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“First dentistry was painless.
Then bicycles were chainless,
Carriages were horseless,
And many laws enforceless.
Next cookery was fireless,
Telegraphy was wireless,
Cigars were nicotineless,
And coffee caffeineless.
Soon oranges were seedless,
The putting green was weedless,
The college boy was hatless,
The proper diet fatless.
New motor roads are dustless,
The latest steel is rustless,
Our tennis courts are sodless,
Our new religion–godless.”
“The most important kind of freedom is to be what you really are. You trade in your reality for a role. You trade in your sense for an act. You give up your ability to feel, and in exchange, put on a mask. There can’t be any large-scale revolution until there’s a personal revolution, on an individual level. It’s got to happen inside first.”
“People are afraid of themselves, of their own reality; their feelings most of all. People talk about how great love is, but that’s bullshit. Love hurts. Feelings are disturbing. People are taught that pain is evil and dangerous. How can they deal with love if they’re afraid to feel? Pain is meant to wake us up. People try to hide their pain. But they’re wrong. Pain is something to carry, like a radio. You feel your strength in the experience of pain. It’s all in how you carry it. That’s what matters. Pain is a feeling. Your feelings are a part of you. Your own reality. If you feel ashamed of them, and hide them, you’re letting society destroy your reality. You should stand up for your right to feel your pain.”
“That’s what real love amounts to – letting a person be what he really is. Most people love you for who you pretend to be. To keep their love, you keep pretending – performing. You get to love your pretence. It’s true, we’re locked in an image, an act – and the sad thing is, people get so used to their image, they grow attached to their masks. They love their chains. They forget all about who they really are. And if you try to remind them, they hate you for it, they feel like you’re trying to steal their most precious possession.” Jim Morrison
Monday, 24th of February, 6:02AM… I awaken. I had a dream and in this dream, I got there. I got there… I reached the promised land. I don’t know how I got there. I don’t even know where it was… but I got there with nothing but the coat on my back. No bag, no wallet, no money, no ID, no phone, no pills, no computer… off the grid, if there was one where I was… no nothing. No running… no airport… I was not trying to get somewhere or away from something, including myself. I just was there.
This was not a night terror. I knew no one. I was all alone, but in a crowd… which in and of itself is not disturbing. I’m used to being alone. I always traveled alone… particularly when no one knew I was leaving the country. In reality, I never traveled with anything or so much it needed to be checked… I had no baggage when traveling, just a backpack and purposeful tactical clothing with more than 70 pockets. In this dream, I made it with nothing and remember not much but walking around in circles (so to speak)… following the flow of people, wondering what I was going to do. Thinking that whenever i get home from wherever I am I will still have nothing. I had a coat and that’s all.
More than one month of half the normal dose of that which kept the monsters from my dreams… prevented the terrors, the sweats, the panics. The intended dose reduction to bring my dreams closer than the last fifteen seconds that I could remember under the influence of a good sleeper pill. I’m different now. I’ve evolved. I’ve experienced personal and spiritual growth that I never had an opportunity to explore up to this point in my life. If last night means anything, I hope that it is that my night terrors are gone forever.
That which haunted me my entire life is no longer so haunting and not much more than an ever more distant memory. In this dream, there was a huge building and I don’t know what it was, but all others were moving towards it and going into it… and I couldn’t go into it because I had a coat. I had nothing, yet I had too much. My intended migration towards minimalism during consciousness has moved from reality to a dream. My baggage is gone. It’s been wide open for all to see into for about four years now… but now, the baggage isn’t just open… it’s gone.
This was no requiem. It was dream. I had a real dream. Am I reborn? At the point I told someone IN my dream what was happening to me… with nothing… not knowing if it was lost… gone forever… I awakened and left my bedroom to look at the clock and the time. 6:02AM
“Survivors who have actively faced their healing are some of the most lively, spunky, brave, fun, wonderful people I know. There’s something about diving into the deepest pain in life and coming out whole, that leads us to enjoy each precious moment in life, because we know it’s all we’ve got. Instead of responding to the pain of the past, survivors learn to appreciate the wild beauty of the present.”
“The average human being is actually quite bad at predicting what he or she should do in order to be happier, and this inability to predict keeps people from, well, being happier. In fact, psychologist Daniel Gilbert has made a career out of demonstrating that human beings are downright awful at predicting their own likes and dislikes. For example, most research subjects strongly believe that another $30,000 a year in income would make them much happier. And they feel equally strongly that adding a 30-minute walk to their daily routine would be of trivial import. And yet Dr. Gilbert’s research suggests that the added income is far less likely to produce an increase in happiness than the addition of a regular walk.”
? Kerry Patterson, Influencer: The Power to Change Anything
If you are absolute and refuse to read, learn, understand, empathize, or even speak to who or what you demonize, how will you ever learn more about you… yourself, and cultivate deeper perception, awareness, comprehension into what you believe yourself? The things that have the most value when it comes to learning and understanding are exactly the things worth exploring and are worth reading, have the most value and, more accurately, those that challenge our convictions. Before you use a simple label for anything you question or take issue with, no matter what, you must be knowledgable enough to think for yourself and come to your own conclusion. Trust no one’s voice but your own, but before you judge others, make sure you have clean hands and use a purely factual challenge without any labels. It doesn’t matter if it is political, social, cultural or religious… the same mandate applies. [Marc Gilbert-Widmann January 29, 2014]
“In a world as electronically connected as ours, other than shooting Bieber into the silent void of space (which the Geneva Convention lists as a war crime against space), there is nothing we can do to protect our children from the toxic effect this stunted Vanilla Ice has and will continue to have on our culture.
