Why I Left Academia

When I started my doctoral dissertation and the associated research, I was absolutely full of love toward what I was doing. I worked on understanding how specific hormones in the brain (neuropeptides) modify human decision-making. I ran clinical trials and published several articles. Here is chapter 2 of my dissertation published in PLOS One. It is one of their top papers in terms of citations. Great stuff! But then the troubles start. You get your PhD and you are on your own.

Publish or Perish

When you are in academia, you need to publish as well as teach. This is not an easy combination, because teaching itself is a full time job and when you are just starting out, you are hit with a bigger teaching load than once you become an “accepted” member of academia. So academics publish and publish and publish, and here comes trouble!

Most research is in teams and team members come from different locations, different fields, and often with conflicting opinions. For example, when I worked at the Max Planck Institute in Germany as a postdoc visiting scholar, I teamed up with several people to run an experiment. The idea was mine, I worked with a Max Planck researcher on setting the research up, and several other people joined us: a statistician graduate student to help with the statistics, the radiologist that helped us use the fMRI machine, the lead at Max Planck Institute where I was working at the time, and a professor from the University that had the student body form the volunteer group. The actual experiment ran in 2008. Today, in 2022, we still don’t have a publication because every time I get the paper and try to help, I am shot down by the professor at the university. I don’t think that this research paper will ever be published because it is very poorly written but there is this one person that won’t let me get in there and make any changes. I think you understand where I am going with this. But there is another problem.

The Main Problem

I bumped into this video the other day and though I am really not a fan of the DietDoctor for much fake information on their website, I decided to watch this video because it was short and the topic was of interest to me. The topic is associated with my experience in scientific research.

You can find the video here if you prefer to watch on YouTube: https://www.youtube.com/watch?v=xYLrMq240xk

In this video one of the authors of a recent study explains why the recent study they published misleads completely those who read the abstract and why even the newsflash was also completely wrong! The paper they wrote can be found here.

The paper summary (the abstract) suggests that while the ketogenic diet beat the Mediterranean diet in most aspects, since it increased LDL, the so called “bad cholesterol”, the Mediterranean diet won and keto failed. Yet, if you read the paper all the way through, you will find that they actually found the exact opposite! The ketogenic diet won over the Mediterranean diet in every aspect of the study, even in the case of increased LDL, because when placed into the context of its effect on metabolic health markers, the increased LDL ended up with metabolically healthier people ==> better outcome.

Why Was the Paper Misleading?

You will see in the video that of the many authors, the lead author and 4 more authors are plant-based dieters, and so the findings actually disagreed with their biases. They could not stomach that the ketogenic diet worked better than the Mediterranean, and so they “twisted” the story toward their bias.

In addition, the speaker in the video was in charge of writing the paper but the part that explained why the increased LDL was a benefit, was removed by the lead author. With this, the lead author changed the entire meaning of the paper and has basically falsified the research by misrepresenting the findings.

Unfortunately, as this is also my experience, this happens more often than not.

Is Peer Review The Hallmark?

While most scientists (and the public especially) will always want to see only peer reviewed papers considered, my experience with peer review, both as a reviewer and also as an academic submitting articles for peer review has been a challenging one, and one I no longer trust.

When I was a peer reviewer, there were always 3 reviewers per paper and two had to agree on what will happen. In nearly every case, my statistical knowledge forced me to reject over 95% of the papers but they still published because the other two reviewers had weaker statistical experiences and simply didn’t catch the problems.

And when I was the author and submitted to peer review, I could pick and choose who I did not want on the peer review committee and I could also recommend any reviewers I preferred. This alone is already a form of “cheating”. And in some cases when I didn’t see any familiar names and the paper went to whoever, they had the right to request that I cite their paper, even if it was not appropriate to do so, given my topic.

Academic Publications Have Serious Problems

The attached video will help you understand why studies are often completely taken out of context by the abstract and why the headlines are often reported to present the exact opposite of what the study found. This also means that if you aren’t a scientist and don’t understand academic papers or have no access to them, and you only listen to the headlines and what is reported in the news, you will completely be misguided and will believe the opposite of what was in the actual research article.


Don’t listen to newsflashes! Don’t believe an article reported by the Media! If you are really interested in the topic, get the original article and if you don’t understand it, ask an academic friend to help you understand it. Life is full of traps where money can be made! Don’t fall into the trap!

Comments are welcome, as always, and are moderated for appropriateness,


About Angela A Stanton, Ph.D.

