On Testimonials and Diet Books

Recently, a woman (let’s call her “Jane”) commented to me after reading some of my Whole30 critiques that:

“How can you fact check the testimonies people have from this diet!? Are you really disregarding a whole food diet??”

Her implication seemed to be that the anecdotes of hundreds of people who had found success on this diet plan were all that mattered. Science and reason be damned! I replied back that:

“Every diet book has testimonials from people describing how said diet changed their lives and improved their health. This does not mean that those diet books are based on [or promote] good science. The problem with the Whole30 is that [in my opinion] they do not seem to care if the information they provide their fans is accurate or not.”

To my knowledge, no efforts have been made to try and correct any of the dietary misinformation that is prevalent in their book, It Starts With Food (ISWF), or the Whole30 website.

But that got me thinking about the testimonials in the book. At the beginning of every chapter in ISWF, you are inspired by stories from people who have experienced miraculous health improvements on this diet. On their website, the Whole30 has this to say:

“…many people have reported the “magical” elimination of a variety of symptoms, diseases and conditions – in just 30 days.

diabetes · high cholesterol · high blood pressure · obesity · acne · eczema · psoriasis · hives asthma · allergies · sinus infections · migraines · acid reflux · celiac disease · Crohn’s · IBS · bipolar disorder · depression · seasonal affective disorder · eating disorders · ADHD endometriosis · PCOS · infertility · arthritis · Lyme disease · hypothyroidism · fibromyalgia”

That’s quite a list. Naturally, all the testimonials presented would be positive (that’s just good marketing). But if Jane would like to use these testimonies as the basis for why the Whole30 is a good diet plan, she should take into account the totality of the anecdotes. When looking at a question scientifically, it’s important to look at all the available evidence. Not everything is all rainbows and sunshine as we see from the 10 comments below that were posted in the Whole30 Forums:

1 - Two Weeks in, Rashes are MUCH WORSE!

"I am a little over 2 weeks into my Whole30, which I started in the hopes of finally clearing up a rash on my ankle. A few days into it, the rash appeared on my elbows (where I had it about 5 years ago but went away with a Rx cream). By a week into, the rash appeared on my other leg as well, and now two weeks in, I have growing patches on both legs and arms and my scalp itches like crazy."

2 - Weight gain, no change in size

"I have been on Paleo for 5 weeks and whole30 for a month now.
Finally, I got on the scale....
The first week I lost 2.5 lbs. then I stopped weighing myself. After whole 30, I gained it all back +1.5 lbs."

3 - At what point do you decide it's not working?

"I'm on day 24 and have battled with exhaustion and bad sleep the past few weeks just like before w30. My diet hasn't radically changed apart from no dairy or alcohol and this is the first time I've eaten consistently clean for so long. I've had lots of help on the forum and I am pretty sure my food balance is right. Is it really worth another 6 days? I can do it; I'm not craving anything but it seems a bit pointless. I’m not sure it’s good for me thinking about food all the time."

4 - Failure - Six months on Whole30

"As soon as I started my Whole30, my belly started retaining water like crazy. It got so huge it looked like I was pregnant…My belly was so big, I had difficulty breathing. I tried experimenting with the sources of protein I was eating…I tried not to get discouraged, and so I continued my Whole30 for six months. But the problem persisted. Also, I gained like 15 pounds. Which is really depressing because I'm already very overweight."

5 - Excess gas & Farting on Whole30

"I've nearly completed the Whole30 with a few minor slip-ups for which I don't feel regret. Starting around Day 20 I've noticed a huge spike in frequency and smell of farts. They happen as frequent as once every 5-30 minutes, depending on how lately I've eaten…This is getting to be a pretty huge problem. My parents are angry at me, I'm embarrassed at my work cubicle, my car smells rancid, and I'm uncomfortable whenever my girlfriend's around."

6 - Constipation/bloating

"I've been Paleo/Whole9 for about 4 weeks, and my gut has slowed down like nobody's business! I was eating fish, eggs, grains, legumes before this (I was dairy-free), but no chicken, beef, etc... until I started paleo. I'm sure this could be a big factor with constipation, but I thought I'd have a flatter stomach without all the sugar and lectins. I take probiotics and fish oil daily."

7 - Day 15 - Only feeling more tired!

"So I'm now on Day 15 of my first Whole30 and am still waiting for that big energy lift to come. Fatigue was my main reason for starting the Whole30, but I'm more tired than ever. It's not long after dinner that I'm ready to crash. I've put in the time to get 8-9 hours of sleep each night, but I have been turning and tossing a lot more than usual as well. So is it normal to feel this tired this late in the game?"

8 - High Cholesterol!!!

"I had blood work done two weeks ago and found out that I have high cholesterol! I was shocked because I have eaten healthy my whole life, lots of lean meats and vegetables, small amounts of oatmeal and rice, but all whole foods, and I have been sticking to the whole30 guidelines for the most part for the last 4 months. This was the first time I've ever had my cholesterol tested, but now I'm worried that all of the fatty meats, eggs, and clarified butter I've been enjoying are negatively affecting my health…I am really worried because my level is so high that the doctor mentioned medication, but I'm only 20!"

9 - We can't sleep

"Hubby and I are on Day 26. We have been 100% compliant with the program from Day 1…But we are both exhausted. Not only from all the cooking (does anyone else feel they're chained to their kitchen?!?!?) but because we can't sleep.

It started in the first week and it's been about three weeks now. We go to bed, toss and turn for a long time before being able to sleep, then wake up in the middle of the night - 2, 3, 4 am. Sometimes we manage to go back to sleep after a long time and wake up again before or around 6 am. Other times one of us, or both, can't go back to sleep at all.

I'm getting very grumpy and struggling to perform at work…I haven't eaten absolutely anything that is not on the shopping list and have stuck to the meal template - a portion of meat wit loads of veggies and some good fat, three times a day. I drink lots of water. Once a day I have a portion of berries. I haven't been overeating nor undereating. I have kept my usual level of exercise - not a lot, but I take stairs, walk to places instead of driving and so on. I have no idea what's going on."

10 - Just keep gaining weight...

"I finished my first Whole30 a few weeks ago. I try to avoid scales, but I compete in martial arts, so I know what my weight was in June because I had a weigh-in for a competition. Because I am typically smack in the middle of my weight class, I didn't do anything out of the ordinary to prepare to weigh in. I simply didn't need to. Today, I went to the doctor and I have gained 12 pounds since then…I have always had a flat stomach gain in my hips/thighs. I now have a little spare tire…I was healthy before I started, I was just looking to lose those last few pounds and in a way where I was healthy while doing it and could maintain energy while working out. And that weight gain changes my weight class, so I really have to do something about it. I want to cry. I guess I should try to start with smaller portions? I'm not sure what else to do. I'm wondering if I fall into the "it doesn't work for everyone" category."

Now, I do not think that anecdotes are worthless nor do I think that the Whole30 has never been able to help people improve their eating habits. Anecdotes may have some relevance when dealing one-on-one with a patient in a clinical setting or as a means to help generate a hypothesis to be tested in future clinical trials. The Whole30 may be able to improve people’s health but it does so by grossly misinforming the public about the foods they eat and about their personal health. There are countless evidence-based resources out there that can instill the same positive eating behaviors encouraged in the Whole30 and do so without pushing pseudoscience onto their clients and customers.

With any diet book, you will get compliments and complaints. The point here is to please, please don’t buy something based solely on the testimonials alone. Caveat emptor.

Nutrition Sources You Should Avoid

**Need to quickly fact check a source or claim? Try using the NutriSearch.info search engine. All search results only come from 2,000+ websites and articles that deliver accurate, evidence-based content.

The internet is a cesspool of god awful nutrition advice. Some of this terrible information is delivered in such a way that makes it seem legitimate and can fool even the most intelligent among us. I created this guide as a resource to help cut through the hype you see in media headlines and on your Facebook feed. If you see an article/book/talk/product from one of the sources below please proceed with caution as it may be a load of nonsensical, pseudoscientific rubbish (especially if it's from The Food Babe). 

To land a spot on this list, a significant portion of the dietary information provided by the source must be scientifically erroneous or misleading. Some of these sources fall into the category of "quacks, frauds, and charlatans" and while others are in the "questionable" category. The common pitfalls I've seen in these sources can be grouped into four general categories:

  1. Cherry-picking sources that agree with their beliefs while ignoring those that don't.
  2. Not interpreting data within the full context of what is known about a topic.
  3. Over-extrapolating study results (like saying that findings from an animal trial apply directly to humans).
  4. Citing invalid or uncredible sources (using anecdotes as hard evidence as opposed to peer-reviewed literature).

Overall, the theme of this list are people who have misconstrued nutritional science. In my opinion, the sources below meet one or more of these criteria. 

Some of you are bound to see people on here that you consider to be good resources or may even like. Their appearance on this list does not mean everything they have ever published is erroneous, simply that they have also published too much unsound material to be considered a reliable nutrition information source as defined in my Good Nutrition Sources post.

How to Fact Check a Source

By no means is this a comprehensive list as new dubious sources pop up frequently. If you are attempting to determine the reliability of a source that is not listed, here are a few options to try. First, head on over to QuackWatch.com. If they are on that site, it’s probably best to steer clear. A second option is to take the name of the person in question and search it in google (or on NutriSearch) followed by one of these phrases/words: “debunked”, “critique”, “fact check”, “quack”, or “fraud”. You may be able to get some useful articles using this second method. Don’t be afraid to try and find out if they have any reliable credentials as well. Do they have relevant degrees or respected certifications in the field of nutrition such as those listed on the Good Sources page? If not, you may want to view what they’re saying with some skepticism until you can confirm it with a reliable source. 

For a list of reliable nutrition sources you can use, head on over to this page or try using the NutriSearch.info search engine. This list is fluid and will be edited as new unreliable sources emerge. If you have one you think should be on here, drop it in the comments section. 

Note: I don’t link directly to any of these sources (because why would I?). Instead, I’ve linked to resources demonstrating why they are on this list. 

Full disclosure: I do research for Examine.com, which is not affiliated with this blog in any way.


Abel James a.k.a The Fat-Burning Man
Andreas Eenfeldt a.k.a The Diet Doctor
Andrew Weil
Barry Sears
Billy DeMoss
Bob Harper
Chris Kresser
Dallas and Melissa Hartwig / The Whole30 / Whole9Life / Healthy Mama, Happy Baby 
Dana McDonald a.k.a The Rebel Dietitian
Daniel Amen
Dave Asprey
David Perlmutter
David Wolfe
Deepak Chopra
Diane Sanfilippo
Dr. Oz
Erin Elizabeth a.k.a The Health Nut
Gary Taubes
Greg Glassman
Gwyneth Paltrow
Jason Fung
Jeffrey Smith
Jillian Michaels
Jimmy Moore
Joel Fuhrman
Jonathan Bailor
Joseph Mercola
Josh Axe
Katie Tietje a.k.a Modern Alternative Mama
Katie Wells a.k.a Wellness Mama
Kevin Trudeau
Kris Carr
Mark Hyman
Mark Sisson
Michael Greger
Mike Adams a.k.a The Health Ranger
Nina Teicholz
Oprah Winfrey
Pete Evans
Peter D'Adamo
Ray Peat
Robb Wolf
Robert Atkins
Robert Lustig
Sally Fallon Morell
Sarah Wilson
Stephanie Greunke
Suzanne Somers
Ted Naiman
The Kardashians (All of them)
Tim Ferriss
Tim Noakes
Tom Naughton a.k.a Fat Head
Tom O’Bryan
Vani Hari a.k.a The Food Babe
William Davis
Zoë Harcombe


CrossFit Journal
Healthy Mama, Happy Baby (Mamas.Whole30.com)
RayPeat.com and RayPeatForum.com


If there’s one thing gurus love to do, it’s to write multiple diet and health books. Far too many to list here - so please don’t waste your money on diet books written by the people listed above. Here is a brief list of popular diet books to skip.

Pro Tip - Skip all of Gary Taubes' books. You're welcome.

21 Day Sugar Detox - Diane Sanfilippo
Always Hungry - David Ludwig
Cholesterol Clarity - Jimmy Moore
Dr. Atkins Diet Revolution - Robert Atkins
Dr. Kellyann's Bone Broth Diet - Kellyann Petrucci
Eat Bacon, Don't Jog: Get Strong, Get Lean, No Bullshit - Grant Petersen
Eat Right for Your Type - Peter D'Adamo
Fat Chance - Robert Lustig
Good Calories, Bad Calories - Gary Taubes
Grain Brain - David Perlmutter
I Quit Sugar for Life - Sarah Wilson
It Starts With Food - Dallas and Melissa Hartwig
Keto Clarity - Jimmy Moore
Knockout - Suzanne Somers (and all of her other books)
Low Carb, High Fat Food Revolution - Andreas Eenfeldt
Optimum Healing - Tom O'Bryan
The 4-Hour Body - Tim Ferriss
The Big Fat Surprise - Nina Teicholz
The Bulletproof Diet - Dave Asprey
The Calorie Myth - Jonathan Bailor
The Case Against Sugar - Gary Taubes (another critique here)
The China Study - T. Colin Campbell and Thomas M. Campbell
The Food Babe Way - Vani Hari
The Genotype Diet - Peter D'Adamo
The Obesity Code - Jason Fung
The Optimum Nutrition Bible - Patrick Holford
The Paleo Solution - Robb Wolf
The Plant Paradox - Steven R. Gundry
The Real Meal Revolution - Tim Noakes and Jonno Proudfoot
The Whole30 - Dallas and Melissa Hartwig
The Wild Diet - Abel James
The ZONE Diet - Barry Sears
Wheat Belly - William Davis
Why We Get Fat - Gary Taubes


Cereal Killers
Fat Head
Fed Up
Food Matters
Forks Over Knives
Genetic Roulette
Genetically Modified Food: Panacea or Poison
Hungry For Change
Perfect Human Diet
Seeds of Deception
Sweet Misery: A Poisoned World
That Sugar Film
The Beautiful Truth
The Big Fat Fix
The Future of Food
The Gerson Miracle
The World According to Monsanto
We Love Paleo
What The Health

TV Shows

The Doctors
The Dr. Oz Show
Extreme Weight Loss
My Diet Is Better Than Yours
The Biggest Loser


Environmental Working Group
Institute for Functional Medicine
Institute for Integrative Nutrition
Institute for Responsible Nutrition
Institute of Responsible Technology
PETA (People Eating Tasty Animals. JK JK - People for the Ethical Treatment of Animals)
Weston A. Price Foundation

Suspect Credentials and Universities

A list of credentials and universities (often unaccredited) that do not properly teach nutritional science or prepare their graduates to work in dietetics. 

American Board of Holistic Medicine (ABIHM)
American Nutrimedical Association
Bernadean University
Bulletproof Certification
Certified Clinical Nutritionists (CCN), Certified Nutritionists (CN), or Certified Nutrition Consultants (CNC) from The Society of Certified Nutritionists (SCN) 
Certified Nutritional Consultant (CNC) from the American Association of Nutritional Consultants
Certified Gluten Practitioner
Certified Nutritionist (CN) from the American Health Science University
Clayton College of Natural Health
Clinical Nutrition Certification Board (CNCB)
Columbia Pacific University (CPU)
Doctor of Chiropractic (DC)
Hawthorn University
National Academy of Research Biochemists
Naturopathic Doctor (ND)
Nutritionist (not to be confused with the legitimate credential of RDN – Registered Dietitian Nutritionist)
Primal Blueprint Expert Certification

Facebook Groups

In addition to the sources above, here are some other pages not to follow (or unfollow).