But that doesn’t mean we have to let him stay in our home.
Every day we deport those who come here with no agenda other than to work hard, keep their head down, pay taxes, raise a family, and pursue the American Dream in a noble and honorable way. But we’re housing this little pantywaist and his posse?
>”Promoting ‘responsible drinking and driving’ is like promoting ‘responsible drive-by shootings’.”—MADD’s Driven Magazine, Fall, 1997. (This was in their nationally distributed magazine.)
>”The only safe amount of alcohol when you are mixing driving and drinking is zero – double zeros, no alcohol,” says MADD’s Tina Pascoe. (They swear they are not for Prohibition.)
“Forget limits on BAC. It’s just not acceptable to drink and drive, period” – Madd President Wendy Hamilton. (And since we can’t eliminate driving, let’s eliminate drinking.)
>”…I had ceased my affiliation with M.A.D.D. when they would no longer allow me to say the name God or Jesus Christ when I spoke to people about the story of my daughter.”—Former MADD coordinator, Vicki Soles. (Must be the disturbing fact that Jesus drank wine.)
>“Last year, 24,000 nationwide lost their lives because of drunk drivers.”— Theresa McNeil, MADD spokeswoman on WXON-TV. (Misspoken again? The MADD message loud and clear: Already inflated Alcohol-related death numbers equal drunk driving deaths.)
>Chief Justice William Rehnquist in 1990, “No one can seriously dispute the magnitude of the problem…drunken drivers cause an annual death toll of over 25,000.” –from the Supreme Court decision allowing sobriety checkpoints. (Alcohol-related deaths equal drunk driving deaths. Now where did he get that idea?)
> ”Once you’ve consumed your first drink, you’ve lost that ability to make a sound judgment.” —MADD Chapter President, Penny Wagner. (That explains a lot about our lawmakers.)
>”Drunk driving is one of the most frequently committed violent crimes in the United States, killing 16,653 people last year, according to the National Highway Traffic Safety Administration.”—Nationwide Insurance Poll press release, Dec, 2001. (They have also learned the art of misspeaking. Nationwide is a financial contributor to MADD and reaps 2-300% higher premiums from DUI arrestees.)
>“Education is important, but we’re to the point where almost everyone knows they shouldn’t drink and drive. The people who are still doing it are choosing to do it. The most effective way to deal with them is to arrest them.” David Kelly, MADD, Virginia chapter. (All 80% of the population—and hurry up about it!)
>July, 03 NHTSA radio script: “Impairment starts with the first drink and driving impaired is a crime,” “If you drive impaired you’ll get caught.” (MADD policy, government policy. Same people. The distinction blurs.)
>“Lowering the legal [arrest] standard will be a deterrent for light drinkers as well as heavy drinkers. There is no safe blood alcohol level, and for that reason, responsible drinking and driving means no drinking and driving.”—Catherine Prescott, former President, MADD. (They swear they are not for Prohibition, really.)
“Drunk driving is the most frequently committed crime in the nation today. DWI arrests in 1987 totaled an estimated 1,728,000, more than three times the total for all otherviolent crimes (murder, forcible rape, robbery and aggravated assault).”—MADD pamphlet. (Drunk driving=violent crime=rape, murder. Get the message.)
>Drunk driving continues to be the most frequently committed violent crime. —MADD’s Wendy Hamilton, Nov 21, 2002. (To be violent, shouldn’t a crime always have a victim?)
>From the NHTSA: “Although every year 1.5 million impaired drivers are arrested, only one arrest is made for every 772 occurrences of driving under the influence of alcohol.” (That’s 1.158 Billion occurrences of violent, mostly victimless crimes every year! And 1,158,000,000 potential arrests each year. We need one BIG jail. Note also that drunk driving is now impaired driving.)
“…we do not want to overlook the casual drinker. If you choose to drink, you should never drive. We will not tolerate drinking and driving-period.”—MADD President, Karolyn Nunnallee. (They swear they are not for Prohibition, honest.)
>“Mr. Howarth, how many fatal accidents do cell phone users cause every year versus drunk drivers?”
“I have absolutely no idea, nor do I care.” — Brian Williams and MADD lobbyist Tom Howarth, MSNBC, March 4, 1998. (Cell phone use has been equated to a BAC of .10 (drunk). MADD supports cell phone use while driving, so you can report drunk drivers.)
“In El Salvador, a first offense results in execution by firing squad.” In fact, an attorney from the Salvadoran Embassy phoned Chaloupka demanding that MADD stop lying about El Salvador’s driving laws.—Detroit News, 4-27-91. (Lucky we live here where it’s only jail, fine & license suspension.)
>”Good morning, I’m James Fell. I am a national board member for Mothers Against Drunk Driving and the Director of Traffic Safety and Enforcement Programs at the Pacific Institute for Research and Evaluation [PIRE]. Before joining PIRE, I spent 30 years at the National Highway Traffic Safety Administration.” (MADD policy, government policy. Same people, same policy.)
MADD board member and PIRE researcher Robert Voas admitted, “Drivers in the .08 to .09 range often do not exhibit the blatant erratic driving of higher BAC offenders, so that the evidence for probable cause may not be present for stopping a vehicle.” (Note to MADD, “He forgot to say drunk drivers.” Perhaps we should call them closet drunks since they don’t exhibit any clues to their real identity. PIRE is responsible for many of the alcohol studies that MADD & the NHTSA use.)
