The Blood Type Diet has been used to success by millions of individuals over the past twenty years. Despite the tremendous amount of success stories and robust scientific literature on blood groups and secretor status, many individuals still attempt to discount the Blood Type Diet as a ‘fad diet’ and state that there is very little scientific evidence behind it.
A point that is commonly brought up is the lack of scientific evidence supporting the Blood Type Diet, which is quite to the contrary. The Blood Type Diet was developed by Dr. Peter D’Adamo and is based upon decades of research on blood group science, physiology, immunology, biochemistry and hematology. Many of the critics of the Blood Type Diet are not versed in the plethora of research on how blood groups and secretor status can affect nearly every system within the body and how they can affect how individuals react to different foods. Dr. Peter D’Adamo spent years developing and formulating the Blood Type Diet based upon his research and from scientists around the world. To name a few, blood type and secretor status have been shown to have the following numerous effects:
- Blood group specificity is listed as one of the nine major factors that influence how lectins bind to cells in the gut[i]
- The ability for bacteria, viruses and lectins to attach and persist in the walls of the intestinal tract[ii]
- Levels of intestinal enzymes, which are involved in the breakdown of dietary fat, proteins, cholesterol and the absorption of calcium[iii],[iv],[v],[vi],[vii]
- Distinct differences in gut microbiome population[viii],[ix]
- Levels of blood clotting factors[x],[xi],[xii],[xiii]
- Risk of heart disease and metabolic syndrome[xiv],[xv],[xvi],[xvii],[xviii], [xix],[xx],[xxi]
- Regulation of the immune system[xxii],[xxiii],[xxiv],[xxv]
- Risk of stomach and duodenal ulcers[xxvi],[xxvii],[xxviii],[xxix]
- Risk of H. pylori infection, which can lead to gastritis, inflammation and ulcers[xxx],[xxxi]
The above are just a few of the many scientific parameters that the Blood Type Diet was formulated upon.
In 2014, a study was released by a team of authors to determine if there were any favorable effects on cardiometabolic markers in participants following the Blood Type Diet.[xxxii] Numerous outlets have used this study as a basis to argue that the Blood Type Diet is not effective. Analysis of this study revealed that the participants were not following the Blood Type Diet at all. In fact, only 13.7% of the foods from the study matched foods in the Blood Type Diet. Within the study, foods such as ‘hotdogs’, ‘mac & cheese’, ‘pizza’ and ‘processed meat sandwich’ were assigned to different blood types as either beneficial, neutral or avoid.[xxxiii] First, these foods are made up of many different individual ingredients, and it is impossible to categorize them as beneficial, neutral or avoid for any specific blood group. Second, anyone who has even skimmed the Blood Type Diet books would know that these are not foods are certainly not recommended for any blood group.[xxxiv][xxxv]
While research is incredibly important when it comes to nutrition, the anecdotal success stories of thousands of individuals who have used the Blood Type Diet are overwhelming. Individuals have experienced weight loss, improved blood sugars, cholesterol, and blood pressure and even recovered from debilitating conditions by using the Blood Type Diet. By tailoring an individual’s diet to their blood type, one can prevent and combat diseases by changing the foods they eat.
References:
[i]. Trends in Glycoscience and Glycotechnology; 8:149-165
[ii]. Triadou N, Audran E, Rousset M, et al. Relationship between the secretor status and the expression of ABH blood group antigenic determinants in human intestinal brush-border membrane hydrolases. Biochim Biophys Acta 1983;761:231-236
[iii]. Domar U, Hirano K, Stigbrand T. Serum levels of human alkaline phosphatase isozymes in relation to blood groups. Clin Chim Acta 1991;203:305-313.
[iv]. Matsushita M, Irino T, Stigbrand T, et al. Changes in intestinal alkaline phosphatase isoforms in healthy subjects bearing the blood group secretor and non-secretor. Clin Chim Acta 1998;277:13-24.
[v]. Stolbach LL, Krant MJ, Fishman WH. Intestinal alkaline phosphatase in chylous effusion: role of ABO blood group and secretor status. Enzymologia 1972;42:431-438.
[vi]. Walker BA, Eze LC, Tweedie MC, Evans DA. The influence of ABO blood groups, secretor status and fat ingestion on serum alkaline phosphatase. Clin Chim Acta 1971;35:433- 444.
[vii]. Bayer PM, Hotschek H, Knoth E. Intestinal alkaline phosphatase and the ABO blood group system—a new aspect. Clin Chim Acta 1980;108:81-87.
[viii]. Hoskins LC, Boulding ET. Degradation of blood group antigens in human colon ecosystems. I. In vitro production of ABH blood group-degrading enzymes by enteric bacteria. J Clin Invest 1976;57:63-73.
[ix]. Hoskins LC, Boulding ET. Degradation of blood group antigens in human colon ecosystems. II. A gene interaction in man that affects the fecal population density of certain enteric bacteria. J Clin Invest 1976;57:74-82.