Collective Evolution
Gary Taubes Fan Club
Modern Alternative Mama
Natural Cures Not Medicine
Nutrition WOD
Prevention Magazine
The Mind Unleashed


None (so far)

YouTube Channels

Any from the above-mentioned websites/organizations/people


Via QuackWatch.com

Because the titles "nutritionist" and "nutrition consultant" are unregulated in most states, they have been adopted by many individuals who lack recognized credentials and are unqualified. In addition, a small percentage of licensed practitioners are engaged in unscientific nutrition practices. The best way to avoid bad nutrition advice is to identify and avoid those who give it. I recommend steering clear of:

  • Anyone who says that everyone needs vitamin supplements to be sure they get enough. Most people can get all the vitamins they need by eating sensibly.
  • Anyone who suggests that most diseases are caused by faulty nutrition. Although some diseases are diet-related, most are not.
  • Anyone who suggests that large doses of vitamins are effective against a large number of diseases and conditions. That is simply untrue.
  • Anyone who suggests hair analysis as a basis for determining the body's nutritional state or for recommending vitamins and minerals. Hair analysis is not reliable for this purpose.
  • Anyone who claims that a wide variety of symptoms and diseases are caused by "hidden food allergies"
  • Anyone who uses a computer-scored "nutrient deficiency test" as the basis for prescribing vitamins. There are valid ways that computers can be used for dietary analysis. But those used for recommending vitamins are programmed to recommend them for everyone.
  • Be wary of those who sells vitamins in their offices. Unscientific practitioners often do sell unneeded supplements — usually at a considerable profit.

Nutrition Sources You Can Trust

**It's a challenge to keep this list up to date, so if you have a nutrition or health question you can now search all of the sources listed below plus 2,000+ more sites and articles at once using the NutriSearch.info search engine.

One of the questions I get asked the most is where to turn for reliable sources of nutrition information. Well, from now on I will have this handy guide to direct them to. I’ve broken it down into categories so you can browse depending on what you are looking for. To make this list, the vast majority of the dietary information published must be based on quality scientific evidence. No one can be 100% accurate 100% of the time, but you must be handing out valid information on nutrition for at least ~90-95% of your content to remain on the list. The sources listed here:

  1. Regularly discuss topics within the full context of available data
  2. Do not cherry-pick their sources and include those that may challenge their beliefs
  3. Interpret relevant clinical trials accurately and take into account their limitations
  4. Frequently cite valid and credible sources

In my opinion, those listed below meet the above criteria and promote high-quality science-based information.

Always keep in mind that no one person is beyond reproach and that you should think critically about everything you read, even if they are on the Good Sources list. This directory is fluid and will be edited as new reliable sources emerge. If you have one you think should be on here, drop it in the comments section. 

For the list of nutrition sources you should be wary of, head on over to this page. In that post, we also discuss how to check any source that may appear on either of these lists. 

Note: Nobody paid or in any way compensated me to be on this list.

Full disclosure: I do research for Examine.com, which is not affiliated with this blog in any way.


Adel Moussa
Alan Aragon
Amber Rogers
Armi Legge
Arya Sharma
Asker Jeukendrup
Bill Shrapnel
Brad Dieter
Brad Schoenfeld
Colby Vorland
Dan Pardi
Danny Lennon
David Despain
Denise Minger
Eric Helms
Evelyn Carbsane
James Fell
James Krieger
JC Deen
Jeff Nippard
Jeff Rothschild
Johan Leech
John Berardi
Jose Antonio
Kamal Patel
Kevin Hall
Kevin C. Klatt
Laurent Bannock
Layne Norton
Leah McGrath
Leigh Peele
Lyle McDonald
Maria Brilaki
Martin MacDonald
Menno Henselmans
Michelle a.k.a The Fat Nutritionist
Mike Howard
Mike Israetel
Mike Sweeney
Patrick Umphrey
Peter Clark
Rosanne Rust
Seth Yoder
Sheila Kealey
Spencer Nadolsky
Stephan Guyenet
Steven Novella
Tim Crowe
Yann Le Meur
Yoni Freedhoff


I use Feedly.com to monitor new posts on these pages.

Eat, Train, Progress.
Harvard - The Nutrition Source
NIH’s Body Weight Planner
NutritionAsIKnowIt.com (duh)
PubMed Central
PubMed Health
The Nutrition Source (Harvard)
The Salt (NPR)


These are some non-obvious pages. All the organizations, people, and websites listed above will usually have a page you can like or subscribe to if you search for them. To access some groups you must be logged into Facebook.

Build Up Dietitians
Eat, Train, Progress
Eating The Food
ERD Private Forum
FACTS Followers
Fitness Conversations
Health Skepti-Forum
Healthy Skepticism
International Society of Sports Nutrition (ISSN)
Lean Minded
Macros Inc.
Nutrition As I Know It (duh again)
Nutritional Sciences Research
Science-Based Nutrition
Smart Training & Flexible Dieting (page)
Smart Training & Flexible Dieting (group) 
The Cruise Ship

Online Nutrition Coaching

Dr. Spencer's Inner Circle
Dr. Spencer's Online Coaching
JCD Fitness
SeanFlanaganWellness.com - The Habit Project
The Ideal Weight Program

Online Weight Loss/Gain Calculators

The two links below both use the same calculations to predict weight gain or weight loss. They just have different layouts so pick the one you like better. A video on how to use these calculators can be seen here

NIH Body Weight Planner
Precision Nutrition’s Weight Loss Calculator


A Guide to Flexible Dieting - Lyle McDonald
Fat Loss on a Budget - Amy Dix
Girth Control - Alan Aragon
Lose It Right - James Fell
Starve Mode - Leigh Peele
Talking Back to Diet Gurus - Mike Howard
The Diet Fix - Yoni Freedhoff M.D.
The Fat Loss Prescription - Dr. Spencer Nadolsky
The Hungry Brain - Stephan Guyenet
The Lean Muscle Diet - Lou Schuler and Alan Aragon
The Muscle & Strength Pyramid - Eric Helms
Why Do We Gain Fat, and How Do We Lose It? - Dan Pardi and Stephan Guyenet Ph.D.


All of these are available through iTunes in addition to the links provided below.

3D Muscle Journey
An Unbalanced Breakfast
Dietitians Unplugged
Eat, Move and Live Better
Eat To Perform
Evil Sugar Radio
Focus on Nutrition and Nutrition Science by ReachMD
Iraki Nutrition
Lipid Luminations
Nutrition Talks
Physique Science Radio
Rationally Speaking
Real Nutrition Radio
Shredded by Science Radio
Sigma Nutrition Radio
Sound Bites with Melissa Joy Dobbins
Talking Biotech Podcast
The Complete Fitness Professional
The Deliberate Life Podcast
The Dietitian's Dilemma
The Ingles Information Aisle
The Skeptics Guide to the Universe
We Do Science! The Guru Performance Podcast


You can find my playlist of nutrition and health related videos here.

Dr. Spencer Nadolsky
Food Insight
GMO Answers
Healthcare Triage
Jeff Nippard
Jeff Rothschild, MS, RD
Picture Fit
The Checkout


Clean Eating - The Dirty Truth
Does the anti-GMO foods movement go against science? - TechKnow
Frontline: Supplements and Safety
License to Farm
Science Moms
Why Diets Fail

TV Shows

Bullshit! by Penn & Teller
The Checkout


Academy of Nutrition and Dietetics
American Cancer Society
American Diabetes Association
American Heart Association
British Dietetic Association
CDC’s Division of Nutrition, Physical Activity, and Obesity
Celiac Disease Foundation
Cochrane Collaboration
European Food Safety Authority
Food Allergy Network
Institute of Medicine
National Academy of Sciences
National Cancer Institute
National Diabetes Education Program
National Institute of Diabetes & Digestive & Kidney Disease
NIH’s MedlinePlus
NIH’s Office of Dietary Supplements
The International Society of Sports Nutrition
USDA’s Choose My Plate
USDA’s National Agricultural Library
USDA's National Nutrient Database
USDHHS’s Health Finder
Vegetarian Resource Group

Certifications and Credentials

CDE - Certified Diabetes Educator
CEDRD - Certified Eating Disorder Registered Dietitian
CISSN - Certified Sports Nutritionist of the International Society of Sports Nutrition
CSSD - Board Certified Specialist in Sports Dietetics
DTR - Dietetic Technician, Registered
Eat To Perform - Nutrition Certification for Coaches
FISSN - Fellow of the International Society of Sports Nutrition
ISSN-SNS - Sports Nutrition Specialist Certification of the International Society of Sports Nutrition
LD/LDN - Licensed Dietitian or Licensed Dietitian Nutritionist
Mac Nutrition University
MPH - Masters of Public Health (may not always be nutrition focused)
PN L1 and L2 - Precision Nutrition Level 1 or 2
RD/RDN - Registered Dietitian or Registered Dietitian Nutritionist
Shredded by Science Academy
Tufts University Certification Programs
Wellness/CV - Wellness and Cardiovascular Health

Online Nutrition Classes

An Introduction to the U.S. Food System: Perspectives from Public Health - Johns Hopkins University
Child Nutrition and Cooking - Stanford University
Critical Analysis of Popular Diets and Dietary Supplements - Johns Hopkins University
Eating to Win: Activity, Diet and Weight Control - OpenLearn
Food for Thought - McGill
Fundamentals of Human Nutrition - University of Florida
Gut Check: Exploring Your Microbiome - University of Colorado, Boulder
International Nutrition - Johns Hopkins University
Introduction to Food and Health - Stanford University
Nudge-It: Understanding Obesity - The University of Edinburgh
Nutrition and Health Part 1: Macronutrients and Overnutrition - Wageningen University
Nutrition and Health Part 2: Micronutrients and Malnutrition - Wageningen University
Nutrition and Health Part 3: Food Safety - Wageningen University
Nutrition and Medicine - Tufts OpenCourseWare
Nutrition and Physical Activity for Health - University of Pittsburgh
Nutrition for Health Promotion and Disease Prevention - UC San Francisco
Nutrition Made Clear - The Great Courses (paid)
Nutrition, Health, and Lifestyle: Issues and Insights - Vanderbilt University
Nutrition: Healthy Food for Better Living - Wageningen University
Principles of Human Nutrition - Johns Hopkins University
The Meat We Eat - University of Florida
The New Nordic Diet: from Gastronomy to Health - University of Copenhagen
The Psychology, Biology and Politics of Food - Open Yale Courses
The Science and Politics of the GMO
The Science of Gastronomy - The Hong Kong University of Science and Technology


Aegis Shield Mobile (Apple | Android)
Body Weight Simulator (Apple)
Fit Genie App (Apple)
My Fitness Pal (Apple | Android)
Monash University Low FODMAP Diet App (Apple | Android)
My Macros+ (Apple)
My Net Diary (Apple iPhone | Apple iPad | Android)
NSF for Sport (Apple | Android)
Spoon Guru (Apple | Android)
Target Weight for Adults (Apple)
Target Weight for Teens (Apple)
YouAte (Apple)


Alan Aragon’s Research Review
Examine.com Research Digest
Examine.com Supplement Stack Guides
Examine.com Supplement-Goals Reference Guide
Science Driven Nutrition Journal

Myth: Artificial Sweeteners are “Hundreds of Times” Sweeter than Sugar

While reviewing the Whole30’s It Starts With Food, I came across an interesting tidbit I thought deserved its own post. If you have ever read anything about artificial/low-calorie/nonnutritive sweeteners, it’s likely you’ve come across the following statements [1]:

  • Aspartame (Equal) is 200 times sweeter than table sugar
  • Stevia (Truvia) is 200-400 times sweeter than table sugar
  • Sucralose (Splenda) is 600 times sweeter than table sugar
  • Saccharin (Sweet’N Low) is 200-700 times sweeter than table sugar

These statements may lead you to believe that high potency nonnutritive sweeteners (NNS) like the ones listed above are many times sweeter than sugar, causing the reward and pleasure signals in your brain to go haywire. Would you be surprised to hear that in reality sugar actually ranks higher in sweetness than common NNS? 

The myth of the exorbitantly sweet NNS stems from a misunderstanding of how sweetness is measured. When testing for sweetness, both potency and intensity are recorded from trial participants. Dr. Walters, Ph.D. gives a good overview of the testing procedures [2,3].

“Sucrose is the standard to which all other sweeteners are compared. Humans can recognize sweetness in about 1% or 2% sucrose solution. Coffee is typically sweetened to about the level of 5% sucrose [and] soft drinks about 10%. At 15%, sucrose is really sweet and starts to feel a little syrupy. Taste panelists are often trained to quantitate sweetness on a 0-15 sweetness scale…using [a range of] 2-15% sucrose solutions as references. Other sweeteners are then tasted at a series of dilutions to determine the concentration that is as sweet as a given sucrose concentration.  For example, if a 1% solution of sweetener X is as sweet as a 10% sucrose solution, then sweetener X is said to be 10 times as potent as sucrose”.

So when someone says “aspartame is 200 times sweeter than table sugar” what they are really saying is that it is 200 times more potent than table sugar because you can use a lower dose to obtain the same perception of sweetness. It is not an indication that aspartame delivers a higher-intensity stimulus than sugar; merely that it triggers the taste receptors for sweetness on your tongue at a lower dosage.

Intensity, not potency, is what we really want to look at when comparing natural and NNS. Intensity is the true measure of sweetness perception. While early research has provided rankings of sweeteners most have used small sample sizes [3,4]. However, a study published in the International Journal of Obesity tested 3 nutritive sweeteners (sucrose, maple syrup and agave nectar) and 4 NNS (acesulfame-K (AceK), rebaudioside A (RebA), aspartame and sucralose) using a large cohort of 401 participants [5]. Ranked from most to least sweet, the results were as follows:

  1. Maple Syrup
  2. Agave Nectar
  3. Sucrose (table sugar)
  4. Aspartame
  5. Sucralose
  6. RebA
  7. AceK

All 3 nutritive sweeteners beat out the 4 tested NNS. A probable cause for why NNS rank lower than sugar may be due to the suppression of the sweet taste by bitter and metallic compounds that become more prominent as the dosage increases. 

The researchers concluded the following [5]:

“Non-Nutritive Sweeteners (NNS) are not supernormal stimuli. Although NNS have low psychophysical detection thresholds compared with sugars, it is not valid to use thresholds or the dose over threshold to estimate the perceived intensity of these sweeteners…present data do not support the claim that NNS produce deleterious health effects by overstimulating sweet taste receptors to produce hyper-intense sweet sensations.”

So the next time you hear someone claiming that NNS are frying the pleasure centers of your brain, kindly explain to them the myth of the supernormally stimulating nonnutritive sweetener. 

For more info check out the YouTube videos below.

Evil Sugar Radio Interview

I had the pleasure to be interviewed by Antonio Valladares and Scott Kustes on the Evil Sugar Radio podcast. We touched on a bunch of topics, including my critique of the lackluster science behind the Whole30's It Starts With Food, low carb diets and gestational diabetes, and looking at if sugar kills your sex drive

Head on over to their site to listen to the podcast in full. 

Evil Sugar Radio #84: Mike Hull – Abuse of Science & Supplement Scams

Episode 84 Overview
Here’s an overview of what we’ll be talking about in this episode:

1:10 – What made you interested in going in-depth in analyzing the Whole30 program?
2:20 – What is the biggest misconception of what they’re promoting?
4:30 – Do you see the same type of ideas and claims made throughout the industry?
5:10 – What do you think when health gurus make the claim that “you didn’t do it right” when a program doesn’t work for you?
10:00 – You mentioned claims about hormonal contraception and brain cancer. Can you discuss?
11:30 – What is the hierarchy of evidence? How do we know what is high-quality evidence?
14:50 – What about other dietary boogiemen like high-fructose corn syrup and MSG?
17:40 – So how do we explain when people experience positive or negative effects when eating or removing certain foods?
18:50 – What about low-carb and gestational diabetes?
21:10 – You wrote about sugar and sex drive. What’s that about?
26:00 – What about supplement regulation issues and scams in the supplement industry?
31:00 – What are your thoughts on self-experimentation (the “n=1 study”)?
33:15 – What are you up to next?
36:30 – How can the fitness industry better serve clients and provide better information?