>”In Fairfax County, Virginia the cops are arresting drunks — get this — in bars. That’s right. They are going into bars and dragging people outside to determine if they are drunk. And if they are, wham-bam, it’s into the slammer, Sam!” —Dec, 02. FOX news. (The Untouchables, Virginia style.)
MADD’s reaction to the news: “In our view, law enforcement is doing its job,” said Chuck Hurley, an official with the National Transportation Council and former national board member of Mothers Against Drunk Driving. (MADD policy, government policy. Same people, same policy.)
>“If .08% is good, .05% is better. That’s where we’re headed, it doesn’t mean that we should get there all at once. But ultimately it should be .02%.”—Steve Simon, Chairman, Minnesota State DUI Task Force (Why stop there? “00” is such an easy number to remember.)
>“We may wind up in this country going to zero tolerance, period.”—U.S. Senator and MADD supporter Barbara Boxer (D-CA). (California always wants to be first.)
>”The National Crackdown is a partnership of criminal justice and traffic safety partners in all 50 States joining forces to catch impaired drivers and to lock them up.”—NHTSA, July, 2003 (Impaired drivers are the new violent criminals and police are now called traffic safety partners. The proposal is to stop 93 million drivers at sobriety checkpoints as soon as taxpayer funds are received. Look for a catchy label without the work checkpoint in it, maybe “Safe & Secure Streets Campaign”.)
>”Because of the heightened visibility checkpoints give to DWI law enforcement, they are especially valuable and effective as a general deterrent… If the public is aware the police will be conducting checkpoints… they drink less,” From a MADD speech.(Fear of the government and the police is a desirable thing, evidently.)
>“We cannot have the kind of country we want if people are afraid of those folks who are trying to protect them.” -President William Clinton. (Unlike George Bush, Clinton was never arrested for drunk driving and his chauffeur doesn’t drink.)
>U.S. Transportation Secretary Norm Mineta said “If you drink and drive, you lose. Today we’re putting drunk drivers on notice: If we catch you drinking and driving, we will arrest you and prosecute you.” (Now drunk driving is a federal offense!)
>Last year 17,274 Americans lost their lives on our nation’s highways in alcohol-related fatal traffic crashes. This number constituted the first increase in drunk driving fatalities in a decade. Katherine P. Prescott, President, (MADD) Senate speech, May 7, 1997. (Here in the same paragraph is alcohol related equated to drunk driving. This in a speech to Congress.)
>”This compendium incorporates MADD ‘s position on each issue, sample laws, sample testimony or speeches, and other useful resource information…“— NHTSA Zero Tolerance Underage Drinking website. (To save money they could combine the NHTSA and MADD logos.)
>Paul Mulshine, Star-Ledger Staff, July 20, 2003—“[Quote by]…MADD president Wendy Hamilton in a Reuters article just prior to the July 4, (2003) weekend: “Last year, 18,000 people were killed in drunk driving crashes.” This not true, however. The MADD people admitted that when I phoned their Washington office.
“She may have been misquoted or she may have misspoken,” said spokesperson Stephanie Manning when I asked her about Hamilton’s statement. “The official line is to say ‘alcohol-related deaths.'”
I asked Hamilton if she knew exactly how many people were actually killed by drivers who were legally drunk in 2002. She said she didn’t, but she invited me to call the National Highway Traffic and Safety Administration.
The NHTSA spokesman said he didn’t know either. But he was kind enough to point out that the “alcohol-related” category employed by Mothers Against Drunk Driving includes a great number of accidents in which the participants were either not drunk or not driving. If a car hits you as you walk across the street after having a glass of wine with dinner, for example, then the .01 blood-alcohol content in your corpse will be sufficient for NHTSA to classify your untimely demise as alcohol-related – even though the driver was totally sober…” (Just an innocent misspoken statement, ala another president, named Nixon.) CLICK HERE for the complete news article
>”Lowering the legal [arrest] standard will be a deterrent for light drinkers as well as heavy drinkers.”—Former MADD President, Prescott. (“And vengeance is mine,” said the Lord.)
quotes compilation compliments of MADD (Mothers Against Drunk Driving)
FACT CHECK: My first impression of this study is that while they recognize certain factors and results as anecdotal, I find ALL results and assumptions anecdotal because of the nature and uncontrollable variables of the study.
Scientific factors and explanations aside, this study is flawed. This study (by design) does not meet the standards of scientific testing. It is not double blind. The sampling is too small and uncontrolled. There is no represented control over the test subjects and the results are based on blood testing and surveying the participants.. “Since the scoring system in the present study only assessed relative adherence to each of the four ‘Blood-Type’ diets, we could not determine the absolute number of people who strictly followed any of the diets”.True compliance by test subjects is not known.
It is readily and repeatedly stated with different language that residual confounding is: “the observed associations between ‘Blood-Type’ diet scores and cardiometabolic disease risk factors could be due to residual confounding. However, residual confounding is not likely to explain why there would be no differential association among ABO genotypes.” I disagree. For your convenience to understand word phrases, I present a high levelsummary of residual confounding:
Residual confounding is the distortion that remains after controlling for confounding in the design and/or analysis of a study. There are three causes of residual confounding:
There were additional confounding factors that were not considered, or there was no attempt to adjust for them, because data on these factors was not collected. Control of confounding was not tight enough. For example, a study of the association between physical activity and age might control for confounding by age by a) restricting the study population to subject between the ages of 30-80 or b) matching subjects by age within 20 year categories. In either event there might be persistent differences in age among the groups being compared. Residual differences in confounding might also occur in a randomized clinical trial if the sample size was small. In a stratified analysis or in a regression analysis there could be residual confounding because data on confounding variable was not precise enough, e.g., age was simply classified as “young” or “old”.
