the rat. Cancer Research 43, 2150-2154 (1983).
14. N. Jolliffe, M. Archer, Statistical associations between international coronary heart disease death rates and certain environmental factors. J. Chronic Dis. 9, 636-652 (1959).
15. D. Armstrong, R. Doll, Environmental factors and cancer incidence and mortality in different countries, with special reference to dietary practices. International Journal of Cancer 15, 617-631 (1975).
16. W. B. Grant, An ecologic study of dietary links to prostate cancer. Altern Med Rev 4, 162-169 (1999).
17. K. K. Carroll, L. M. Braden, J. A. Bell, R. Kalamegham, Fat and cancer. Cancer 58, 1818-1825 (1986).
18. W. E. Connor, S. L. Connor, The key role of nutritional factors in the prevention of coronary heart disease. Prev Med 1, 49-83 (1972).
19. B. J. Abelow, T. R. Holford, K. L. Insogna, Cross-cultural association between dietary animal protein and hip fracture: a hypothesis. Calcif. Tissue Int. 50, 14-18 (1992).
20. D. M. Hegsted, Calcium and osteoporosis. J. Nutr. 116, 2316-2319 (1986).
21. T. C. Campbell, J. Chen, C. Liu, J. Li, B. Parpia, Non-association of aflatoxin with primary liver cancer in a cross-sectional ecologic survey in the People's Republic of China. Cancer Research 50, 6882-6893 (1990).
22. J. Chen, T. C. Campbell, J. Li, R. Peto, Diet, life-style and mortality in China. A study of the characteristics of 65 Chinese counties. (Oxford University Press; Cornell University Press; People's Medical Publishing House, Oxford, UK; Ithaca, NY; Beijing, PRC, 1990), pp. 894.
23. J. Chen, R. Peto, W. Pan, B. Liu, T. C. Campbell, Mortality, biochemistry, diet and lifestyle in rural China. Geographic study of the characteristics of 69 counties in mainland China and 16 areas in Taiwan. (Oxford University Press, 2006), pp. 825.
24. T. C. Campbell, A nutritional link for COVID-19? EC Nutrition 16, 18-26 (2021).
25. R. C. Bell, K. A. Golemboski, R. R. Dietert, T. C. Campbell, Long-term intake of a low-casein diet is associated with higher relative NK cell cytotoxic activity in F344 rats. Nutrition and Cancer 22, 151-162 (1994).
26. H. H. Mitchell, A method of determining the biological value of protein. Journal of Biological Chemistry 58, 873-903 (1924).
27. D. Kritchevsky, Dietary protein, cholesterol and atherosclerosis: a review of the early history. Journal of Nutrition 125, 589S-593S (1995).
28. S. Clarkson, L. H. Newburgh, The relation between atherosclerosis and ingested cholesterol in the rabbit. J. Exp. Med. 43, 595-612 (1926).
29. J. Hu et al., Repression of hepatitis B virus (HBV) transgene and HBV-induced liver injury by low protein diet. Oncogene 15, 2795-2801 (1997).
30. T. C. Campbell, Chemical carcinogens and human risk assessment. Fed. Proc. 39, 2467-2484 (1980).
31. R. H. Chittenden, The nutrition of man. (F. A. Stokes & Co., New York, 1907), pp. 321.
32. R. H. Chittenden, Physiological economy in nutrition. (F.A. Stokes, New York, 1904), pp. 478.