Dietary Macronutrient Composition Per Capita

Via ChartsBin

This map shows dietary macronutrient composition per person. The dietary energy consumption per person is the amount of food, in kcal per day, for each individual in the total population.

  • USA: 3770 kcal/person/day (Carb: 49%, Proteins: 12%, Fats: 38%)
  • World: 2780 kcal/person/day (Carb: 63%, Proteins: 11%, Fats: 26%)
  • Developed countries: 3420 kcal/person/day (Carb: 53%, Proteins: 12%, Fats: 34%)
  • Developing World: 2630 kcal/person/day (Carb: 67%, Proteins: 11%, Fats: 23%)
  • Sub-Saharan Africa: 2240 kcal/person/day (Carb: 72%, Proteins: 10%, Fats: 19%)
  • Central Africa: 1820 kcal/person/day (Carb: 75%, Proteins: 11%, Fats: 26%)

Kilocalorie: A unit of measurement of dietary energy. One kcal equals 1,000 calories and one kJ equals 1,000 joules. In the International System of Units (ISU), the universal unit of dietary energy is the joule (J). One kcal = 4.184 kJ.

Pamela Ronald: The Case For Engineering Our Food

This TED talk provides a nice high-level overview of what genetic modification is, how it can benefit humanity and helps to dispel some of the fears surrounding GMO's.

Pamela Ronald studies the genes that make plants more resistant to disease and stress. In an eye-opening talk, she describes her decade-long quest to help create a variety of rice that can survive prolonged flooding. She shows how the genetic improvement of seeds saved the Hawaiian papaya crop in the 1950s — and makes the case that it may simply be the most effective way to enhance food security for our planet’s growing population.

O Gluten! My Gluten!

Media outlets are notoriously awful at interpreting scientific publications. A study done in the UK found that among the top 10 papers there, up to 72% of the dietary advice given in the period surveyed was unsubstantiated or false [1]. So it should not be a surprise that a while back the media bungled yet another publication. 

I wanted to comment on the scope and clinical applicability of the following article, No Effects of Gluten in Patients With Self-Reported Non-Celiac Gluten Sensitivity After Dietary Reduction of Fermentable, Poorly Absorbed, Short-Chain Carbohydrates, since it has made the rounds on the internet and people continue to misinterpret it. 

Since Non-Celiac Gluten Sensitivity (NCGS) does not have a formal clinical diagnosis (yet, it’s being worked on), practitioners have to rely on questionnaires that have patient’s rate things like pain, bloating, stool consistency, nausea, tiredness, and overall symptoms. NCGS is defined as “One or more of a variety of immunological, morphological, or symptomatic manifestations that are precipitated by the ingestion of gluten in individuals in whom Celiac Disease has been excluded” [3].

This study was designed to find out if “in subjects who report having NCGS, [does] gluten induce dose-dependent, reproducible gastrointestinal and systemic symptoms” [2].


The 37 subjects selected all had Irritable Bowel Syndrome (IBS) and had self-reported improvement while on a gluten free diet. All were placed on a low FODMAP and gluten-free diet for two weeks and then randomized into one of three groups:

  1. High gluten
  2. Low gluten + lactose-free whey protein
  3. No gluten + lactose-free whey protein

This study contained two parts. During the first portion of the study, participants remained on the above diets for 1 week, followed by a 2-week washout period before crossing over into the next diet. All participants went through all 3 diets for 1 week. 

In the second part of the trial, 22 of the original patients were on one of the following three diets for 3 days:

  1. High gluten
  2. High lactose-free whey protein
  3. Placebo

Natural and artificial food chemicals or additives that could potentially trigger symptoms were also excluded. After three days on the diet, they went through a 3-day washout period and were then crossed over into another group. 

In addition to assessing symptoms, biomarkers such as serum and fecal markers of intestinal inflammation/injury and immune activation, and indices of fatigue were also measured. 


In the first part of the trail, a dose effect of gluten was not observed and gluten specificity of symptomatic responses was observed in only 3 subjects (8%). A dose effect means that as a dose of something increases, you expect to see the symptoms increase with it. In this case, because a dose-response was not observed, it is highly unlikely that gluten alone is a possible trigger for those with IBS. 

These results were further confirmed in the second half of the trial when 2 patients that had symptomatic responses to gluten in the first trial did not experience those symptoms while taking gluten in the second trial. In fact, gluten specific symptoms were not reproduced in any subject in the second trial. 


Only 1 participant had a positive T-cell response after the high gluten portion of the trial. There were no significant differences in markers of inflammation, immune activation, or fatigue across the treatment periods. “No correlation existed between mean overall symptom score on high-gluten and any of the [bio]markers” [2].


So what can be drawn from this study? As always, nuance is important. The conclusions I would draw would be to advise those with IBS to talk to a doctor or dietitian about going FODMAP’s free, but I would not tell them that they need to go on a gluten-free diet, although they are welcome to try. The evidence to back such a claim is currently lacking. Future research would need to elucidate on whether gluten is working in combination with other wheat components in inducing GI symptoms in those with IBS, although this paper is a great start. It is one of the better designed, well-controlled trials I have seen looking into the issue of NCGS. 

I want to make it clear that this paper does not speak to what gluten will do in an otherwise healthy person nor does it conclude that gluten sensitivity does not exist. It is only looking at the effects of gluten and those with IBS. 

When addressing the topic of gluten it is important to note that the best available research shows that the combined prevalence of wheat allergies, Celiacs Disease/Sub-Clinical Celiac Disease, Non-Celiac Gluten Sensitivity/Wheat Sensitivity, dermatitis herpetiformis (DH), and gluten ataxia affect only 10% of the population at the highest estimations [4,5,6]. Gluten often gets scapegoated for a whole host of illnesses, but it’s important to ensure that there is quality science to back up those claims. And please, do not go gluten-free just because Gwyneth Paltrow told you to

1 - http://www.ncbi.nlm.nih.gov/pubmed/23832153
2 - http://www.ncbi.nlm.nih.gov/pubmed/23648697
3 - http://www.ncbi.nlm.nih.gov/pubmed/22345659
4 - http://www.ncbi.nlm.nih.gov/pubmed/21181303
5 – http://www.ncbi.nlm.nih.gov/pubmed/19122516
6 – http://www.ncbi.nlm.nih.gov/pubmed/17206762

A Tale of Low Carb Diets and Gestational Diabetes

With the rising popularity of low carb/paleo type diets has come a curious unintended consequence: expecting mothers receiving a false positive on their Gestational Diabetes Mellitus (GDM) test. 

The Rise in Popularity of the Paleo Diet

Gestational Diabetes Mellitus (GDM)

GDM is diabetes (“Type 4 Diabetes”) diagnosed in the second or third trimester of pregnancy that is not obviously type 1 or 2 [1]. Women with diabetes in the first trimester would be classified as having type 2 diabetes [1]. The essential contributing factor to GDM is pancreatic insufficiency [2]. Basically, your pancreas is not making enough insulin for your body to overcome the increased insulin resistance due to the placental hormones of pregnancy and increased maternal adipose tissue, which could potentially cause your blood glucose levels to remain high. 

GDM = weak pancreas. Not making enough insulin for you and the baby. 


There are two test for GDM: the one step and two step strategy. 

The One-Step test is the first test for diagnosing GDM. The diagnosis of GDM is made when any of the following plasma glucose values are met or exceeded [3]:

  • Fasting: 92 mg/dL (5.1 mmol/L)
  • 1 hour into the test: 180 mg/dL (10.0 mmol/L)
  • 2 hours into the test: 153 mg/dL (8.5 mmol/L)

If for whatever reason you do not pass the One-Step Oral Glucose Tolerance Test (OGTT), ask for the Two-Step test or ask them to check your HbA1C, as it shows blood sugar levels over time as opposed to the brief snapshot these one and two step tests provide. HbA1C can be measured with a simple blood test. The Two-Step test involves the following [3]:

  • Step 1: Perform a 50-g Glucose Loading Test (GLT) (non-fasting), with plasma glucose measurement at 1 h. If the plasma glucose level measured 1 h after the load is ≥140 mg/dL (7.8 mmol/L), proceed to a 100-g OGTT.
  • Step 2: The 100-g OGTT should be performed when the patient is fasting. The diagnosis of GDM is made if at least two of the following four plasma glucose levels (measured fasting and 1 h, 2 h, 3 h after the OGTT) are met or exceeded:
Carpenter/Coustan NDDG (57)
Fasting 95 mg/dL (5.3 mmol/L) 105 mg/dL (5.8 mmol/L)
1 Hour 180 mg/dL (10.0 mmol/L) 190 mg/dL (10.6 mmol/L)
2 Hours 155 mg/dL (8.6 mmol/L) 165 mg/dL (9.2 mmol/L)
3 Hours 140 mg/dL (7.8 mmol/L) 145 mg/dL (8.0 mmol/L)

Low Carb Diets and OGTT

So if you are on a low carb diet (approximately less than 130g a day) you have probably developed something called peripheral insulin resistance (AKA physiological insulin resistance). During this state, any carbohydrate that you eat is most likely going to be diverted to your brain because the tissues in the rest of your body will not be taking up glucose as readily [4]. 

If you take either the one or two step test while on a low carb diet the results are more than likely to indicate you have gestational diabetes. This is because the muscles and adipose tissues will not be able to absorb the large dose of glucose provided in these tests, thus causing your blood glucose levels to remain high. 

In order to prevent a false positive, 5-7 days before the test starts make sure you are eating plenty of carbs, 250-300+ grams a day. Go ham with those sweet and white potatoes, rice, oats, squash, grains, etc., especially on workout days. If you are already eating sufficient carbs then this shouldn’t be a problem. 

A Final Note

It is not advised that women try to lose weight while pregnant. If you are eating low carb with the intent of losing weight, please speak with your doctor. Below, the folks at Precision Nutrition have put together an infographic on what to eat while pregnant. Click on the picture to jump to their site.


1 - American Diabetes Association. Classification and diagnosis of diabetes. Sec. 2. In Standards of Medical Care in Diabetes—2015. Diabetes Care 2015;38(Suppl. 1):S8–S16


2 - Retnakaran R, Qi Y, Sermer M, Connelly PW, Hanley AJG, Zinman B. β-Cell Function Declines Within the First Year Postpartum in Women With Recent Glucose Intolerance in Pregnancy. Diabetes Care 2010;33(8):1798-1804. doi:10.2337/dc10-0351.


3 - American Diabetes Association. Diagnosis and Classification of Diabetes Mellitus. In Standards of Medical Care in Diabetes—2015. Diabetes Care January 2014 vol. 37 no. Supplement 1 S81-S90.


4 - Rennan de Oliveira Caminhotto, Fabio Bessa Lima. Impaired glucose tolerance in low-carbohydrate diet: maybe only a physiological state. American Journal of Physiology - Endocrinology and Metabolism. Published 15 December 2013. Vol. 305 no. 12, E1521DOI: 10.1152/ajpendo.00580.2013.


GMO’s Cause Cancer, Part II: Much Ado About Monsanto

In my last post, we took a look at the infamous Séralini study, Long-term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize [1]. The study was poorly conducted and ultimately added little to the scientific understanding of the safety of Monsanto’s Roundup-tolerant NK603 genetically modified (GM) maize.

You can read my full analysis of the paper here.

This article will examine the original Monsanto paper that spawned this GMO melodramatic episode [18]. I'll also be using this post to deliver some broader educational points about the safety, science, and regulations behind genetically modified organisms.

From Lab To Market

To get a GM food to market is a long, drawn-out, expensive process. From the initial discovery of a desirable gene or trait to the point where it can be sold on the market takes an average of 13.1 years (but can range from 7 to 24 years) and costs $136 million [2]. The regulatory step in this process is the longest, taking 8 or more years to complete, due to the fact that there are three US agencies that regulate GMO crops: the FDA, USDA, and EPA [2].

The USDA, under The Plant Protection Act of 2000, has the authority to conduct mandatory reviews of GM plants to assess their potential impact on current agriculture and the environment [3,4,6]. Data is collected on the new plant by conducting a series of small field trials. In order to pass regulatory review, the USDA requires “a molecular, biochemical, and cellular characterization of the GE plant, along with data on the life cycle, reproductive characteristics, and any expected or unexpected changes from non-engineered plants of the same species” [7].

The FDA conducts voluntary reviews to assess the safety of GMO consumption for humans and animals. They evaluate the presence of new or increased toxins, allergens, and examine alterations in overall nutritional composition. While this system is still technically voluntary, all currently available GMO’s in the US have undergone this consultation [3,5].

The EPA deals mainly with the health and environmental risks of pesticides. The EPA does not specifically assess the GM food but rather any pesticide, herbicide, insecticide, or fungicide that may be used in tandem, such as the use of Roundup (glyphosate) with Roundup Ready corn [3,8]. 

Internationally, the Organization for Economic Cooperation Development (OECD) sets additional testing standards, including the requirement of a 90-day animal toxicity study [7,9]. It was this type of trial that was performed in the Monsanto paper we’re about to review. 90-day trials are performed by feeding rodents high amounts of the GE crop, typically up to 1/3 of diet, and then comparing them to a control group eating the closest isogenic, non-GM form of that crop. Typically measured toxicology endpoints include “body weight, food consumption, clinical findings, clinical chemistry parameters (hematology, serum chemistry, and urinalysis), macroscopic observations at necropsy, organ weights, and microscopic findings at histopathological examinations” [9]. To date, two independent reviews of animal feeding trials, including long-term and multi-generational trials, have not found any evidence of toxicological harm in animals fed GE crops [10,11]. 

Conflicts Of Interest

While there is not a conflict of interest section in this paper there is little need for one, as it shows right in the title the scientists conducting this study are employed by Monsanto. 

The Monsanto Study

Onto the paper!

This 2004 study looks at the toxicological effects of Roundup Ready corn (NK603) fed to Sprague Dawley rats over 13 weeks. The GM corn in this study has been modified to resist the herbicide Roundup by introducing the CP4 EPSPS gene sequence into the corn’s genome so it will produce CP4 EPSPS enzymes, which have a low affinity for glyphosate [12]. In plants that do not produce these CP4 EPSPS enzymes, glyphosate will inhibit EPSPS activity and prevent the biosynthesis of 5-enolpyruvyl-shikimate-3-phosphate (EPSPS) proteins. This EPSPS inhibition will halt the production of aromatic amino acids essential for the plants growth; primarily phenylalanine, tyrosine, and tryptophan. In essence, the plant will starve to death. 

Additionally, the CP4 EPSPS protein is rapidly digested in mammals, reducing exposure, and has no significant structural similarities to known toxins or allergens [12,17]. However, CP4 EPSPS does share a homology of 7 contiguous amino acids with the dust mite allergen, der p 7 (more on this later) [22]. CP4 EPSPS has also not been shown to be toxic in any other organisms [12]. 

It should be noted that the pathway through which Roundup (glyphosate) acts on Roundup Ready plants is not present in mammals (that’s us), fish, birds, reptiles or insects [12,13]. The absence of this pathway in humans in one of the reasons why glyphosate has a relatively low toxicity (LD50 5,108 mg/kg) [16]. Both table salt (LD50 3,000 mg/kg) and caffeine (LD50 192 mg/kg) are more toxic than glyphosate [14,15,16]. 

But I digress.