There were many errors in the classification of subjects with respect to confounding variables.” (*Confounding and Effect Measure Modification, http://sphweb.bumc.bu.edu/… Boston University of Public Health). The sampling and length of the study is insignificant, There is not enough data (from this study) to make the declaration of “no differential association among ABO genotypes”. To state of (the blood type diet): “its recommendations do not specify any actual amount of consumption.” is materially incorrect and the statement is deceptive.
Dadamo and his book do not make a claim without scientific facts and complete references. This study does not reflect enough of the lectin factor… and a complete dismissal of Dadamo’s (among other) research with regard to specific lectin effect on aglutenation ofeach of the ABO blood types. It is stated: “In summary, the present study is the first to test the validity of the ‘Blood-Type’ diet and we showed that adherence to certain diets is associated with some favorable cardiometabolic disease risk profiles.
This may explain anecdotal evidence supporting these diets, which are generally prudent diets that reflect healthy eating habits. However, the findings showed that the observed associations were independent of ABO blood group and, therefore, the findings do not support the ‘Blood-Type’ diet hypothesis.” this statement corresponds to the preferred result of nutrigenomics who appear to focus less on the blood type and more on genetic factors. They say there is no corresponding conflict and the fact a grant from nutrigenomics helped pay for this “OPINION PAPER”.
Peer review is a mis-used phrase and implies real science where it is generally evaluation of meta-data and not real science.
MY INDIVIDUAL CASE STUDY: I started the blood type diet, not to lose weight… my weight was already dropping from me via an eating disorder called… “I don’t feel like eating get that food away from me.” Or more commonly referred to as PTSD. I had to go about the task of finding a “DIETary” lifestyle that allowed me to eat without wanting to vomit or the smell of food that would would make me nauseated. I actually selected the blood-type diet because of the foods, which made food preparation easier with more raw foods and vegetables.
The first meal of the day is still difficult for me… and if I don’t have reminders, I will usually forget to eat all day long and around supper time say… humm… I haven’t eaten anything all day. As far as my health. At the start, I was in the middle of a cardiac intervention… pulmonary intervention… and anemia that followed me my entire life… no matter what treatment was tried. In 2009/2010, my carotid and femoral arteries had significant plaque. I had a leaky heart valve. I had an aFib issue and was told I would be on heart medication the rest of my life. I had peptic ulcers, edema of the transverse colon… I can’t remember what I have forgotten to list I was at the door of death and passed through it when as a man, I waited beyond the point of no return before I went to the ER… where I coded on Oct 17, 2009 when two of four heart chambers were crushed by fluid. I was conscious and watched the flatline that lasted about 15 seconds. This all came to a head after eating SUSHI… where I got a food borne bacteria… not e.coli, or any other type of food poisoning… In fact, after a two week hospitalization it was another three weeks before they were able to determine what had made me accumulate fluids. Three liters in the right lung (pleural effusion) and 550cc’s in my pericardia (pericardial effusion).
Draining the lung was simple enough and I was amused when the fluid was coming out of the tube inserted between a few ribs in my back… saying… “wow, all that is coming out of me?”… The pericardiocentesis (spelling) was a bit more complicated. I had no blood pressure when laying flat so they could not sedate me for the procedure to insert the chest tube to drain my pericardia… so… I had to man up and take the needle and tube going snap crackle pop through my chest wall and into the pericardia and wrapped around the heart with NO SEDATION… I suppose the training I received as a child getting dental care done all the way to exposed nerves with no Novocain (as a form of punishment) was helpful. It was NOT comfortable and was made tolerable by watching the ultra-sound guided tour of the needle and tube in my chest. Remarkably… the initial insertion of the needle was surprisingly painless, but for the look on the cardiologist’s face as he was trying to shove the needle into my chest and asking the ultra sound tech… “Is that the right ventricle?.
I was the walking dead getting five different antibiotics (IV) and was walking around with a fifty foot oxygen hose and a pole with seven infusers on it. They didn’t know what they were treating so they treated everything. At this time I normally had high blood pressure (but not during the intervention). Total cholesterol almost 300. Triglycerides over 400. Low RBC (<4.1), low WBC(<3.8), low hemoglobin(<12.9), low platelets (<135), high MCV (>106) causing macrocytosis (spelling). A wild range of glucose (fasting). Along came the choice of the blood-type diet.
I have a good relationship with my primary care physician and I went to him to tell him what I was going to do… He was a bit indifferent at first… but after a full year he finally said… “I’m not really sure exactly what you are doing, but it is working”… so keep doing it and don’t worry about being too skinny, because you are not… you do have low % of bdy fat but normal BMI”… Thank you Dr Dino Gonzalez.
All of my blood markers are NOW within normal range. A lifetime of anemia has been for all practical purposes completely resolved. There is no cure, but I am as close as it comes. Total cholesterol is now hovering between 140-150, Triglycerides 93. The only blood marker out of range at last blood testing (12/18/2k13) is creatinine (0.7). I no longer take blood pressure medication. I no longer take a statin and before that tricor. I no longer need iron supplementation, which never really helped the anemia but kept me out of crisis. I have not had to have a blood transfusion in three years. My blood pressure is 110/70 (+/-). My resting heart rate is 63 with no aFib or heart medication.