[x]. Orstavik KH, Kornstad L, Reisner H, Berg K. Possible effect of secretor locus on plasma concentration of factor VIII and von Willebrand factor. Blood 1989;73:990-993.
[xi]. Wahlberg TB, Blomback M, Magnusson D. Influence of sex, blood group, secretor character, smoking habits, acetylsalicylic acid, oral contraceptives, fasting and general health state on blood coagulation variables in randomly selected young adults. Haemostasis 1984;14:312-319.
[xii]. Orstavik KH. Genetics of plasma concentration of von Willebrand factor. Folia Haematol Int Mag Klin Morphol Blutforsch 1990;117:527-531.
[xiii]. Green D, Jarrett O, Ruth KJ, et al. Relationship among Lewis phenotype, clotting factors, and other cardiovascular risk factors in young adults. J Lab Clin Med 1995;125:334-339.
[xiv]. Hein HO, Sorensen H, Suadicani P, Gyntelberg F. The Lewis blood group—a new genetic marker of ischaemic heart disease. J Intern Med 1992;232:481-487.
[xv]. Ellison RC, Zhang Y, Myers RH, et al. Lewis blood group phenotype as an independent risk factor for coronary heart disease (the NHLBI Family Heart Study). Am J Cardiol 1999;83:345-348.
[xvi]. Zhiburt BB, Chepel’ AI, Serebrianaia NB, et al. The Lewis antigen system as a marker of IHD risk. Ter Arkh 1997;69:29-31. [Article in Russian]
[xvii]. Slavchev S, Tsoneva M, Zakhariev Z. The secretory type of persons who have survived a myocardial infarct. Vutr Boles 1989;28:31-34. [Article in Bulgarian]
[xviii]. Petit JM, Morvan Y, Viviani V, et al. Insulin resistance syndrome and Lewis phenotype in healthy men and women. Horm Metab Res 1997;29:193-195.
[xix]. Hein HO, Sorensen H, Suadicani P, Gyntelberg F. Alcohol consumption, Lewis phenotypes, and risk of ischaemic heart disease. Lancet 1993;341:392-396.
[xx]. Petit JM, Morvan Y, Mansuy-Collignon S, et al. Hypertriglyceridaemia and Lewis (A-B-) phenotype in non-insulin-dependent diabetic patients. Diabetes Metab 1997;23:202-204.
[xxi]. Clausen JO, Hein HO, Suadicani P, et al. Lewis phenotypes and the insulin resistance syndrome in young healthy white men and women. Am J Hypertens 1995;8:1060-1066.
[xxii]. Al-Agidi SK, Shukri SM. Association between immunoglobulin levels and known genetic markers in an Iraqi population. Ann Hum Biol 1982;9:565-569.
[xxiii]. Shinebaum R. ABO blood group and secretor status in the spondyloarthropathies. FEMS Microbiol Immunol 1989;1:389-395
[xxiv]. Grundbacher FJ. Immunoglobulins, secretor status, and the incidence of rheumatic fever and rheumatic heart disease. Hum Hered 1972;22:399-404.
[xxv]. Grundbacher FJ. Genetic aspects of selective immunoglobulin A deficiency. J Med Genet 1972;9:344-347.
[xxvi]. Odeigah PG. Influence of blood group and secretor genes on susceptibility to duodenal ulcer. East Afr Med J 1990;67:487-500.
[xxvii]. Suadicani P, Hein HO, Gyntelberg F. Genetic and life-style determinants of peptic ulcer. A study of 3387 men aged 54 to 74 years: The Copenhagen Male Study. Scand J Gastroenterol 1999;34:12-17.
[xxviii]. Hein HO, Suadicani P, Gyntelberg F. Genetic markers for stomach ulcer. A study of 3,387 men aged 54-74 years from The Copenhagen Male Study. Ugeskr Laeger 1998;160:5045- 5046. [Article in Danish]
[xxix]. Sumii K, Inbe A, Uemura N, et al. Multiplicative effect of hyperpepsinogenemia I and nonsecretor status on the risk of duodenal ulcer in siblings. Gastroenterol Jpn 1990;25:157-161.
[xxx]. Su B, Hellstrom PM, Rubio C, et al. Type I Helicobacter pylori shows Lewis(b)-independent adherence to gastric cells requiring de novo protein synthesis in both host and bacteria. J Infect Dis 1998;178:1379-1390.
[xxxi]. Alkout AM, Blackwell CC, Weir DM, et al. Isolation of a cell surface component of Helicobacter pylori that binds H type 2, Lewis(a), and Lewis(b) antigens. Gastroenterology 1997;112:1179-1187.
[xxxii]. Wang J, García-bailo B, Nielsen DE, El-sohemy A. ABO genotype, 'blood-type' diet and cardiometabolic risk factors. PLoS ONE. 2014;9(1):e84749.
[xxxiii]. http://www.dadamo.com/txt/index.pl?3030