400 rats were broken up into 10 groups. Each group had 20 males and 20 females. The animals were divided into groups via stratified randomization so that body weights were not significantly different (P<0.05). The groups comprised of the following:

  1. Control (40) – 11% Non-GMO corn. Genetically similar to GM corn but lacking CP4 EPSPS trait
  2. Control (40) – 33% Non-GMO corn. Genetically similar to GM corn but lacking CP4 EPSPS trait
  3. Roundup Ready Corn (40) – 11% NK603 Corn
  4. Roundup Ready Corn (40) – 33% NK603 Corn
  5. Reference Control A (40) – 33% Non-GMO grown in Ohio
  6. Reference Control B (40) – 33% Non-GMO grown in Iowa
  7. Reference Control C (40) – 33% Non-GMO grown in Indiana
  8. Reference Control D (40) – 33% Non-GMO grown in Ohio
  9. Reference Control E (40) – 33% Non-GMO grown in Colorado
  10. Reference Control F (40) – 33% Non-GMO grown in Colorado

The incorporation of the reference groups was justified as such in the paper:

“The purpose of these reference controls was to approximate the normal range of responses of rats fed different commercial, non-transgenic corn grain since these data were not available.”

Others have criticized this, saying that the reference groups just add noise to the data and the only comparison that matters is the control to GMO group. As we will see in the results section, a direct comparison was made between the control rats and the Roundup Ready (RR) rats in addition to the reference controls. 

All grain samples used were analyzed for nutrient components, pesticide residues, and mycotoxins (mold). The identity of the GMO and Non-GMO corn used in the study was confirmed via polymerase chain reaction (PCR) analysis. In the control and Roundup Ready groups where rats were consuming 11% corn, corn grain was supplied by Purina TestDiet to bring total corn content up to 33% to be comparable to the other diets. 

Clinical observations included:

  • Twice daily monitoring for mortality and moribundity
  • Once daily monitoring for overt signs of toxicity
  • Weekly physical examination
  • Weekly weigh-ins
  • Individual food consumption tracked weekly after baseline food consumption was taken

Blood samples were taken from 10 rats per sex per group. Urine was collected from the same rats used for blood samples. At the end of the 13-week trial, the rats were anesthetized and given a complete pathologic examination. Organs, bones, and tissues were harvested for further testing and analysis. 


In no particular order, here were the findings of the paper. 

Body Weight And Food Consumption – no statistically significant differences

Clinical Pathology Parameters – no statistically significant differences

Hematology – no statistically significant differences

Serum Chemistry – no statistically significant differences

Urine Chemistry – from the paper:

“There were no differences between the control and treated groups that were considered to be test article related (data not shown). Urine phosphorus and potassium were increased slightly in males from the high dose Roundup Ready corn group when compared to the control group, but were within the mean ±2 standard deviations of the population of reference controls. Values for the male control group were lower than the reference control groups and test groups that contributed to the observed statistical differences.”

I'll note here that I think they should have included a table with this data, as they had done for most of the others.

Organ Weights - from the paper:

“The only statistical difference in organ weight was a slight increase in absolute heart weight of high dose test males (1.98 grams) relative to control (1.78 grams) and reference control males (1.87 grams). However, this difference was within the mean ±2 standard deviations of the reference control population…there was no dose response as the 11% Roundup Ready male heart weight was 1.99 grams, similar to weights for 33% Roundup Ready males, and similar to 2 reference control groups (1.92 and 1.94 grams).”

Pathology results – no statistically significant differences


My biggest beef with all these papers is that they do not release their raw data. I find this absurd. Head on over to AllTrials.net to read more about this issue. 

The OECD guidelines do not explicitly call for blinding when performing post-mortem examinations, but it seems like such a simple thing to do in order to eliminate potential bias. Like the Séralini paper, no blinding measures were taken. 

Food intake was recorded but not presented. Only data on what the feed contained the test substance was given. 

No values for the urine chemistry were given. 

Details on the storage conditions of the feed were not provided per EFSA guidelines. 

I've seen some bloggers complain that only 10 rats from each group of 20 were used to collect data for hematology and urine chemistry. The OECD Guidelines at the time only recommended the use of 10 out of the 20 rats per group for biochemical analysis [23]. Séralini and this Monsanto study both used the prescribed 10 rats. 

No isogenic corn was used as the control. Instead “background genetics representative of the test line [was used that lacked] the nk 603 transgene” [18]. I’m not sure how big of an impact this would have had on the results given the variability we saw in the reference controls. 

Speaking of the reference controls, I understand why they included them in the study but I'm not convinced that they needed to be there. Neither the EFSA nor the OECD guidelines call for their use and yet they seem to be pretty standard in GMO 90-day toxicology studies. At least in this paper, no scientific explanation is given for their inclusion. 

Oh, and how in the hell am I supposed to decipher these graphs?!

Additional Feeding Studies

I was able to find three additional animal studies looking at the same NK603 strain of corn. The first study was conducted in 800 broiler chickens where the intervention group was fed 63% NK603 GMO corn for 6 weeks. No clinically significant differences were observed in “weight gain, feed intake, feed efficiency, carcass, and quality measures” [18,19]. The second study looked at 304 grower and finisher pigs, where the intervention diets ranged from 68% to 82% NK603 GMO corn, also found no significant differences in growth performance or carcass characteristics [20]. The second looked at 396 feedlot steer being fed 73-79.5% NK603 corn. Again, no statistically significant differences were found between the control and intervention groups [21]. 

Free Data!

Via the EFSA’s website:

“Given the level of public interest, EFSA will make all data on genetically modified (GM) maize NK603 publicly available on its website today (14 January, 2013). While the Authority has already made available these data upon specific request on several occasions, any member of the public or scientific community will now be able to examine and utilize the full data sets used in this risk assessment.”

You can grab a copy of that data here

. Be warned, it’s a 500 megabyte ZIP file and takes a while to download off of their sluggish servers. Unfortunately, they did not release the data on safety tests with glyphosate. They remain confidential, as it is the “general rule for pesticide data” [24].

A Call For Clearer Guidelines

OECD guidelines need to be updated for animal study models. They were originally designed for use in chemical toxicology tests and are in need of some tweaking to make them better suited for food toxicology tests. The current and future guidelines need to be enforced as well. As they currently stand, application of these rules are not consistent [24]. At the moment, I would give enforcement a B/B+. 

The EFSA is also working on procedures for 1-2 year animal feeding studies [25].

A Side Note on Allergies

Remember 30 paragraphs ago when I mentioned that the CP4 EPSPS protein in NK603 Roundup Ready corn shared a homologous amino acid sequence with the dust mite allergen? Well, I started looking into this issue of GMO’s and increased risk of allergenicity to see if it was a justifiable concern. After writing about 8 pages on the topic, I realized it needed to be its own separate post. Look for that soon. 

Inconsistent Expectations

When you hear people talk about their concerns over GMO safety for human consumption, it usually boils down to something along these lines:

“I’m concerned that GMO’s will introduce some unknown substance/allergen/toxin into the food system.”


“Sure, we can change some of the genes, but we cannot predict the downstream effect it will have on the entire genome.” (AKA the Pleiotropic Effect: where you have multiple effects resulting from a single genetic change).

I believe that those who genuinely hold these reasonable concerns don't understand that GMO is an umbrella term. Your average Joe/Jane probably thinks of a GMO as a plant that has been injected with a gene from another plant or animal. In fact, there are many different methods of genetic modification. Here is a brief overview [26]:

Hybrids/Artificial Selection

– “Traditional” breeding. Crossing two plants in hopes of creating a new plant with favorable attributes. I.E. higher yield, resistance to cold weather, drought tolerance, etc…


– where whole genomes are duplicated or added.

Examples: apples, strawberries, wheat, and bananas.

Mutation Breeding

– Exposing seeds to chemicals or radiation to damage DNA that hopefully yields desirable traits.

Examples: peppermint, grapefruit, pears, apples, rice, and mint. 

Crossing Species Barriers

(Interspecific Hybridization) – crossing two distinct species to create a new one.

Examples: tangelo, plutos, rice, wheat, some apples.


– what is typically thought of as a ‘GMO’. Recombinant DNA (rDNA) molecules are designed to bring genetic sequences to new sources.

Examples: corn, canola, soybeans, cotton, and papaya

So here’s the kicker. When transgenic technology is used to make corn express the CP4 EPSPS protein, an average of 1-3 genes are affected. We know exactly which genes are affected, what they do, and where they sit in the genome. All of the other genetic modification methods change anywhere from 10,000 to 800,000+ genes. 

There are people who rant and rave about the evils of transgenic GMO’s. They want them labeled, out of our food system, or banned completely. And yet they never make a peep about other methods of genetic modification; none of which are tested to nearly the degree of transgenic crops before being released into the food system and none of which are labeled. 

Those that would see GMO’s continue under their current heavily regulated status should be equally vocal about having those same regulations applied to traditional hybridization, polyploids, mutation breeding, and interspecific hybridization. 

Let me be abundantly clear. Transgenic GMO 'breeding' carries no greater health risk than any other breeding method, including traditional breeding. The 8 years and three regulatory agencies that transgenic GMO’s have to go through for approval make them some of the most well studied and arguably safest foods we have available.

In the 20 years that transgenic GMO’s have been available for human consumption there have been no documented cases of harm to health [33,34]. The same cannot be said of traditional breeding methods, which undergo far less scrutiny. 

In 1974, the USDA had to recall a potato bread through "traditional" methods called Lenape. It turns out that the Lenape had particularly high levels of an alkaloid called solanine, a natural defense mechanism of the potato. When ingested it induces “vomiting, diarrhea, loss of consciousness, and convulsive twitching” [27,28].

Celery is another example. Using conventional breeding methods, breeders tried to increase insect-resistance by creating a strain that produced higher amounts of psoralens. Grocers and harvesters that came into regular contact with the vegetable experienced cases of dermatitis and severe skin rashes [29,30,31].

I know this has been a grinder of a blog post, so I'll wrap this up with an apropos

 quote from the FDA:

“Virtually all breeding techniques have potential to create unexpected, including pleiotropic, effects. For example:
  • Mutations unrelated to the desired modification may be induced
  • Undesirable traits may be introduced along with the desired traits
  • Newly introduced DNA may physically insert into a transcriptionally active site on the chromosome, and may thereby inactivate a host gene or alter control of its expression
  • The introduced gene product or a metabolic product affected by the genetic change may interact with other cellular products to produce a deleterious effect
Plant breeders, [plant geneticists, and bioengineers] using well established-practices have successfully identified and eliminated plants [and genes] that exhibit unexpected, adverse traits prior to commercial use” [32] [my additions].

GMO’s Cause Cancer, Part I: The Curious Case of Séralini’s Rats


1 - http://www.sciencedirect.com/science/article/pii/S0278691512005637

2 - https://croplife.org/wp-content/uploads/2014/04/Getting-a-Biotech-Crop-to-Market-Phillips-McDougall-Study.pdf

3 - http://www.ncbi.nlm.nih.gov/pubmed/17956539

4 - http://www.aphis.usda.gov/wps/portal/aphis/ourfocus/biotechnology

5 - http://www.fda.gov/Food/GuidanceRegulation/GuidanceDocumentsRegulatoryInformation/Biotechnology/ucm096126.htm

6 - http://www.aphis.usda.gov/brs/pdf/PlantProtAct2000.pdf

7 - http://anrcatalog.ucdavis.edu/pdf/8179.pdf

8 - http://www.epa.gov/scipoly/biotech/pubs/framework.htm

9 - http://www.ncbi.nlm.nih.gov/pubmed/24579994

10 - http://www.sciencedirect.com/science/article/pii/S0278691511006399

11 - http://link.springer.com/article/10.1007%2Fs00003-012-0777-9

12 - http://www.ncbi.nlm.nih.gov/pubmed/22541883

13 - http://www.ncbi.nlm.nih.gov/pubmed/11248008

14 - http://www.sciencelab.com/msds.php?msdsId=9924972

15 - http://www.sciencelab.com/msds.php?msdsId=9927475

16 - http://www.cdms.net/LDat/mp07A005.pdf

17 - http://www.ncbi.nlm.nih.gov/pubmed/8598558

18 - http://www.ncbi.nlm.nih.gov/pubmed/15110110

19 - http://www.ncbi.nlm.nih.gov/pubmed/12705406

20 - http://www.ncbi.nlm.nih.gov/pubmed/14974557

21 - http://www.ncbi.nlm.nih.gov/pubmed/14552389

22 - http://link.springer.com/article/10.1186%2F1472-6807-2-8/fulltext.html

23 - http://www.oecd.org/chemicalsafety/testing/oecdguidelinesforthetestingofchemicals.htm

24 - http://www.enveurope.com/content/25/1/33

25 - http://www.efsa.europa.eu/en/efsajournal/pub/3347.htm

26 - http://kfolta.blogspot.com/2012/06/more-frankenfood-paradox.html

27 - http://grist.org/list/potato-bred-to-make-perfect-potato-chips-will-kiiiiiill-you/

28 - http://link.springer.com/article/10.1007%2FBF02863068?LI=true#page-1

29 - http://www.cdc.gov/mmwr/preview/mmwrhtml/00000464.htm

30 - Ames BN, Gold LS. 1999. Pollution, pesticides and cancer misconceptions. Pp. 18-39 in Fearing Food, J. Morris and R. Bate, eds. Oxford, UK: Butterworth Heinemann

31 - http://www.ncbi.nlm.nih.gov/pubmed/2404325

32 - http://www.fda.gov/Food/GuidanceRegulation/GuidanceDocumentsRegulatoryInformation/Biotechnology/ucm096095.htm

33 - http://www.nap.edu/openbook.php?record_id=10977&page=8

34 - http://www.who.int/foodsafety/publications/biotech/biotech_en.pdf

GMO’s Cause Cancer, Part I: The Curious Case of Séralini’s Rats

Gilles-Éric Séralini had some rats. He fed them some GMO corn and some Roundup herbicide and they got cancer and died. Therefore, GMO’s cause cancer.

I think you'll find it’s a bit more complicated than that.

What follows is an attempt to thoroughly dissect the Séralini paper and subsequent republication. This will be a gloriously meticulous exercise in demonstrating how bad science can muddy the public’s scientific understanding.


Séralini is a professor of molecular biology at the University of Caen, France, and president of the scientific board of CRIIGEN (Committee of Independent Research and Information on Genetic Engineering). He published a study in 2012 in the journal of Food and Chemical Toxicology (FCT) that was supposed to be a replication of a 2004 study conducted by Monsanto looking into the safety of Monsanto’s Roundup Ready resistant corn (NK603 R-tolerant maize) [1,2]. Séralini’s study has since been retracted by FCT and republished in another journal but before we dive into the meat of the paper let’s take a brief look at Séralini’s history and potential conflicts of interest.

In 2006, Monsanto published a study looking at the safety of YieldGard Rootworm Corn (MON 863) which designed to protect against feeding damage caused by corn rootworm larvae [3]. The findings showed that MON 863 was as “safe and nutritious as existing conventional corn varieties” [3]. After being compelled by appellate court action in Germany, Monsanto released the raw data of its study, which was reanalyzed by Séralini [4]. This reanalysis showed that MON 863 allegedly caused kidney and liver damage in rats. This reanalysis was roundly criticized for its poor statistical methods in a 2007 paper published by a panel of experts. This paper found the following [5]:

“In each case, statistical findings reported by both Monsanto and Séralini et al. were considered to be unrelated to treatment or of no biological or clinical importance because they failed to demonstrate a dose–response relationship, reproducibility over time, association with other relevant changes (e.g., histopathology), occurrence in both sexes, difference outside the normal range of variation, or biological plausibility with respect to cause-and-effect. The Séralini et al. reanalysis does not advance any new scientific data to indicate that MON 863 caused adverse effects in the 90-day rat study.”