At the start of this in 2009 I weighed 205. After the hospitalization I was down to 170 and went back up to 185 after discharge when resuming (ab)normal carnivorous diet. Those blood markers have to be combined with the fact I now hover between 140-145lbs and have been there for two years now. % of body fat about 11%, BMI 22, bone density 66. I am released from cardiac care. The plaque that WAS in my carotid and femoral (among other places I’m sure) is COMPLETELY GONE. I have no aFib. I don’t have a six pack stomach… I have an eight pack stomach. My peptic ulcers are gone. The edema of my transverse colon (IBS) is gone. There are other resolved minor issues.
I am the picture of health… other than a pulmonary embolism in September which there as of yet is no explanation for. I do not fit the profile of sedentary lifestyle… so it may end up being a little chunk of the big “C” somewhere. Nothing invasive to explore can be done because i’m on rat poison… coumaden/warfarin, which took me from the blood type diet to the warfarin diet.
The latest lab results were after three months of NOT eating the vegetables, nuts, grains, seeds, legumes, seafood and all other foods high in vitamin K that resolved so many of my medical issues… including completely reversing cardiovascular disease but for that pesky right lung. I haven’t been an angel my whole life and the 2009 crisis uncovered, stage 1 emphysema, asthma, severely reduced lung capacity just n the right lung and a lot of scar tissue. I did not start the blood type diet to lose weight but rather gain health. I am the poster boy BUT… according to this “peer-reviewed” piece it doesn’t count because I am blood type A+. ANY QUESTIONS???
When the science you learned in school and the science you read in the newspaper don’t quite match up, the Meet Science series is here to help, providing quick run-downs of oft-referenced concepts, controversies, and tools that aren’t always well-explained by the media.]
ABO Genotype, ‘Blood-Type’ Diet and Cardiometabolic Risk Factors
Jingzhou Wang, Bibiana García-Bailo, Daiva E. Nielsen, Ahmed El-Sohemy
Published: January 15, 2014
The ‘Blood-Type’ diet advises individuals to eat according to their ABO blood group to improve their health and decrease risk of chronic diseases such as cardiovascular disease. However, the association between blood type-based dietary patterns and health outcomes has not been examined. The objective of this study was to determine the association between ‘blood-type’ diets and biomarkers of cardiometabolic health and whether an individual’s ABO genotype modifies any associations.
Subjects (n = 1,455) were participants of the Toronto Nutrigenomics and Health study. Dietary intake was assessed using a one-month, 196-item food frequency questionnaire and a diet score was calculated to determine relative adherence to each of the four ‘Blood-Type’ diets. ABO blood group was determined by genotyping rs8176719 and rs8176746 in the ABO gene. ANCOVA, with age, sex, ethnicity, and energy intake as covariates, was used to compare cardiometabolic biomarkers across tertiles of each ‘Blood-Type’ diet score.
Adherence to the Type-A diet was associated with lower BMI, waist circumference, blood pressure, serum cholesterol, triglycerides, insulin, HOMA-IR and HOMA-Beta (P<0.05). Adherence to the Type-AB diet was also associated with lower levels of these biomarkers (P<0.05), except for BMI and waist circumference. Adherence to the Type-O diet was associated with lower triglycerides (P<0.0001). Matching the ‘Blood-Type’ diets with the corresponding blood group did not change the effect size of any of these associations. No significant association was found for the Type-B diet.
Adherence to certain ‘Blood-Type’ diets is associated with favorable effects on some cardiometabolic risk factors, but these associations were independent of an individual’s ABO genotype, so the findings do not support the ‘Blood-Type’ diet hypothesis.
Citation: Wang J, García-Bailo B, Nielsen DE, El-Sohemy A (2014) ABO Genotype, ‘Blood-Type’ Diet and Cardiometabolic Risk Factors. PLoS ONE 9(1): e84749. doi:10.1371/journal.pone.0084749
Editor: Nick Ashton, The University of Manchester, United Kingdom
Received: August 15, 2013; Accepted: November 18, 2013; Published: January 15, 2014
Funding: This work was supported by grant 305352 from the Advanced Foods and Materials Network (to AE-S). JW is a recipient of an Ontario Graduate Scholarship. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: AE-S holds shares in Nutrigenomix Inc., a genetic testing company for personalized nutrition. This does not alter the authors’ adherence to all the PLOS ONE policies on sharing data and materials.
A link between ABO blood group and diet was proposed by P.J. D’Adamo in his book “Eat Right For Your Type” published in 1996 . The ‘Blood-Type’ diets have gained widespread attention from the public with more than 7 million copies sold in over 60 languages, and making the New York Times bestseller list . D’Adamo postulates that the ABO blood group reveals the dietary habits of our ancestors and adherence to a diet specific to one’s blood group can improve health and decrease risk of chronic diseases such as cardiovascular disease. Based on the ‘Blood-Type’ diet theory, group O is considered the ancestral blood group in humans so their optimal diet should resemble the high animal protein diets typical of the hunter-gatherer era. In contrast, those with group A should thrive on a vegetarian diet as this blood group was believed to have evolved when humans settled down into agrarian societies. Following the same rationale, individuals with blood group B are considered to benefit from consumption of dairy products because this blood group was believed to originate in nomadic tribes. Finally, individuals with an AB blood group are believed to benefit from a diet that is intermediate to those proposed for group A and group B . The ‘Blood-Type’ diet also proposes that lectins, which are sugar-binding proteins found in certain foods , could cause agglutination if they are not compatible with an individual’s ABO blood group.