Angela A Stanton, PhD, is a Neuroeconomist focusing on chronic pain--migraine in particular--physiology, electrolyte homeostasis, nutrition, and genetics. She lives in Southern California. Her current research is focused on migraine cause, prevention, and treatment without the use of medicine. As a forever migraineur from childhood, her discovery was helped by experimenting on herself. She found the cause of migraine to be at the ionic level, associated with disruption of the electrolyte homeostasis, resulting from genetic variations of all voltage dependent channels, gates, and pumps (chanelopathy) that modulate electrolyte mineral density and voltage in the brain. In addition, insulin and glucose transporters, and several other variants, such as MTHFR variants of B vitamin methylation process and many others are different in the case of a migraineur from the general population. Migraineurs are glucose sensitive (carbohydrate intolerant) and should avoid eating carbs as much as possible. She is working on her hypothesis that migraine is a metabolic disease. As a result of the success of the first edition of her book and her helping over 5000 migraineurs successfully prevent their migraines world wide, all ages and both genders, and all types of migraines, she published the 2nd (extended) edition of her migraine book "Fighting The Migraine Epidemic: Complete Guide: How To Treat & Prevent Migraines Without Medications". The 2nd edition is the “holy grail” of migraine cause, development, and prevention, incorporating all there is to know. It includes a long section for medical and research professionals. The book is full of academic citations (over 800) to authenticate the statements she makes to make it easy to follow up by those interested and to spark further research interest. It is a "Complete Guide", published on September 29, 2017. Dr. Stanton received her BSc at UCLA in Mathematics, MBA at UCR, MS in Management Science and Engineering at Stanford University, PhD in Economics with dissertation in neuroscience (culminating in Neuroeconomics) at Claremont Graduate University, fMRI certification at Harvard University Medical School at the Martinos Center for Neuroimaging for experimenting with neurotransmitters on human volunteers, certification in LCHF/ketogenic diet from NN (Nutrition Network), certification in physiology (UPEN via Coursea), Nutrition (Harvard Shool of Public Health) and functional medicine studies. Dr. Stanton is an avid sports fan, currently power weight lifting and kickboxing. For relaxation (yeah.. about a half minute each day), she paints and photographs and loves to spend time with her family of husband of 45 years, 2 sons and their wives, and 2 granddaughters. Follow her on Twitter at: @MigraineBook, LinkedIn at https://www.linkedin.com/in/angelaastantonphd/ and facebook at https://www.facebook.com/DrAngelaAStanton/
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5 Responses to Why I Left Academia

  1. gail says:

    Good morning! I have two questions, where can I make a donation, and is there a place online where you discuss how GKI is an inaccurate measure of ketones/ketosis relative to ingestion of protein and insulin/glucagon signaling? I’ve heard you mention this a few times in interviews, but it is so fast and I really want to dive deeper into the biochemistry and such so I can understand the process better. Your work is outstanding!! Thank you!!

    Liked by 1 person

    • Gail,

      Superb questions! I will answer here very shortly and I think you are right, I should write up a blog article on this. I may just do that.

      Question 1: The donation is welcomed at the nonprofit website: https://www.stantonmigraineprotocol.org/timetable/event/support-us/ this link takes you straight to the donation page. And thank you very much if you are considering to donate. 🙂

      Question 2: GKI and what it means. GKI is a division between glucose (in mmol/L) and ketones as you read it in with your blood testing kit. It assumes that low glucose and high ketones mean you are in ketosis, but this isn’t necessarily true, and so it misleads many people.

      Question 3: The physiology associated with the triad of glucose, insulin, and ketones is a very complicated one. In short: ketones are created when insulin is not released but glucagon is. Therefore, whether one GENERATES ketones or not is dependent on insulin levels and not glucose levels, while the USE of ketones is dependent on glucose levels but not insulin levels. So there is a disconnect right here, because if I have, for example, low insulin but high glucose, I can produce ketones and it will increase in my blood, but I am actually not using it because my glucose is high.

      You may say: but if your glucose is high, insulin surely must release. And yes, it will, but there is a delay. In this time delay the liver is still producing ketones only the body isn’t using them. In other words: the feedback system takes time but the use of energy is constant. And glucose will be used as energy before ketones by all organs that can use glucose, simply because glucose is toxic in the blood in excess, whereas ketones are less dangerous in excess.

      Another point here is the excess ketones in the blood. Ketones are fatty “acids” and thereby acidify the blood, so having high ketones is not only undesired, but can be fatal–the famous “ketoacidosis”. GKI would suggest that a blood ketone level of 5 mmol/L is great, but actually at that point the blood acidity is changed and is more acidic than is should be, causing harm.

      It is important to realize that ketones and glucose are “just” fuels and too much fuel isn’t going to make your car go faster, it just overspills. In our body, glucose overspill occurs in the kidneys, damaging the kidneys, and ketone can also overspill there, though the glucose we use as fuel, beta-hydroxybutyrate (BHB) can be converted back into acetoacetate, the base ketone body from with BHB and also acetone–the “keto breath”–spontaneously generates. So if a person has excess BHB in the blood, it can revert back into acetoacetate, which is urinated out and acetoacetate can also waste it as acetone, by breathing it out. So there are 3 ways in which the human body can get rid of ketones, but only two ways for glucose: burn t or urinate it out.

      Back to the connection of insulin for a second: if you are in good strong ketosis, with blood glucose between 80-99 mg/dL and BHB around 1-2 mmol/L, and you remain there continuously whether you are eating or not, the GKI then works fine. If you eat and this value changes, then insulin entered the picture. An increase in ketones in the blood after eating means insulin was released and ketones backed up. Therefore, at this time, you are not in ketosis, even though you are showing higher ketones.

      By contrast, as your body used up all excess sugar after eating from the blood and your ketones are dropping, say from 1 mmol/L to 0.3 mmol/L, this means you are burning ketones faster than you are making them. So you are actually in strong ketosis. And this is where the GKI completely fails, because it will tell you the exact opposite from what really happens.

      I hope this helped explain the process. It is longer than I thought but I may still write ths up into an article one day. 🙂



      • gail says:

        Oh thank you so much for such a detailed reply!! It is so helpful to my understanding! I so appreciate the time it took to write that!! This is such an important concept to understand. Again, thank you so much!! I look forward to following your work and presentations in the future.

        Liked by 1 person

  2. Jonathan Couchman says:

    Thank you. This is a brilliant and educational article, a real eye-opener. I am so impressed and grateful.

    Liked by 1 person

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