In 2009, Séralini attempted the same tactic and published a paper that reanalyzed the toxicity data for three Monsanto strains of genetically modified (GM) maize: NK603, MON 810, and MON 863. NK603 is tolerant of the herbicide Roundup and MON810 and MON863 synthesize Bacillus thuringiensis (Bt) toxins which are insecticides [6]. Séralini's re-analysis also found that these strains caused damage to the liver, kidney, heart, adrenal glands, spleen, and haematopoietic system. Once again, these findings were disputed by the European Food Safety Authority (EFSA) and Food Standards Australia New Zealand [7,8].

Conflicts Of Interest

Since then, Séralini has moved on from re-analyzing papers and decided to conduct a study himself. In 2012, he published the study “Long term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize” [1]. Curiously, he did not list any conflicts of interest even though there were plenty he could have mentioned. For one, the Foundation for Human Progress (FHP) gave €1 million euros to help fund this €3.2 million euro study. FHP is very active in funding anti-GMO groups [9]. He also published a book and documentary right after the study was released, both entitled ‘Tous cobayes?’, which translates into ‘We Are All Guinea Pigs!’ [10,11]. He also has a few other books, such as ‘Genetically Incorrect’ and ‘We Can Clean Up’, both of which talk about how genetic manipulation is dangerous [21].

Séralini is also a consultant with a small company called Sevene Pharma, a homeopathic pharma company. He conducted research on one of their medications and was able to ‘prove’ that it can protect against pollutants, including Roundup [12,13]. These trials were conducted in vitro on human liver cells. No trials were ever conducted in humans but that did not stop Sevene Pharma from selling their Digeodren line of pills, claiming they can protect “against cell death caused by the Roundup” based off of the research Séralini provided [14]. 

The idea that this homeopathic remedy, let alone any homeopathic remedy could work is absurd. Homeopathic pills take active ingredients and dilute them to the point where there is no trace of the original substance left. Hundreds of randomized clinical trials have found over and over that they do not work [40,41,42,43,44,45,46].

Oh, and remember CRIIGEN? The organization where Séralini is the president of the scientific board? It’s an anti-GMO lobbying group that helped fund his study [22].

The Embargo System

Then there is the problem of Séralini abusing the embargo system. Usually, one week before a paper is released, journalists get a sneak peek at the paper. During this week they can fact check the paper by talking it over with their peers and seeking out expert opinion on the research. This is an important and useful process to help control media hysteria that often occurs after a paper is released. Journalist’s conduct these activities under the agreement that they will not publish anything until after the journal says they can; typically after the paper is published.

This was not the case for the Séralini paper. Journalists that wanted access early access to the paper had to sign a non-disclosure agreement stating that they were prohibited from sharing the results with any outside experts before the embargo was lifted [15]. So any journalist that saw the paper early could not seek out expert opinion on the study. Journalists were left to their own devices to fact check the paper. The result was that the first round of news on this paper was largely unskeptical and did not address any scientific concerns [17]. Anyone who broke the non-disclosure agreement was threatened with a harsh fine: “A refund of the cost of the study of several million euros would be considered damages if the premature disclosure questioned the release of the study” [11].

When the abuse of the embargo system was discovered, the “French National Centre for Scientific Research (CNRS)…decried the public-relations offensive as inappropriate for a high-quality and objective scientific debate, and reminded researchers working on controversial topics of the need to report results responsibly to the public” [11].

All that and we haven't even reached the paper yet!

The Study

Let’s do a rundown of the paper. In the introduction, the following claims are made [1]:

  • There is international debate as to the necessary length of mammalian toxicity studies in relation to the consumption of genetically modified (GM) plants including regular metabolic analyses
  • Significant disturbances have been found [in regard to GMO subchronic toxicity] and may be interpreted differently
  • Detailed analyses have revealed alterations in kidney and liver functions that may be the signs of early chronic diet intoxication, possibly explained at least in part by pesticide residues in the GM feed

For each of these claims, the only citations he provides are back to his own published papers. He does not cite any other sources or include the fact that his previously published papers were heavily criticized for methodological and statistical issues. But I digress.

The rats were either fed the Roundup-tolerant maize (GMO), maize treated with Roundup (GMO+R), water mixed with Roundup (R), or a control non-GMO maize (non-GMO). The maize was then mixed in with the standard rat chow at three different levels. The result was 10 different groups, 10 males and 10 females in each, which were broken down as follows:

  1. Controls (20) – Non-GMO corn
  2. 11% GMO (20) – 11% GMO corn + rat chow
  3. 22% GMO (20) – 22% GMO corn + rat chow
  4. 33% GMO (20) – 33% GMO corn + rat chow
  5. 11% GMO + R (20) – 11% GMO corn treated with Roundup + rat chow
  6. 22% GMO + R (20) – 22% GMO corn treated with Roundup + rat chow
  7. 33% GMO + R (20) – 33% GMO corn treated with Roundup + rat chow
  8. R(A) (20) – 0.00000005g/L or 0.000000011% Roundup in water
  9. R(B) (20) – 0.4g/L or 0.09% Roundup in water
  10. R(C) (20) – 2.25g/L or 0.5% Roundup in water

Blood samples were taken at 1, 2, 3, 6, 9, 12, 15, 18, 21 and 24 months: 11 measurements were obtained for each animal alive at 2-years. Over 56 parameters were measured from various blood, urine, and liver samples. 34 tissue and organ samples were taken after the rats died for further analysis. The following methods were used for statistical analysis: Principal component analysis (PCA), partial least-squares to latent structures (PLS), and orthogonal PLS (OPLS) [1].

The next part is very important and is an excellent example of why it is crucial that researchers release their raw data. In the results section, Séralini states that not “all data [can] be shown in one report, and [only] the most relevant are described here” [1]. Now this is certainly true, that is can be difficult to show all of your finding in a paper, but it also leaves a window open for cherry picking data that is in line with your beliefs. This is why it’s imperative that raw data be released, so methods can and findings can be independently verified.  

The paper goes on to detail many of the findings. You can read them all in the original paper, which is free online, but the gist of the findings show that the control rats fared the best and the intervention groups had a greater incidence of mortality, tumors, liver and kidney problems to name a few.

Methodological Issues

Below I've broken down the relevant areas and discussed the issues in each.


What exactly was he trying to measure? He was testing three different hypothesis in his trial:

  1. Gm corn
  2. Gm corn + Roundup
  3. Roundup

Reference data was not provided, such as the levels of Roundup normally found in maize (GM or non-GM), the levels of Roundup metabolites found in products made from the maize, “the stability of Roundup after food processing, and the circulating or tissue levels of Roundup or any surrogate metabolites…[this data] is critical for any study based on adsorption, distribution, metabolism and excretion (ADME)” [18].


The gap between the high doses (2.25g/L or 0.5% Roundup in water) and the low dose (0.00000005g/L or 0.000000011% Roundup in water) is too large to be able to determine a dose-response relationship [30,31].

Roundup is highly unlikely to be found in the drinking water supply. In France, they conducted 43,741 tests that screened for glyphosate in 21,864 stations. Only 95 tests (0.2%) detected glyphosate and at levels below 5ng/L (0.000000005 g/L). The French study noted that it only tested for glyphosate and not the other chemicals in Roundup because the “co-formulants [are] not mobile in the soil”. The French findings concluded that “The likelihood of finding the tested quantities in groundwater appears negligible. Therefore, the route of administration described in the study protocol (oral exposure) is not the most appropriate for assessing the risks related to the product's application” [30,31]. 

These findings show that all three doses used by Séralini are unlikely to be found in drinking water and have no real world applicability [30,31].

To further compound things, water consumption was recorded but not reported. We have no way of knowing how much of the water these rats actually ingested over the study.


Food consumption was recorded, but not reported.

Non-GMO corn was never verified that it was non-GMO through lab tests.

No analysis was done to see if any of the non-Roundup treated food was cross contaminated.

Rat Strain and Number of Rats

Here is where one of the biggest methodological issues of this study manifests. Séralini had 200 rats in total. 20 were included in the control group and 180 were in the various intervention groups. That gives you an intervention to control ratio of 1:9. That is far too few control rats to leverage any statistical power. There was no power analysis reported to justify the number of mice chosen in the study.

The other big issue was the duration the study ran with the Sprague Dawley (SD) strain of mice; a strain that is susceptible to cancer. SD rats are typically used in short-term experiments of 90-days to ascertain tumorigenicity or toxicity. If tumors form before 90-days, whatever is being tested is considered to be tumorigenic.

The Séralini study ran for two years. This is an issue because SD rats have been shown to spontaneously grow tumors when left to live out their lives in undisturbed conditions [33-37]. This makes the SD strain inappropriate for long-term studies of this nature, as it is difficult to determine if the tumors were caused by the intervention or by chance. Cancers also affect many types of metabolism in the body, which will add noise to the toxicity test data collected. This is why SD rats are only used for 90-day toxicity studies.

The Results of two, 2-year long studies where the rats lived undisturbed

The high tumor incidence of these rats is further compounded by the low number of rats chosen for a study of 2 years. 20 per group is only justified in a short 90-day test as it provides enough statistical test power to detect differences between groups. Because the study lasted for two years, the sample size was too small [30,31].

The Organization for Economic Co-operation and Development (OECD) recommends “20 rats per group for a 12-month chronic toxicity study (Test Guideline 452 (OECD, 2009b)) and 50 rats per group for a 24-month carcinogenicity study (Test Guideline 451 (OECD, 2009a)) or a combined chronic toxicity/carcinogenicity study (Test Guideline 453 (OECD, 2009c)). With 10 rats per group, this study falls short of the recommended number considered necessary to infer statistically significant effects of long-term treatment for the two types of analysis undertaken (chronic toxicity, carcinogenesis)” [11,30,31].

Furthermore, SD rats show “high mortality rates and high incidence rates for mammary tumors in control groups, which were the main abnormalities observed by Séralini et al. (2012). These phenotypic characteristics should have been taken into account when calculating the required number of animals” [30,31].

An article in Nature notes that “data provided…by Harlan Laboratories, which supplied the rats in the study, show that only one-third of males, and less than one-half of females, live to 104 weeks. By comparison, its Han Wistar rats have greater than 70% survival at 104 weeks, and fewer tumors” [11].

Survival Analysis – Lifespan

The following are observations made in the EFSA’s Final review of the Séralini et al. publication [30,31].

"Séralini explains that “Control male animals survived on average 624 ± 21 days, whilst females lived for 701 ± 20”. These values are the result of an incorrect calculation because the data is censored (we do not know when the animals still alive at the end of the study would have died naturally since they were euthanized). Instead, what has been calculated is the empirical mean and standard deviation of the uncensored observed values joined with the censored values for still-alive rats (as if a rat still alive at T=720 days is considered dead at T=720 days). The results given are therefore inexact because this procedure introduces a bias by underestimating the average date of death and clearly also the standard error of the estimator. To have chosen not to consider everything that occurs after 624-21=603 days is therefore not justified because this value comes from an incorrect calculation" [30,31].

"Correct calculation of the survival distribution for different groups requires the introduction of a parametric model, but the use of such an approach is constrained, given the limited amount of data per group. For example, if we fit a Gaussian model for the survival time of the males, the 24 estimated mean and standard deviation are respectively 626 and 68 days. For the females, it is 892 and 206 days. It is not correct to proceed as the authors have done and calculate the standard error for the mean merely by dividing the standard deviation by √10, as would be done for uncensored Gaussian variables. Due to censoring, the distribution of the estimator of the mean is much more spread out and asymmetric, meaning that the use of the standard error for calculating confidence intervals is not meaningful" [30,31].

No confidence intervals or p values are reported for mortality data and it appears the mortality data was not statistically analyzed. When analyzed, “there is no evidence that mortality to the end of the experiment was significantly different in the groups of rats fed either the GMO, GMO + R, or when R was administered in the drinking water at three different levels. The claim by the authors that ‘‘In females, all treated groups died 2–3 times more than controls, and more rapidly’’ is not true” [20].

Table A1 shows the mortality to the end of the experiment in each group [20].

Results of Log-Rank tests on reduced life expectancies with and without correction for multiple testing [30,31].

Naturally occurring mortality rates were also not taken into consideration. Below is a table of studies showing natural mortality rates.


The study was neither single nor double-blinded.

Mechanisms and Other Issues

Effects of feeding Roundup Ready maize to the SD rats and the effects of feeding them Roundup were identical; a highly suspicious result for two completely separate substances. No plausible mechanism for this was provided.

Growth data was not provided.

Organ weight was not provided.

No dose-response curve was observed. You would expect to see things like mortality increase as the rats ate higher concentrations of roundup or GM corn but no such curve happened.

Statistical Issues

No statistical tests on treatment differences for mortality and pathology incidence [18].

No estimation of dose/sex/ROUNDUP GMO effects or calculation of confidence intervals for these effects [18].

No adjustment for survival [18].

No analysis of cumulative tumor risks relative to survival duration [18].

No analysis of time to tumor formation [18].

No discussion or presentation of test facility historical control tumor incidence data [18].

Kaplan–Meier statistics (or similar methodologies) are absolutely required to analyze tumor prevalence and survival across time and populations. The use of mean centering and unit-variance could also artificially reduce the level of background variability, therefore, causing the significance of the observed variation to be exaggerated [18].

The results on mortality and tumor incidence are presented descriptively and are not statistically analyzed, no p-value was given [30,31].

54 comparisons were made in the study but only five were significant (P < 0.05) before False Data Rate (FDR) correction. The following were significant before the correction:

  • Hepatic pathologies‟ described by the author as liver congestions, macroscopic spots and microscopic necrotic foci [30,31]
    • for the males in the group fed 22% GMO,
    • for the males in the RB group.
    • Mammary tumors
      • for the females in the RB group.
      • Pathological signs in the mammary glands (other than tumors described by the authors as galactoceles and mammary hyperplasias) [30,31]
        • for the females in the RA group,
        • for the females in the RB group.

After FDR correction for multiple testing, there are no significant differences at the 5% level [30,31].

OPLS-DA analysis was used to discriminate between the control group and experimental groups. The application of this method is a bit peculiar. As noted in the EFSA report [30,31]:

  • Whatever the method used, it is important to validate the model obtained (i.e. ensure that it possesses good predictive properties) by:
    • an independent test set, which helps to ensure that the model fitted to the training set retains good predictive properties for new data not previously used to fit the model;
    • cross-validation methods, where different subsets of the data are used alternately as training set and test set.
    • The study’s authors have not validated the models obtained, which cannot, therefore, be used for predictive purposes.
    • Use of this method assumes a symmetric distribution of predictor variables. Biochemical parameters may have an asymmetric distribution; pre-transformation is therefore necessary. There is nothing to suggest that this was done.
    • Calculating confidence intervals for each parameter is not relevant when many parameters are used, since potential correlations between parameters are totally ignored.

For a more detailed statistical analysis with programming notes, please read these two blog entries: 

Why I Think The Séralini GM Feeding Trial Is Bogus

Séralini Rat Study Revisited

Conclusions on the Study Results

During the EFSA hearing, the study’s authors “admitted that this study was not conclusive by itself and that, though subject to improvement, it had the merit of opening up an interesting line of research…The team’s members firmly believe that, having used all techniques available, what they observed was not random. The study could certainly be improved but the team simply opened up a path and we must now collectively do better…These experiments need to be repeated since this was the first time that tests were undertaken with a pesticide as a whole at a low dose (Extracted verbatim from the report of the hearing with the study’s authors)” [30,31].