The ABO blood group is a classification of blood based on the structural variation of a certain carbohydrate antigenic substance on red blood cells. As one of the first recognizable genetic variants in humans, the ABO blood group has been studied extensively for its association with a variety of diseases including cancer , , , , malaria , and cholera . Regarding cardiometabolic diseases, individuals with blood group O were found to have lower levels of von Willebrand factor (VWF)  and had a reduced risk of venous thromboembolism compared to the other blood groups . Furthermore, group B individuals were found to have lower levels of E-selectin  and a lower risk of type 2 diabetes compared to group O . These findings demonstrate the potential importance of the ABO blood group in altering risk of disease, including cardiometabolic disease. However, little is known about whether the ABO blood group modifies an individual’s response to diet. A recent systematic review concluded that no evidence exists to support the proposed health benefits of ‘Blood-Type’ diets . Considering the lack of scientific evidence and the popularity of the ‘Blood-Type’ diet, the objective of this study was to determine the association between ‘Blood-Type’ diets and biomarkers of cardiometabolic health and whether an individual’s ABO genotype modifies any associations.
Materials and Methods
The study protocol was approved by the Research Ethics Board at the University of Toronto, and all subjects provided written informed consent.
Subjects (n = 1,639) were participants of the Toronto Nutrigenomics and Health (TNH) Study, which is a cross-sectional examination of young adults aged 20 to 29 years. All subjects were recruited between October 2004 and December 2010 and completed a general health and lifestyle questionnaire, which included information on age, sex, ethnocultural group and other subject characteristics. Subjects who were likely under-reporters (less than 800 kcal per day) or over-reporters (more than 3,500 kcal per day for females or 4,500 kilocalories per day for males) of energy intake were excluded from the analyses. Subjects were also excluded if they had missing data for any of the biomarkers of interest or ABO genotype (n = 184). After exclusions, 1,455 subjects (993 women and 462 men) remained. Individuals were categorized into four major ethnocultural groups: White (n = 703), East Asians (n = 491), South Asians (n = 155), and others (n = 106).
Dietary adherence score assessment
Dietary intake was assessed by a one-month, Toronto-modified Willet 196-item semi-quantitative food frequency questionnaire (FFQ) as described previously . Briefly, each subject was given instructions on how to complete the FFQ by using visual aids of portion sizes to improve the measurement of self-reported food intake. Subject responses to the individual foods were converted into daily number of servings for each item. In order to quantify the adherence to each of the four ‘Blood-Type’ diets, four different diet scores were given to each subject regardless of his or her own blood group. Based on the food items listed in the ‘Blood-Type’ diets , subjects received one positive point for consuming one serving of each recommended food item and one negative point for consuming one serving of an item on the list of foods to avoid. Foods that are listed as “Neutral” were not included in the equation and do not contribute to the final score. The lists of recommended foods to eat or avoid for each ABO blood group are shown in the Appendix S1. Subjects were then grouped into tertiles based on their scores for each diet, with the top tertile representing those whose diet most closely resembles the corresponding ‘Blood-Type’ diet.
Cardiometabolic risk factor assessment
Anthropometric measurements including height, weight, blood pressure and waist circumference were determined as previously described . Body mass index (BMI; kg/m2) was calculated and physical activity was measured by questionnaire and expressed as metabolic equivalent (MET)-hours per week, as described previously , . Overnight 12-hour fasting blood samples were collected to measure serum biomarkers of cardiometabolic disease including triglycerides, free fatty acids, C-reactive protein, glucose, insulin, and total-, HDL- and LDL-cholesterol, as described previously . The homeostasis model of insulin resistance (HOMA-IR) was calculated by using the formula: (insulin * glucose)/22.5, and the homeostasis model of beta-cell function (HOMA-Beta) was calculated by using the formula: (20 * insulin)/(glucose – 3.5).
ABO genotype identification
The Sequenom MassArray® multiplex method was used to determine the blood group of study participants by genotyping two single nucleotide polymorphisms (SNPs) (rs8176719Del>G; rs8176746A>C) in the ABO gene. The rs8176719 SNP indicates O-allele-specific 261delG while rs8176746 determines the galactose specificity of the encoded A/B transferases and thus the expression of A and B antigens on erythrocytes .
Statistical analyses were performed using the Statistical Analysis Systems (SAS) Software program (version 9.2; SAS Institute Inc., Cary, North Carolina). The a error was set at 0.05 and reported p-values are 2-sided. Variables that were not normally distributed were either loge or square root transformed prior to analysis, but the mean values and standard errors are displayed without transformation to facilitate interpretation. Subject characteristics were compared across ABO blood groups by using chi-square tests for categorical variables and analysis of covariance (ANCOVA) for continuous variables. ANCOVA was also used to compare means of biomarkers of cardiometabolic disease risk across tertiles of diet scores. Means compared between groups were adjusted for multiple comparisons using the Tukey-Kramer procedure. Age, sex, ethnocultural group and energy intake were used as covariates in the ANCOVA analysis. Physical activity and smoking were also considered, but not included in the final model because they did not significantly (P<0.05) alter the results. The p-values for the associations between ‘Blood-Type’ diet and cardiometabolic biomarker profile remained significant (P<0.001) regardless of whether or not these two variables were included in the model. To determine whether matching the blood group with the corresponding diet was associated with a more favorable cardiometabolic disease risk profile, we stratified the entire population into two groups; one with the matched blood group for the diet, and the other unmatched. We next examined the interaction between diet score and the matching status on levels of each cardiometabolic disease risk factor for each ‘Blood-Type’ diet by using the Tukey-Kramer correction. When a significant interaction effect was observed, we further compared the differences in the outcome between subjects with the matched blood group and the unmatched group in each of the tertiles of diet score.