Other Long Term Studies

Séralini claimed that long-term experiments had never been conducted outside of his study [18]. This is not true. Two such studies (Malatesta et al. 2008; Sakamoto et al. 2008) have been conducted using a more appropriate rat strain (F344 for Sakamoto) and a larger number of rats. Neither found evidence of GMO related effects. However, these two studies cannot be fully compared to Séralini’s study. Both were conducted with glyphosate-tolerant soybeans but this tolerance was obtained through the synthesis of a CP4 EPSPS protein, just like the NK603 maize Séralini and Monsanto tested [30,31]. It should be noted that in  Malatesta et al. the study was conducted on a limited number of rats and only on female mice [30,31].

Séralini is correct that there should be more publications looking at the long-term toxicological effect of herbicides/pesticides and GMO’s. The EFSA is currently updating their guidelines to ensure that this can happen [30,31,32].

Raw Data Release/Selection of Data Reported

Here are some issues that could be cleared up if Séralini would release his raw data to the public, as noted in the EFSA report:

"Data required to interpret the toxicity study, such as data on composition and contaminants in diets, dietary intakes and weight gain of animals, are not reported in the paper. Consumption data and the energy balance of the various diets are all the more important as tumor incidence can vary according to dietary intake (Keenan et al., 1997)" [30,31].
"Without any justification, the authors have chosen to report the results of the four biochemical parameters and two hormonal parameters that they consider to exhibit 9 the greatest variation from the control group (Fig. 5B). This choice was made after the results were obtained. It is obviously to be expected that there will be differences between the 864 (18 experimental groups x 48 biochemical parameters = 864) comparisons made by the authors for the 48 biochemical parameters in the 15th month of the study" [30,31].

When his paper was republished, he bizarrely opted to only release part of his data.

His team took blood samples at 1, 2, 3, 6, 9, 12, 15, 18, 21, and 24 months but only released the data for month 15.

“They released the tumor and mortality data for each group of rats, but not for the individual rats — which makes it impossible to test for in-group variation” [16]

When asked by the EFSA to release his raw data, Séralini said he would not release his data until “the EFSA makes public all the data underpinning its 2003 approval of NK603 maize for human consumption and animal feed” [11]. This move is somewhat ironic considering he took Monsanto to court to have their raw data released and won. His argument basically boils down to “I will if they will”, as if his ability to practice good science is somehow dependent on the actions of others.

Other Concerns


I do not know if the graphs he used in his paper are standard, but they certainly were confusing as hell

Males that drank the most Roundup had decreased mortality compared to those that drank untainted water or water with less Roundup in it.

Male Rats That Drank Roundup. Y-axis is mortality (# rats/group)

0, A, B, C = dotted, thin, medium, and bold lines, respectively. Lifespan during the experiment for the control group is represented by the vertical bar ± SEM (grey area). In bar histograms, the causes of mortality before the grey area are detailed in comparison to the controls (0). In black are represented the necessary euthanasia because of suffering in accordance with ethical rules (tumors over 25% body weight, more than 25% weight loss, hemorrhagic bleeding, etc.); and in hatched areas, spontaneous mortality.

Males that ate the highest concentration of GM corn died less.

0, 11, 22, 33 = dotted, thin, medium, and bold lines, respectively

Is any of this statistically significant? Probably not, but note that Séralini drew conclusions from this untested data the same way I just did.

Pictures of Rats

It was very odd that he included pictures of the tumor-ridden rats in his paper. The pictures were sensationalist and did not add any scientific understanding. He only included pictures of the intervention rats and not the control rats, even though both groups had tumors.

The most curious part of including these pictures is that at the very beginning of his paper he stated this: “All data cannot be shown in one report, and the most relevant are described here” [1]. 

If space was so limited why not leave out the pictures? By excluding them, he gains ½ a page more to discuss findings.

European Hearing

During the EFSA hearing, Séralini acknowledged that the study design was not suitable to assess long-term carcinogenicity (cancer incidence) and his paper was only designed to measure long-term toxicity [30,31]. I get that the words tumor and cancer are not synonymous, but the paper repeatedly referred to tumors and spent a lot of time discussing them. A report in Nature notes that Séralini, “…has promoted the cancer results as the study’s major finding, through a tightly orchestrated media offensive that began last month and included the release of a book and a film about the work” [11]. If this was truly a toxicity study it makes the pictures of the rats with tumors all the more irrelevant.

From the EFSA hearing:

“Séralini et al. (2012b) do not address any of the open issues for the statistical methods as raised in EFSA’s first Statement (EFSA 2012). They state that statistical methods for the analysis of tumors endpoints cannot allow to conclude on a mortality linked or not to the treatment groups. EFSA notes that this is inconsistent with the conclusions with respect to the tumors and mortality as drawn by Séralini et al. (2012a). [30,31]”
“Séralini et al. (2012b) mentioned that a scientific publication is limited with respect to space and can therefore only show the data necessary to understand and discuss the conclusions, and refer to future publications that will provide more data. It is unclear how the authors have selected the endpoints for reporting and why, for reported endpoints, the complete analysis was not provided (e.g. biochemical data were reported only for selected treatment groups, and only at one time point”) [30,31]. At this time no further papers discussing the data have been released by Séralini.

Answers To Critics

Before and after his paper was retracted, Séralini published letters defending his paper. Below is the summary arguments of those two papers and the counter-arguments I provide. I have extracted the arguments where he tries to defend his paper. Other arguments were made that do not pertain to the papers quality and are not included below but can be read in full at these two citations > [26,27]. I have also included arguments from the website http://www.gmoSéralini.org/ [29]. Many arguments we have already covered earlier in the paper but I will summarize them here.

Argument 1 – Selection Of Rats

Sprague Dawley rats are used routinely in such studies for toxicological and tumor-inducing effects, including those 90-day studies by Monsanto as a basis for the approval of NK603 maize and other GM crops.

Other studies have used Sprague Dawley rats in 36-month studies by (Voss et al., 2005) or in 24-month studies by (Hack et al., 1995), (Minardi et al., 2002), (Klimisch et al., 1997), (Gamez et al., 2007)

Counter-Argument 1

Yes, these studies use the Sprague Dawley line of rats but for the appropriate 90-day interval as set out by The Organization for Economic Co-operation and Development (OECD) guidelines [28]. The 90-day interval is advised because this strain of rats are susceptible to spontaneously generating tumors under normal conditions [33-37].

Just because other studies used these rats for longer periods than advised does not make the Séralini study good, it makes all of these studies equally bad.

Argument 2 – Number Of Rats

OECD guidelines (408 for 90-day study, 452 chronic toxicity and 453 combined carcinogenicity/chronic toxicity study) always asked for 20 animals per group although the measurement of biochemical parameters can be performed on 10 rats. Monsanto itself measured only 10 rats of the same strain per group on 20 to conclude that the same GM maize was safe after 3 months (Hammond et al., 2004).

Counter-Argument 2

Again, the OECD guidelines are meant for rat studies lasting 90-days, not two years. The OECD guideline state that in a carcinogenesis study there should be 50 rats per group [28]. The authors claim that they “did not perform a carcinogenesis study…but a long-term chronic full study”. Even if that is true they would still need a larger number of rats to compensate for potential rat die off during the study. They would also receive larger statistical power from the larger sample. The second issue is that they did not exactly follow the OECD guidelines anyway, as they had 20 control rats and 180 intervention rats. As for measuring only 10 rats from each group, this is in line with the OECD guidelines but I believe the selection of 10 rats has to be randomized and preferably blinded. There was no mention of this in the paper.

Argument 3 – Number Of Control Rats

Séralini’s control groups were the same size as each treatment dose group, in line with standard scientific practice.

Counter-Argument 3

Yes, each group was the same size (20 each), but there were 180 rats in 9 intervention groups and only 1 group of 20 acted as a control.

Argument 4 – No Food Intake Data Is Presented, So We Don’t Know The Dose Of Toxins Ingested

Séralini measured food intake more often than industry studies on GM foods (2x a week) and the absence of data in his published paper does not invalidate the findings observed. This was a more frequent and detailed measurement than industry tests which measured only food intake, and only on a weekly basis. Monsanto’s 90-day study on NK603 maize also does not present individual food intake data but only the mean amount consumed for each group.

Counter-Argument 4

If he took the food measurements why not release that data? And while Monsanto recorded food consumption once a week rather than twice a week that is not going to change the amount of food consumed. Neither study provided individual food intake in their papers, although Monsanto’s raw data including food intake has since been released via court order. Monsanto’s paper did provide mean amount consumed per group which is more than Séralinis paper, which reported nothing. To date, Séralini has still not released his full data including food and water consumption.

Argument 5 – No Mechanism For The Effects Observed Has Been Established

There is no requirement in any regulatory system to establish a mechanism of action for a toxin before regulatory action can be taken and there is no burden of proof on scientists who find toxic effects to establish a mechanism before they report their findings. This is fortunate because it can take decades to establish a mechanism, and sometimes a mechanism is never found.

Counter-Argument 5

Even if the mechanism of action is not established, it is highly improbable that two completely different treatments, rats fed GMO corn and rats fed Roundup, would experience the exact same outcomes.


In January 2014, the editor of

Food and Chemical Toxicology

A. Wallace Hays sent Séralini a letter asking him to voluntarily retract his study [24]. Séralini refused, so the editor retracted the paper [25].

Should the paper have been retracted?

The Committee on Publication Ethics (COPE) states that the below are the only reason a paper should be retracted:

  • Clear evidence that the findings are unreliable due to misconduct (e.g. data fabrication) or honest error.
  • Plagiarism or redundant publication.
  • Unethical research.

I think you could make the strongest argument for number 1; the data presented is completely unreliable and could be classified under an ‘honest error’, although I'm not so sure the misrepresentation of the data was that honest.

The paper was officially retracted because it was ‘inconclusive’. That is not a good enough reason. Lots of inconclusive papers contribute to the scientific literature. On the other hand, leaving this paper unretracted would have given it credibility. 

The publication of this paper stands as a shining example of the limitations of the peer-review process or perhaps a lapse in editorial judgment from the Journal of Food and Chemical Toxicology.

There are some that argue that the paper should not have been retracted. An article at the Environmental Health Perspectives notes the following:

“Equally troublesome is that this retraction does not really impact how the science will be viewed by scientists, but only how it is viewed by others outside of the scientific community. We feel the decision to retract a published scientific work by an editor, against the desires of the authors, because it is “inconclusive” based on a post hoc analysis represents a dangerous erosion of the underpinnings of the peer-review process, and Elsevier should carefully reconsider this decision” [19].


The paper was re-published June 24, 2014, in the Environmental Sciences Europe journal (ESEU), an open-access journal in which you pay to have your study published [38]. It has been reported that the paper underwent a second peer-review process for this journal. This is not true. Henner Hollert, the editor of ESEU, stated that the “role of the three reviewers hired by ESEU was to check that there had been no change in the scientific content of the paper” [23]. He went onto state that because Food and Chemical Toxicology had already conducted a scientific peer-review, he did not feel the need to conduct a second [23].


1 - There should be more long-term feeding trials to thoroughly evaluate the safety of pesticides and herbicides. The EFSA is currently working on this [32].

2 - Anybody doing research into these areas should be required to release the raw data along with the study. This should not just apply to the areas of food and chemical safety but to all scientific disciplines. More about this issue can be read over at www.alltrials.net

3 - Don't get your science news from gossip magazines. Or The Food Babe.

“Most people are not natural-born statisticians. Left to our own devices, we are not very good at picking out patterns from a sea of noisy data. To put it another way, we are all too good at picking out non-existent patterns that happen to suit our purposes” [39].

GMO’s Cause Cancer, Part II: Much Ado About Monsanto


1 – http://www.sciencedirect.com/science/article/pii/S0278691512005637

2 – http://www.ncbi.nlm.nih.gov/pubmed/15110110

3 – http://www.ncbi.nlm.nih.gov/pubmed/16084637

4 – http://www.ncbi.nlm.nih.gov/pubmed/17356802

5 – http://www.ncbi.nlm.nih.gov/pubmed/17900781

6 – http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2793308/

7 – http://www.efsa.europa.eu/en/events/event/gmo100127-m.pdf

8 – http://www.foodstandards.gov.au/consumer/gmfood/mon863/pages/default.aspx

9 – http://alerte-environnement.fr/2012/11/12/etude-anti-ogm-de-saralini-les-petits-soldats-de-la-fondation-pour-le-progres-de-lhomme/

10 – http://www.imdb.com/title/tt2411114/

11 – http://www.nature.com/news/hyped-gm-maize-study-faces-growing-scrutiny-1.11566

12 – http://files.vkk.me/text/c762d82e4180817b96259041cc71742df293c391.pdf

13 – http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2987375/?tool=pubmed

14 – http://www.sevenepharma.com/complexes-homeopathiques-detoxifier-lorganisme-2/

15 – http://arstechnica.com/science/2012/09/anti-gmo-researchers-used-science-publication-to-manipulate-the-press/

16 – http://www.enveurope.com/content/26/1/14/additional

17 – https://embargowatch.wordpress.com/2012/09/21/stenographers-anyone-gmo-rat-study-co-sponsor-engineered-embargo-to-prevent-scrutiny/

18 – http://link.springer.com/article/10.1007%2Fs11248-013-9692-9

19 – http://ehp.niehs.nih.gov/1408106/

20 – http://www.sciencedirect.com/science/article/pii/S0278691512007946

21 – http://www.amazon.com/s/ref=nb_sb_noss?url=search-alias%3Daps&field-keywords=Gilles+S%C3%A9ralini

22 – http://www.criigen.org/

23 – http://www.nature.com/news/paper-claiming-gm-link-with-tumors-republished-1.15463

24 – http://www.sciencedirect.com/science/article/pii/S0278691513008090

25 – http://www.sciencedirect.com/science/article/pii/S0278691514002002

26 – http://www.gmoSéralini.org/professor-Séralini-replies-to-fct-journal-over-study-retraction/

27 – http://www.ncbi.nlm.nih.gov/pubmed/23146697

28 – http://www.oecd.org/chemicalsafety/testing/oecdguidelinesforthetestingofchemicals.htm

29 – http://www.gmoSéralini.org/category/critics-answered/

30 – http://www.efsa.europa.eu/en/efsajournal/doc/2986ax1.pdf

31 – http://www.efsa.europa.eu/en/efsajournal/doc/2986.pdf

32 – http://www.efsa.europa.eu/en/efsajournal/pub/3347.htm

33 – http://www.ncbi.nlm.nih.gov/pubmed/4748432

34 – http://www.ncbi.nlm.nih.gov/pubmed/13304860

35 – http://www.ncbi.nlm.nih.gov/pubmed/7659952

36 – http://www.ncbi.nlm.nih.gov/pubmed/521452

37 – http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1963.tb13422.x/abstract

38 – http://www.enveurope.com/content/26/1/14

39 – http://books.google.com/books?hl=en&lr=&id=gLlpIUxRntoC&oi=fnd&pg=PR14&ots=A8vyS7Q9D2&sig=3Kz-2CPtiVuR9kIOp5mIAzFb-kE#v=onepage&q=we%20are%20all%20too%20good%20at%20picking%20out%20&f=false

40 - http://www.sciencebasedmedicine.org/reference/homeopathy/

41 - http://www.ncbi.nlm.nih.gov/pubmed/17227742

42 - http://www.ncbi.nlm.nih.gov/pubmed/10649002

43 - http://www.badscience.net/wp-content/uploads/benveniste02.pdf

44 - http://www.ncbi.nlm.nih.gov/pubmed/12492603

45 - http://www.ncbi.nlm.nih.gov/pubmed/22558899

46 - http://www.ncbi.nlm.nih.gov/pubmed/10391656

Is Alcohol Healthy? The Saga Continues

There have been a fair number of epidemiological trials that show light (up to 2/day) to moderate (up to 4/day) drinking is associated with reduced risk of coronary heart disease (CHD) and increased longevity [1,2,3]. Anything above 4 drinks a day and you are increasing your risk of cancer, liver disease, stroke, etc [1]. This is what we call a J-shaped curve. At a lower dose, we see benefits. But as the dose gets higher we see relative risk increase.

But these trials don’t actually prove alcohol reduces certain risk factors, it only shows us an association that should be looked into further. Enter the latest study [4]:

CETP TaqIB genotype modifies the association between alcohol and coronary heart disease: The INTERGENE case-control study

Published in the journal Alcohol (yes, that’s an actual journal), the study asserts that the “cardioprotective effect of alcohol may be restricted to subjects with a particular genotype of the cholesteryl ester transfer protein (CETP) polymorphism.”

Let’s break down the paper. For science!

This was a population-based case-control study. This means that the study pulled patients who did have a disease or certain outcome (cases) and compared them with patients that did not have a disease or outcome (controls). Researchers will then look back and try and determine the relationship between a risk factor and a disease [10]. In this article, we’re looking at the relationship between alcohol, the B2B2 CETP TaqIB genotype, and cardiovascular heart disease. The study randomly selected people from southern Sweden between the ages of 25-74. 618 (453 men and 165 women) in the cohort had experienced a myocardial infarction, unstable angina, or had been diagnosed with coronary heart disease. Another 2,921 (1,378 men and 1,543 women) had been deemed healthy and were the control for this study. The control group was asked about the frequency of their intake of different kinds of alcoholic beverages in the past 12 months and the case group was asked about their alcohol intake in the 12 months prior to their latest coronary event.

It is very important to note that these were self-reported alcohol intake numbers, meaning the accuracy of the data is, as we say in science, ‘sketchy’. Do you remember the frequency and types of alcohol you have imbibed over the past year?

Blood samples were taken from everyone to assess cholesterol and triglyceride concentrations (using enzymatic assays) and HDL concentrations were also measured. Genotyping was performed to see if patients possessed the B2B2 variation of the CETP gene. This gene had been looked at in a few other papers as the possible mechanism for the cardioprotective benefits of alcohol, but the results thus far have been mixed [5,6,7,8]. The working theory is that low levels of alcohol indirectly raise HDL levels via the CETP TaqIB gene, which is partly responsible for the regulation of HDL.

The researchers found that patients that carried the B2B2 genotype saw the greatest reductions in their risk for coronary artery disease. Just to put that into perspective, of the 3,539 patients only 659, or 18.62%, tested positive for the B2B2 genotype. Those lucky few that did possess this gene saw their heart disease risk drop by 79%. On the upside, those that did not have this magical gene still saw an overall risk reduction of 20% with moderate alcohol consumption.

So what is this gene doing that causes this precipitous drop in CHD risk? In a word, they do not know. But they don't think it’s because of the CETP-Alcohol-HDL interaction.

“The cardioprotective effect of alcohol in the CETP TaqIB B2 homozygotes could not be explained by a mediating effect of HDL-cholesterol or an interaction between HDL-cholesterol and genotype, nor was the effect reduced after adjustment for different socioeconomic and lifestyle variables, or explained by selective survival of certain genotype groups. The finding that the protective effect of alcohol is not due to HDL-cholesterol is consistent with the results in a recent Norwegian study (Magnus et al., 2011).”

So what does this all mean for your alcohol consumption? Study author Dag S. Thelle puts it best [9],

“In my view there is not [a message for drinkers]. Not at this time. It's far too early to say anything. The study is too small and has to be repeated.”

And that is how science goes. Sometimes the knowledge we acquire is outpaced by the rate at which we come up with new questions.

Science Checkup: Does Sugar Kill Your Sex Drive?

Do you remember your English classes back in high school? The teacher would assign you some droll book to read and warn you of an impending test on said book. The night before the exam, you would sit down and Google as hard as you could to try and find the Cliffs Notes. Upon finding one, you would read through the summaries and hope it was enough to pass the test. This strategy would usually yield mediocre results. A passing grade but nothing too fancy. Sometimes, this strategy would earn you a big old F. 

Some science writers never grew out of the Cliffs Notes phase and employ this strategy when reporting on journal articles. They will read through the abstract, the summary of a paper, and base their article on that single paragraph. Just like your high school English tests, these articles end up misinterpreting and misrepresenting the full context of the study. 

Enter Dr. Mark Hyman and his latest article,

Killing Your Sex Drive One Bite at a Time: 5 Surprising Ways Sugar Lowers Libido

[1]. In the opening salvos of his article he makes the following claim:

“The biggest culprit that continually knocks sex hormones out of balance is sugar in all its many forms (including all flour products), which raises insulin and creates a hormonal domino effect. Once you understand how insulin can impact other hormones, you begin to connect the dots about how excessive sugar can wreck your sex life.”

He then gives 5 reasons for how sugar kills your sex drive. Let’s review them to see if he was able to make it past the abstracts, shall we?

Claim 1 - Sugar Lowers Testosterone

Key Points

  • In men, insulin resistance brought on by excessive amounts of sugar drives down testosterone
  • Decreased muscle mass and more belly fat are repercussions of low testosterone. Excess body fat can increase levels of the hormone estrogen, leading to low sex drive and trouble getting erections.
  • In a study published in Clinical Endocrinology, where 74 men of varying ages underwent an oral glucose tolerance test, researchers found glucose (sugar) induces a significant reduction in total and free testosterone (T) levels.
  • Imbalanced levels of testosterone in women can reduce desire, increase body fat, lower muscle mass, and create a fuzzy memory.

Here is the cited article - Abrupt decrease in serum testosterone levels after an oral glucose load in men: implications for screening for hypogonadism [2].

The purpose of this study was to assess if “T measurement should be drawn in relation to food intake or if it should be obtained in the fasting state” when testing for hypogonadism, a condition where the sex glands produce little or no hormones [3].

Here’s what the study actually said. 

74 adult men were examined in this study. Ages ranged from 19–74 years (mean 51.4 ± 1.4) and comprised of fifty-nine (80%) Caucasians, 12 (16%) African Americans, 1 (1%) Asian and 2 (3%) Hispanics. Measures of BMI found that 8 were normal weight, 29 were overweight and 37 were obese subjects.  All subjects had gone through puberty and had normal serum levels of prolactin and thyroid-stimulating hormone. Each participant was given a 2-hour oral glucose tolerance test (OGTT) with 75 g of glucose after a 12 hour fast. Blood samples were drawn at baseline and 4 more times every 30 minutes. Free Testosterone levels were calculated using the Vermeulen equation. After the OGTT, it was determined that 42 subjects had a normal glucose tolerance, 22 had impaired glucose tolerance, and 10 were newly diagnosed as type 2 diabetics. Before the OGTT, 8 men had low total Testosterone levels (<9.7 nmol/L, 280 ng/dL) and the other 66 were normal. 

So what happened? During the 2 hour test, Total T went down from 475.50 ng/dL to 403.46 ng/dL (normal is 240-1,000 ng/dL) and Free T went down from 10.09 ng/dL to 7.78 ng/dL (normal is 9-30 ng/dL) [4,5]. So while Total T stayed normal, Free T dipped below the ‘healthy’ range. HOLY CRAP SUGAR IS GONNA MAKE ME IMPOTENT! Slow down there buddy, your penis is going to be just fine. 

First of all, they used a calculation (Vermeulen) to get the Free T numbers instead of a more accurate test, like the Liquid Chromatography/Tandem Mass Spectrometry (LC/MSMS), so there will be some slight variability in the measurements [6]. Secondly, a drop in testosterone levels postprandial (after a meal) is not abnormal. If Mark had thoroughly read this paper, he would have seen this little tidbit. 

“To date, three studies have investigated the T response in men to different caloric and macronutrient (fat) content in meals. Depending on the meal composition, these studies demonstrated either a postprandial decrease in T ranging from 15% to 40% or no change in T levels [over an 8 week period]” [7,8,9]. 

Furthermore, no one is going to sit around all day eating glucose (except maybe a hypoglycemic type 1 diabetic). So saying that a slight drop in T levels while taking 75 g of glucose on an empty stomach somehow translates into eating sugar or flour killing your T production is an utterly ridiculous extrapolation to make based off the data in this study. 

At the end of the study, the authors concluded that “men who present with signs and symptoms of hypogonadism…should have morning measurements taken in a fasting state to obtain a clearer picture of total T levels. This is particularly important as serum T levels have been shown to transiently fall well below the normal range in approximately 15% of healthy men over the course of a day” [2,10].

Not a single mention of sugar's effects on sex drive was stated anywhere in this paper. Not once. Because that’s not what this paper was investigating. 

Let’s review. 

  • Claim 1A - In men, insulin resistance brought on by excessive amounts of sugar drives down testosterone

Putting aside the assumption here that excess sugar causes insulin resistance (overly simplistic, there are many factors at play here) this statement is true-ish. The authors of the paper note that “we, and others, have demonstrated an inverse relationship between testosterone (T) levels and insulin resistance in men with type 2 diabetes and the metabolic syndrome” [2,10,11,12,13,14].

  • Claim 1B - Decreased muscle mass and more belly fat are repercussions of low testosterone. Excess body fat can increase levels of the hormone estrogen, leading to low sex drive and trouble getting erections.

This sounds legit, but no citation is given. 

  • Claim 1C - In a study published in Clinical Endocrinology, where 74 men of varying ages underwent an oral glucose tolerance test, researchers found glucose (sugar) induces a significant reduction in total and free testosterone (T) levels.

True, but as we have seen, he completely misrepresents the study. 

  • Claim 1D - Imbalanced levels of testosterone in women can reduce desire, increase body fat, lower muscle mass, and create a fuzzy memory.

Again, could be true. No citation was provided. Among all these claims, the larger implication is that sugar consumption is the main factor in all these issues, but the data he provides does not affirm this.

Claim 2 - Sugar Creates Leptin Resistance

Key Point:

  • Leptin also monitors sexual behavior. One study in the journal Clinical Endocrinology looked at three groups of men and found those with higher leptin levels—most likely due to leptin resistance—also had significantly higher body mass index (BMI) and lower levels of testosterone.

Here’s the article - Strong association between serum levels of leptin and testosterone in men [14].

Ok, let’s see if I can follow his logic on this one.

Lots of sugar causes leptin resistance > leptin monitors sexual behavior > leptin resistant people have higher BMI’s and lower testosterone > therefore, sugar causes low testosterone.

A causes B and B causes C so A must cause C! That, my friends, is some logical gymnastics. Let’s see what the study said. 

58 adult males were selected for this cross-sectional analysis. Group 1 (n=22) all had untreated hypogonadism (serum T lower than 201 ng/dL), Group 2 (n=20) were hypogonadal patients on androgen substitution therapy and had serum T over 864 ng/dL. For this study Group 2 was treated with testosterone or human chorionic gonadotropin. Group 3 (n=16) had no endocrine disorders, received no treatment, and had serum T levels over 864 ng/dL. At the end of the study, the results showed that Group 1, the men with low T, also had the highest leptin levels. In his article Mark asserts that the higher leptin levels in Group 1 are “most likely due to leptin resistance”. If he had read the paper, he would have seen that their increased leptin levels were due to low testosterone, not leptin resistance. 

When Mark cites this study as proof that leptin resistance, brought on by excess sugar, causes lower serum T levels he misses the fact that these men already had hypogonadism, meaning they already had lower T levels that could have been brought on by anyone of these factors [15]:

  • Klinefelter syndrome
  • Undescended testicles
  • Mumps orchitis
  • Hemochromatosis
  • Injury to the testicles
  • Cancer treatment
  • Kallmann syndrome
  • Pituitary disorders
  • Inflammatory disease
  • Medications
  • Obesity
  • Normal aging
  • Concurrent illness

Let’s review. 

  • Claim 2 – Chronically high leptin levels brought on by excess sugar in the diet causes testosterone levels to drop.

Excess sugar can be a contributing factor to leptin resistance, but the effect of high leptin levels being directly responsible for driving down T levels is not established by this paper. Only an inverse correlation has been shown between serum T levels and leptin. When testosterone was administered in hypogonadal men, leptin went down. Would the inverse be true? Would T levels go down if leptin was administered? Is low T responsible for driving leptin up or are rising leptin levels responsible for driving T down? Those questions, and the question of leptin resistance induced low T, are outside the scope of this paper. Additional studies would be needed to set up causality.

Claim 3 - Sugar Reduces Growth Hormone (GH) Production

Key Point:

  • Studies show insulin reduces your body’s ability to make growth hormone (GH), altering testosterone levels and reducing libido.

The study cited - Elevated insulin levels contribute to the reduced growth hormone (GH) response to GH-releasing hormone in obese subjects  [25]

Time for the breakdown.

First up, the authors note that it is not just insulin but free fatty acids that exert physiological control on growth hormone (GH) release. Which is to say, both high insulin and high free fatty acids (FFA) in the blood will reduce the GH response to Growth Hormone Releasing Hormone (GHRH). In previous studies, the GH response to GHRH was measured by reducing FFA via insulin infusion or by administration of acipimox, an antilipolytic agent that can reduce FFA levels. The researches noticed that the GH response to GHRH was lower in the insulin infusion group than in the acipimox group. The purpose of this trial was to determine to what extent insulin may reduce GH release independent of FFA.

6 obese subjects (4 men, 2 women; age, 30.8 years; BMI, 36.8) and six normal control subjects (4 men, 2 women; age, 25.8 years; BMI, 22.7) were selected. All subjects were in good health: normal endocrine function, normal glucose tolerance, and were taking no medications. Each group underwent three GHRH tests. Test one was an infusion of GHRH with saline and a placebo. Test two was an infusion of GHRH with saline and acipimox. Test three was an infusion of GHRH with insulin and a placebo. 

The results showed that the greater the reduction of FFA in the blood, the higher the GH response to GHRH. The GH response was greater in the control group than in the obese group and the authors speculated it was due to their higher circulating insulin levels. The authors also note that “no correlations were found between the GH response to GHRH and blood glucose levels in both the obese and the normal subjects” [14].

So does Mark’s claim hold up?

  • Claim 3 – Insulin reduces your body’s ability to make growth hormone (GH), altering testosterone levels and reducing libido.

Insulin does not reduce your body’s ability to produce GH. High circulating levels of insulin will inhibit growth hormones response to GH Releasing Hormone. So the GH is still being produced but it might not be getting to where it needs to go. 

As for decreased levels of GH reducing testosterone levels, I suspect this is true, but no citations were given.

Claim 4 - Sugar Makes You Tired

Key Point:

  • A study published in the journal Neuron found amino acids (protein) increase orexin neurons (a neurotransmitter that regulates eating behaviors, wakefulness, and arousal) and boosted alertness. Excessive sugar, on the other hand, decreased orexin, contributing to fatigue and drowsiness.

The article - Activation of central orexin/hypocretin neurons by dietary amino acids [16]

The first thing to note is that this study was performed in vitro and in animals (mice, rabbits). The data showed that amino acids stimulated the orx/hcrt neurons the most, concentrations of pure glucose inhibited the pathway, and mixtures of AA’s and glucose-stimulated orx/hcrt neurons nearly as much as AA’s alone. The authors point out that there is evidence this system should not be over or under-stimulated as it may lead to depression and anxiety [17,18,19,20]. As with most systems in the body, there is a range this system likes to be kept in which seems to be mediated by consuming meals of mixed macronutrient composition [16].

  • Claim 4 – Lots of sugar decreases orexin which makes you tied and (presumably) not want to have sex.

Is this true? Who knows. These trials were not conducted in humans so at best his claim is a hypothesis, even though he states it as a fact. 