Subject characteristics based on the ABO blood group are summarized in Table 1. After adjusting for age, sex, and ethnocultural group, subject characteristics were similar across ABO blood groups, except for insulin, HOMA-IR and HOMA-Beta (p<0.05). Although the overall association between blood group and total cholesterol was significant (p = 0.043), no difference was observed among specific ABO blood group.
Table 1. Subject Characteristics by ABO Genotypea.
Each ‘Blood-Type’ diet was first examined in the entire population without considering ABO blood groups. Figure 1A shows the total number of recommended items that were included in the FFQ for each diet. Briefly, the Type-A diet recommends high consumption of grains, fruits, and vegetables. The Type-B diet recommends high intakes of dairy products and moderate intakes of other food groups. The Type-AB diet is similar to the Type-B diet, but has more restrictions on specific food items. For example, only eggs and fish are recommended as sources of meat for group AB individuals (Appendix S1). The Type-O diet promotes high consumption of meats and avoidance of grain products. Figure 1B shows the diet score distribution. All four scores were normally distributed and did not require any transformation.
Figure 1. ‘Blood-Type’ diet (A). Diet score distribution for each ‘Blood-Type’ diet (B).
Characteristics of each ‘Blood-Type’ diet according to tertile of diet score are summarized inTable S1. Consistent with its recommendations, subjects in the highest tertile of the Type-A diet score consumed more fruits and vegetables and less meat (P<0.001). As for the two diets that recommend dairy consumption, high adherences to the Type-B and Type-AB diets were associated with higher intakes of dairy products (P<0.05). The dietary intake of those following the Type-O diet was also consistent with the diet’s recommendations where more meat and less grain products were consumed as individuals adhered more closely to the Type-O diet (P<0.001).
Mean levels of cardiometabolic disease risk factors based on the tertiles of each diet score are shown from Table 2 to Table5. All associations were adjusted for age, sex, ethnocultural group and energy intake. With increasing adherence to the Type-A diet, subjects, regardless of their ABO blood group, had lower BMI, blood pressure, waist circumference, serum total cholesterol, triglycerides, insulin, HOMA-IR, and HOMA-Beta (P<0.05). Adherence to the Type-AB diet was associated with lower blood pressure, serum total cholesterol, triglycerides, insulin, HOMA-IR, and HOMA-Beta (P<0.05). Adherence to the Type-O diet was associated with lower serum triglycerides (P<0.001). Although the overall association between the Type-B diet adherence and the level of HDL-cholesterol was significant (p = 0.04), no difference was observed between each tertile of the diet score.
Table 5. Cardiometabolic Risk Factors by the Tertiles of Type-O Diet Scoresa.
Table 6, 7, 8 and 9 show the associations between diet scores and cardiometabolic disease risk factors according to the ABO blood group. Different ABO blood groups were equally distributed across the tertiles of each diet score. No significant interactions were observed between diet score and blood group for most of the risk factors, except for fasting glucose (P = 0.02), insulin (P = 0.02), and HOMA-IR (p = 0.01) in the Type-A diet (Table 6), and fasting glucose (P = 0.02) in the Type-AB diet (Table 8). When comparing the levels of fasting insulin and HOMA-IR between group A individuals and the other blood groups, a significant difference was observed in the second tertile, but not in the lowest or highest tertile of the Type-A diet score. No difference in fasting glucose was observed between the two groups in any tertile of the Type-A diet score. For fasting glucose in the Type-AB diet, no difference was observed between individuals with blood group AB and those with other blood groups in any tertile.
Table 9. Cardiometabolic Risk Factors by Matching Type-O Diet Scores and ABO Genotypea.
Our findings show that adherence to certain ‘Blood-Type’ diets is associated with a favorable profile for certain cardiometabolic risk factors in young adults, but these associations were not related to an individual’s ABO blood group. To our knowledge, this is the first study to examine the association between the ‘Blood-Type’ diets and biomarkers of cardiometabolic health, and the findings do not support the ‘Blood-Type’ diet hypothesis.
The association between the Type-A diet adherence and favorable cardiometabolic risk profile is not surprising considering this diet’s emphasis on high consumption of fruits and vegetables, and low consumption of meat products, which is similar to a dietary pattern that has been recommended by various health agencies because of its association with a lower risk of cardiovascular diseases , , , , . Adherence to the Type-AB diet was also associated with favorable levels of several risk factors, despite its recommendation for certain dairy and meat products. Such benefits may be attributed to the list of certain food items considered healthy, which are recommended. For example, individuals with blood group AB are advised to avoid butter and to consume eggs and fish as their main animal-protein source. This is in contrast to the Type-B diet, which has fewer restrictions on many animal products as shown in the Appendix S1. These differences between the two diets may partially explain why a favorable cardiometabolic profile was associated with adherence to the Type-AB diet, but not for the Type-B diet. The Type-O diet is similar to low-carbohydrate diets , which may explain why adherence to this type of diet was associated with lower serum triglycerides (TG), as previously observed for other low-carbohydrate diets , . The reduction in TG may be caused by decreased TG production in the liver and/or increased cellular uptake of TG in response to low carbohydrate intake . By investigating the ‘Blood-Type’ diets in a population with different ABO genotypes, we found that adhering to the Type-A, Type-AB, or Type-O diets was associated with favorable effects on levels of certain biomarkers of cardiometabolic disease risk.
In order to examine whether individuals would benefit more from following their own ‘Blood-Type’ diet, the levels of cardiometabolic disease risk factors were compared between individuals with the matched blood group and the unmatched blood group while sharing similar diet adherence. However, no significant interaction effects were observed between diet adherence and blood group for most of the risk factors, suggesting that effects of following ‘Blood-Type’ diets is independent of an individual’s blood group. Although there were significant interaction effects for fasting glucose, insulin and HOMA-IR for the Type-A diet, and fasting glucose for the Type-AB diet, those interactions may be due to chance, since we did not apply the most conservative Bonferroni post-hoc test to correct for multiple comparisons. Even if the interaction effects were not due to chance, those findings would not support the claim that matching the ‘Blood-Type’ diet with the corresponding blood group results in more favorable effects. In the case of the Type-A diet, the significant interaction effects were mainly driven by higher levels of insulin and HOMA-IR in the second tertile for those with blood group A. Moving from low adherence to high adherence, group A individuals did not demonstrate more favorable changes in these biomarkers. As for fasting glucose levels with the Type-AB diet, subjects with blood group AB had slightly higher glucose concentrations as they adhered to the diet more closely, while the other blood groups showed no differences. These findings, therefore, demonstrate that matching the diet with the corresponding blood group was not associated with any additional benefits and may even be associated with some adverse effects. For those in the unmatched blood group, we also tested whether each ‘Blood-Type’ diet was associated with any of the outcomes by matching to each of the other blood groups (data not shown); however, no significant interactions were observed. Therefore, the associations observed with the ‘Blood-Type’ diets were unrelated to any individual blood group.
Several previous studies have questioned the validity of the ‘Blood-Type’ diets. Based on phylogenetic analysis of human ABO alleles, blood group A has been suggested to be the ancestral human blood group , , rather than group O as postulated by D’Adamo . As for the claim that certain food items contain lectins incompatible with an individual’s ABO blood group, studies to date suggest no ABO-specific agglutination . The absence of scientific evidence was further supported by a recent systematic review , which found no study that directly investigated the effects of the ‘Blood-Type’ diet.
The present study has some limitations. The use of FFQs for dietary assessment could result in some measurement error and cannot give a precise estimate of the absolute intake of food items. However, a FFQ is considered a valid instrument for providing relative estimates of food intake in large populations . Although we adjusted for age, sex, ethnocultural group and energy intake and tested physical activity and smoking as potential covariates, the observed associations between ‘Blood-Type’ diet scores and cardiometabolic disease risk factors could be due to residual confounding. However, residual confounding is not likely to explain why there would be no differential association among ABO genotypes. The study population consisted of an unequal distribution of different ethnocultural groups, which have been shown to have a different prevalence of ABO blood groups  and might have different dietary patterns . However, the associations between diet adherence and levels of biomarkers were still evident after adjusting for ethnocultural group. Previous studies using diet scores have quantified relative adherence by deriving the score proportionally based on the recommended amount of consumption . However, this approach would not be appropriate for quantifying the adherence to the ‘Blood-Type’ diet because its recommendations do not specify any actual amount of consumption. By assigning points based on quantity of consumption for each food item, our scoring system is continuously scaled and normally distributed. Since the scoring system in the present study only assessed relative adherence to each of the four ‘Blood-Type’ diets, we could not determine the absolute number of people who strictly followed any of the diets. However, the observed results showed that even relatively high adherence to Type-A, Type-AB and Type-O diets were associated with favorable levels of cardiometabolic disease risk factors, albeit in an ABO-independent manner. These associations were consistent with previous studies examining similar dietary patterns and cardiometabolic risk factors , , .
In summary, the present study is the first to test the validity of the ‘Blood-Type’ diet and we showed that adherence to certain diets is associated with some favorable cardiometabolic disease risk profiles. This may explain anecdotal evidence supporting these diets, which are generally prudent diets that reflect healthy eating habits. However, the findings showed that the observed associations were independent of ABO blood group and, therefore, the findings do not support the ‘Blood-Type’ diet hypothesis.
The food list was retrieved from the FFQ database of Toronto Nutrigenomics and Health Study. The “+” signs indicate the foods that are recommended for the blood group. The “-” signs indicate the food to avoid for the blood group. The “/” signs indicate the food that are neutral.
Conceived and designed the experiments: AE-S. Performed the experiments: JW. Analyzed the data: JW. Contributed reagents/materials/analysis tools: JW BG-B DN. Wrote the paper: JW. Assisted with the statistical analysis: BG-B. Assisted in data collection and study coordination: DN. Contributed to the manuscript revision for important intellectual content: BG-B DN.
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“Even if it were possible to cast my horoscope in this one life, and to make an accurate prediction about my future, it would not be possible to ‘show’ it to me because as soon as I saw it my future would change by definition. This is why Werner Heisenberg‘s adaptation of the Hays Office—the so-called principle of uncertainty whereby the act of measuring something has the effect of altering the measurement—is of such importance. In my case the difference is often made by publicity. For example, and to boast of one of my few virtues, I used to derive pleasure from giving my time to bright young people who showed promise as writers and who asked for my help. Then some profile of me quoted someone who disclosed that I liked to do this. Then it became something widely said of me, whereupon it became almost impossible for me to go on doing it, because I started to receive far more requests than I could respond to, let alone satisfy. Perception modifies reality: when I abandoned the smoking habit of more than three decades I was given a supposedly helpful pill called Wellbutrin. But as soon as I discovered that this was the brand name for an antidepressant, I tossed the bottle away. There may be successful methods for overcoming the blues but for me they cannot include a capsule that says: ‘Fool yourself into happiness, while pretending not to do so.’ I should actually want my mind to be strong enough to circumvent such a trick.”
? Christopher Hitchens, Hitch-22: A Memoir