Claim 5 - Sugar Triggers Stress & Anxiety

Key Point:

  • High insulin levels also exacerbate chronically elevated levels of cortisol, your stress hormone. When the two hormones stay elevated long after they should taper down, they perform as a team to break down muscle mass, store fat, and dampen libido

The article – none!

Not a single citation was given. This claim could very well be true but it’s hard to analyze when Mark does not provide his sources, as he did in the first four claims. 

So is sugar the “biggest culprit that continually knocks sex hormones out of balance” [1]?


Is sugar a potential contributor to a bigger picture that could result in diminished libido? 

Probably. But to say it is “the biggest” culprit is utter nonsense. 

Here are some things that actually contribute to or cause loss of libido [21,22]:

  • Erectile dysfunction (not synonymous with libido loss)
  • Performance anxiety
  • Stress
  • Fatigue
  • Medical conditions
    • Cancer
    • Depression
    • Hypertension
    • Diabetes
    • Alcoholism
    • Thyroid disorders
    • Medications
      • SSRI’s
      • Tranquilizers
      • Blood pressure medication
    • Surgery
    • Menopause
    • Pregnancy and breastfeeding
    • Anxiety
    • History of sexual abuse
    • Low self-esteem
    • Poor body image
    • Relationship issues

My reasoning for writing this article was not to give you a free pass on sugar. I wrote this piece because there are already numerous, scientifically sound reasons to keep your added sugar intake low [23,24]. The pseudoscientific nonsense pushed by Dr. Hyman will only act to muddy the public’s scientific understanding. The fact that this poorly researched article comes from a doctor just adds insult to injury. He, of all people, should know and do better. 


1 - http://drhyman.com/blog/2014/08/29/killing-sex-drive-one-bite-time-5-surprising-ways-sugar-lowers-libido/#lightbox/0/

2 - http://www.ncbi.nlm.nih.gov/pubmed/22804876

3 - http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002175/

4 - http://www.nlm.nih.gov/medlineplus/ency/article/003707.htm

5 - http://www.mayomedicallaboratories.com/test-catalog/Clinical+and+Interpretive/83686

6 - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240029/

7 - http://www.ncbi.nlm.nih.gov/pubmed/2392062

8 - http://www.ncbi.nlm.nih.gov/pubmed/11319710

9 - http://www.ncbi.nlm.nih.gov/pubmed/11699056

10 - http://www.ncbi.nlm.nih.gov/pubmed/3129947

11 - http://www.ncbi.nlm.nih.gov/pubmed/15983313

12 - http://www.ncbi.nlm.nih.gov/pubmed/15687322

13 - http://www.ncbi.nlm.nih.gov/pubmed/15713702

14 - http://www.ncbi.nlm.nih.gov/pubmed/18319314

15 - http://www.ncbi.nlm.nih.gov/pubmed/9302400

16 - http://www.mayoclinic.org/diseases-conditions/male-hypogonadism/basics/causes/con-20014235

17 - http://www.ncbi.nlm.nih.gov/pubmed/22099463

18 - http://www.pnas.org/content/102/52/19168/F3.expansion.html

19 - http://www.ncbi.nlm.nih.gov/pubmed/17346943

20 - http://www.ncbi.nlm.nih.gov/pubmed/18952152

21 - http://www.ncbi.nlm.nih.gov/pubmed/15862796

22 - http://www.webmd.com/sex-relationships/features/loss-of-libido-in-men?page=2

23 - http://www.mayoclinic.org/diseases-conditions/low-sex-drive-in-women/basics/causes/con-20033229

24 - http://www.mayoclinic.org/healthy-living/nutrition-and-healthy-eating/in-depth/added-sugar/art-20045328

25 - http://www.webmd.com/food-recipes/features/health-effects-of-sugar

26 - http://www.ncbi.nlm.nih.gov/pubmed/10484056

The ‘Natural’ Label: What In The Fresh Hell Does That Even Mean?!

Welcome to another edition of The Nutrition Overlords Knowledge Bombs®: Natural Label Edition

I promise to keep this one short(ish).

So you're walking down the aisle of your local grocery store and you pass by the eggs. Other than there being approximately 30 different brands, you notice some of them carry this fancy 'natural' label (and probably cost $2 more per dozen). So what does this ambiguous label mean anyway?

First, we have to break foods into one of two categories, because heaven forbid food labeling be simple. In the first group, we have meat, poultry, and egg products. In the second group, we have everything else. When the term 'natural' is applied to meat, poultry, and eggs it actually means something! In the USDA's Food Standards and Labeling Policy Book (a joyous read, I assure you) under the Natural Claims section (page 116) it states that meat/poultry/egg products carrying the natural label must meet these two standards [1]:

1 – “The product does not contain any artificial flavor or flavoring, coloring ingredient, or chemical preservative (as defined in 21 CFR101.22), or any other artificial or synthetic ingredient.”
2 – “The product and its ingredients are not more than minimally processed. Minimal processing may include: (a) those traditional processes used to make food edible or to preserve it or to make it safe for human consumption, e.g., smoking, roasting, freezing, drying, and fermenting, or (b) those physical processes which do not fundamentally alter the raw product and/or which only separate a whole, intact food into component parts, e.g., grinding meat, separating eggs into albumen and yolk, and pressing fruits to produce juices.”

These standards are only applied to meat/poultry/eggs because the USDA does not have regulatory jurisdiction outside of these food categories [1].

So what about everything else? Well, this is where the FDA steps in. The FDA has "not developed a definition for use of the term natural or its derivatives. However, the agency has not objected to the use of the term if the food does not contain added color, artificial flavors, or synthetic substances" [2].

So there you have it. All-Natural actually means something…sometimes…depending on the food…because regulatory jurisdiction.

Maybe that will be my next Knowledge Bomb®. Food Labeling: Welcome to Clusterfuckistan.


1 - http://www.fsis.usda.gov/wps/wcm/connect/7c48be3e-e516-4ccf-a2d5-b95a128f04ae/Labeling_Policy_Book_082005.pdf?MOD=AJPERES

2 - http://www.fda.gov/aboutfda/transparency/basics/ucm214868.htm

The Difference Between Natural and Artificial Flavors

Natural vs. artificial flavorings, what’s the deal?

Both of these are terms regulated by the FDA (the term "all-natural" is a different story). The definition of a natural flavoring is anything derived or extracted from a "spice, fruit or fruit juice, vegetable or vegetable juice, edible yeast, herb, bark, bud, root, leaf or similar plant material, meat, seafood, poultry, eggs, dairy products, or fermentation products thereof, whose significant function in food is flavoring rather than nutritional" [1]. An artificial flavor is anything that is not derived from the items listed above, but rather synthesized in a laboratory. Don't freak out, it's not nearly as scary as it sounds! Read on to find out why.

So which one is healthier or better? Well, the answer to that isn't so simple. The first step is to understand that both natural and artificial flavors are just made up of various chemicals. This is not a bad thing! Everything is made up of chemicals. That banana you had for lunch, that avocado you ate for a snack, you, me, and Oprah are all made of chemicals. Chemicals = not inherently evil. The second step is to understand the basic principles of toxicology, or what the effects of chemicals are at certain doses. For example, we can all agree that ~90 milligrams of Vitamin C a day is healthy for you [2]. However, 10,000 milligrams a day will give you diarrhea, nausea, headaches, cramps and possibly kidney stones [3,4]. As the saying goes, the dose makes the poison [5].

You catch all that? Good.

Now back to the original question of natural vs artificial. An argument could be made that the artificial flavorings are safer because all the chemicals allowed in an artificial flavor have been tested for toxicity levels [6,7,8,9]. Chemicals used in a natural flavoring do not have to face the same kind of scrutiny, although there is significant overlap in the types of chemicals used in both kinds of flavorings. Just because a source is natural does not mean it is safe for human consumption (all natural snake venom anyone?). I'm exaggerating of course, but you get the point. These things need to be tested and evaluated, no matter what the source.

Another point to understand is that some artificial and natural flavors have the exact same chemical structure.

The. Exact. Same.

Other times, the chemical structures of an artificial flavor may be simpler than its natural counterpart. This is due to a flavorist eliminating any secondary chemicals that make minimal contributions to the primary flavor when s/he is trying to synthetically mimic a naturally occurring flavor compound [9].

Questions of sustainability can be raised as well. Take coconut flavoring as an example. Coconut flavor is dependent on a chemical called Massoia Lactone which comes from the bark of the Massoia tree [10]. To collect this chemical for use in a natural flavoring, the bark of the Massoia tree is stripped which ends up killing it [9]. This process is far more costly and damaging than if the Massoia Lactone had just been synthesized in a lab. I'll stress this again, both sources have the exact same chemical structure.


From an overall health perspective, an argument could be made against using either of these methods, as both artificial and natural flavors can be employed to make foods hyper-palatable which could lead to overconsumption. This is not the case for all foods, but we cannot forget the primary motivator of food companies is to make money, and added flavorings are a tool they can employ to get us to buy more of their product.

I hope your minds has been sufficiently blown and I have reduced your chemophobia a bit. As some added food for thought, I've included a few pictures from James Kennedy’s series, Ingredients of All-Natural Foods [13].

Please tune in for the next edition of The Nutrition Overlords Knowledge Bombs® - The All-Natural Label: What In The Fresh Hell Does That Even Mean?!?!

Side Note – for a full list of approved synthetic flavoring substances see reference 11 and 12.

The US Is Throwing Measles a “Welcome Back” Party!

I consider America to be a very hospitable place, which is why I'm thrilled to see the US welcoming measles back into the country after 20 years of banishment. Good to have you back measles! You've been missed.

Plus, I think the red splotches all over your body make for a bold fashion statement.

Ok but seriously, let’s talk about this recent resurgence of measles. Measles is an infectious virus that usually manifests as a red, itchy rash 8-12 days after exposure [8,9]. It is highly contagious, can be spread through coughing and sneezing, and will remain alive for up to two hours outside the body [8,9]. It’s a nasty little bugger and complications can include ear infections, diarrhea, pneumonia (infection of the lungs), encephalitis (swelling of the brain), seizures, and death [7].

Measles was declared eliminated back in 2000 within US borders by the CDC [1]. By 2002, it had been eliminated in North and South America [1]. Elimination of infections is defined as “reduction to zero…the incidence of infection caused by a specific agent in a defined geographical area as a result of deliberate efforts; continued measures to prevent re-establishment of transmission are required” [2]. In the US, the overall measles incidence remained less than 1 case per 1,000,000 people from 1997 through 2013 [3]. Of the cases reported, 65% were in unvaccinated patients and 20% had an unknown vaccination status [3]. In all likelihood, the measles occurrences in the unvaccinated patients probably came from the 6 to 11 month (4.1 cases per 1,000,000) and 12 to 15 month age groups (3.6 cases per 1,000,000), as children younger than 12 cannot get the vaccination while others are delayed in their vaccination schedules [3,4]. 

Don't freak out over these unvaccinated infants getting infected from parents that refuse to give their kids the MMR vaccine. Remember, these numbers are from when measles was still classified as eliminated. The effects of vaccinophobia did not manifest via increased measles cases until 2014.

603 cases were reported from January 1st to October 31st 2014, which means there are more coming [5]. In the first 10 months of this year, we have more reported cases than in the past 20 years and more total cases than in the past 5 years combined. That is absurd! But why the sudden spike? Walter Orenstein, M.D., and Katherine Seib, M.S.P.H. suggest two possible explanations in their New England Journal of Medicine article, Mounting a Good Offense Against Measles.

1 – “Susceptible U.S. residents who travel to countries where measles is endemic or epidemic and susceptible residents of those countries who travel to the United States are bringing the virus here.”
2 – “An increasing number of parents in this country are hesitant to have their children vaccinated, and such hesitancy has resulted in an accumulation of unvaccinated populations who can become infected and maintain transmission.”

So why all the fuss over measles? What’s so bad about it anyway? Two reasons: it’s highly contagious and it can kill you dead. Between the 16th and 20thcenturies (1500 - 1999) an estimated 200 million people died of measles [6]. After the measles vaccine became available in 1963, and the combination measles-rubella vaccine in 1971, disease incidence fell quickly [6].

Measles happens to possess the title of being one of the most infectious diseases with a reproduction rate (R0) between 12 and 18 [1,10,11]. This means that once a person has measles, they are capable of passing it on to as many as 18 other people. To see how that stacks up, I've included a comparison to other communicable diseases from NPR.

To keep an outbreak from occurring, we need 92-94% of the population to be vaccinated to ensure herd immunity (see more on herd immunity here) [1]. This threshold is “higher than the thresholds for almost all other vaccine-preventable diseases.” [1].

After reading all that you may be thinking to yourself, “Measles sounds pretty lousy. How do I go about protecting myself and my family?” Well, the graphic below provides some pretty stellar information. If you click on it, you will be taken to a CDC website that can provide you with further assistance.

So if this post was a little too Debbie Downer for you, I'll leave you with a few measles factoids that may brighten your outlook [12].

  • Estimated global coverage with the first dose vaccine is 84% as of 2012
  • The number of countries providing a second dose vaccine increased from 96 (50%) in 2000 to 145 (75%) in 2012
  • 144 million children were vaccinated against measles during vaccination campaigns
  • In 2012, annual reported measles incidence was 33 per 1,000,000, a decline of 77% from 146 per 1,000,000 in 2000
  • Estimated measles deaths decreased 78%, from 562,400 to 122,000
  • An estimated 13.8 million deaths were prevented by measles vaccination during 2000–2012


1 - http://www.nejm.org/doi/full/10.1056/NEJMp1408696

2 - http://www.cdc.gov/mmwr/preview/mmwrhtml/su48a7.htm

3 - http://archpedi.jamanetwork.com/article.aspx?articleid=1787786

4 - http://www.cdc.gov/vaccines/hcp/vis/vis-statements/mmr.pdf

5 - http://www.cdc.gov/measles/cases-outbreaks.html

6 - http://archpedi.jamanetwork.com/article.aspx?articleid=1787785

7 - http://www.cdc.gov/vaccines/pubs/pinkbook/meas.html#complications

8 - http://www.nlm.nih.gov/medlineplus/ency/article/001569.htm

9 - http://www.cdc.gov/measles/about/transmission.html

10 - https://www.elsevier.com/books/vaccines/plotkin/978-1-4557-0090-5

11 - http://smm.sagepub.com/content/2/1/23.abstract

12 - http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6305a5.htm

That Time I Got Involved In An Anti-Vaccination Comment Flame War

Normally I never get sucked into the comment flame wars on FaceBook. I usually read them for amusement and never write anything myself. The trolls got me this time.

I happened to be looking through the comments on an anti-vaccination thread. In these threads, people never link to any legitimate scientific sources to back up their arguments. It just so happened that one woman attempted to back up her anti-vaccination beliefs by providing a link to an FDA document that she says provides "pretty incriminating evidence AGAINST vaccine safety". Stunned by seeing a link to a credible source, I decided to read this document to see if her claims were justified. Below is the exchange that took place.

I wasn't able to catch a screenshot of the next comment Theresa made, but it went something like "Go look up any of the hundreds of Vaccine Information Sheets on the FDA's site and you will see that vaccines cause death, autism, etc..."

When I checked back later, Theresa had deleted all of her comments and her Facebook account as well.

I have exactly 0 issues with people/parents questioning vaccines. I do have an issue with people not taking the time to seek out good sources of information about their safety. Asking the question "what exactly am I injecting into myself/my child" is the first step. Reading about the dangers of vaccinations on Mercola.com or FoodBabe.com is not the second step you should be taking in your investigation.

For those interested in a quick overview of vaccine herd immunity and the studies done on the link between MMR and autism (spoiler: there isn't one) check out these two YouTube videos by Dr. Aaron Carroll, MD.