A case history of high #GGT and #SIBO, with Gut-based root cause - interesting !

Quick post today on interesting case of something that can drive up GGT. With potentially huge increases in liver-related complications later in life. It is based on an email conversation with a person who was struggling to deal with chronically elevated GGT. I'm guessing Dr. Guðmundur F. Jóhannsson will enjoy this one. And it may be important for many people out there who have elevated GGT. As far as I know there is no published literature around this. So this may be a first. Share with anyone who is smart enough to be measuring and monitoring their GGT number. Note also that although not a key factor in Joe's case, a healthy #LCHF regime will hugely assist in improving SIBO for myriad people! Here's a tip from Gabor Erdosi however:  "LCHF with lots of plants is insufficient against SIBO/SIFO, you need to go as far as dairy free zero carb!"

The conversation verbatim below:

JOE (April 2017): I understand you had an issue with elevated GGT and did a lot of research around that problem. I have the same problem. Would you be so kind and share your insights with me? What are the risks if it stays high? How can I lower it? Did you manage to control it? How? Maybe you can point me to the key scientific papers that I should study. Many thanks for your help

IVOR (April 2017):  Two things commonly drive up GGT - Alcohol and Carbohydrate excess. I and other cases had values over 100, whacked down promptly with low carbohydrate (I drink plenty of red wine – but this still ok with low carb regime). The following is a good resource, but they won't mention low carb: http://www.healtheiron.com/ggt-science-library

As can be seen in the above link the risks are for cardiac disease, liver and other cancers, and all-cause mortality. I would aim to be below 30. Serum Ferritin synergistically links to GGT risk - again the way to lower this (and eliminate metabolic syndrome inflammation that drives it) is low carb healthy living. A good site for low carb:  http://www.dietdoctor.com . Attached my metrics driven good by low carb living; excessive sugar and carb drives inflammation and the liver / physiology suffers....

my GGT tumbled in approximately 8 weeks only - this biomarker should respond quickly (e.g. it is often used to verify if alcoholics are staying dry. Their GGT levels drop fairly promptly when off the drink. But due to unknown biological changes that years of drinking have caused in their liver and organs - their GGT rockets up when they drink again. Even a couple of days drinking will do it. The GGT goes up way faster than a non-alcoholic's would when exposed to similar short bursts of alcohol. Amusing that Robert Lustig equates alcohol with sugar as a hepatic poison - he's on the ball…!

There is a director of the Iron Disorders Institute who I traded emails with a couple of years ago; I gave her my hypothesis and she agreed 100% - said she had discovered same link of high carb to high GGT, and was actually writing a book on it; I must get back to her and see if she ever finished !

JOE (Aug 2017): Hi Ivor, I just wanted to close the loop on this: In my case, low carb and low A1c didn't help much. While my TG and HDL improved, my GGT remained in the 150-250 region (where it has been for almost 20 years!). But what did help was the following: it turns out I must have had SIBO and SIFO for most of my life. After a cure with rifaximin and neomycin followed by nystatin, my GGT is now down to 40. Amazing! Bacterial Endotoxins and Mycotoxins must have poisoned my liver. Just wanted to let you know, because I didn't find much written about SIBO/SIFO and GGT. Many thanks again for your help!



http://www.thefatemperor.com/subscribe for more case histories from my massive email backlog...!

Professor Matthew J. Budoff pt 2: Primary Care Physicians and CAC

Dr. Jeff Gerber asks most of the questions in part two of our interview with Professor Matthew J. Budoff. He wrote the atlas of CT technology, and has unparalleled knowledge in this sphere: http://www.springer.com/gp/book/97815...

We focus here mainly on the imperative for primary care physicians to become educated in the power of the CAC score from the Coronary Calcification Scan. The incredible predictive power is summarized here in one of Matthew's countless peer-reviewed published papers:  https://www.hindawi.com/journals/scie...


First and main interview below - covers all the requisite details on CAC ! :

Did you know that 40% of heart attacks occur in the 10% of people with highest CAC Score? Or that ~60% of 'Framingham Middle Risk' people are reclassified after a CAC - into LOW or HIGH risk groups? Or that people with a yearly rising CAC score - have 6 to 8 TIMES the heart attack rate compared to those with stable CAC? That's right - the Calcium Scan is cheap, fast and unparalleled - and it is grossly underutilized.

The CAC is now recommended in the 2013 European and American Cardiology guidelines. But the majority of doctors have no idea about it. To find out more go to http://www.IHDA.ie for great information. And watch David Bobbett's 'The Widowmaker Movie' (2015) with Gillian Anderson and Larry King:



Millions of lives over the past 30 years have been lost due to ignorance of the scan's power (and no small amount of politics and profiteering).

Time to fix the situation.


Calcification and CAC with the expert: Professor Matthew J. Budoff, MD, FAAC

Dr. Jeff Gerber and myself finally caught up with Professor Matthew J. Budoff in California. He was a pivotal figure in recognizing the power of the CT Scan of the Heart - and decades ago to boot. He has led extensive cardiac research efforts over the past decades, publishing an enormous number of papers on calcification scanning and many other areas of cardiac research. Here is just one example - an excellent summary of CAC's power:


He also wrote the atlas of CT technology:  http://www.springer.com/gp/book/9781573402675

Did you know that 40% of heart attacks occur in the 10% of people with highest CAC Score? Or that ~60% of 'Framingham Middle Risk' people are reclassified after a CAC - into LOW or HIGH risk groups? Or that people with a yearly rising CAC score - have 6 to 8 TIMES the heart attack rate compared to those with stable CAC? That's right - the Calcium Scan is cheap, fast and unparalleled - and it is grossly underutilized. Learn the key points in this interview, in less than 20 minutes:

Second part of interview below - focus on the primary care physician imperative:

The CAC is now recommended in the 2013 European and American Cardiology guidelines. But the majority of doctors have no idea about it. To find out more go to www.IHDA.ie for great information. And watch 'The Widowmaker Movie' (2015) with Gillian Anderson and Larry King (best dollar you'll ever spend!). David Bobbett founded www.IHDA.ie and funded this excellent movie to awaken the people - link below:  

Also direct link below:


Millions of lives over the past 30 years have been lost due to ignorance of the scan's power (and no small amount of politics and profiteering).

Time to fix the situation.


London Calling ! BACPR #Cardiovascular Event this October 5th #LCHF

A most interesting event will be taking place in London later in October It is being run by the British Association for Cardiovascular Prevention and Rehabilitation (BACPR). Welcome will be cardiologists, doctors, nurses, nutritionists - and interested members of the public. 

The 2017 conference sessions will include many fantastic speakers. Oh, and me too :-). Link below has the current schedule, which includes Dr. Aseem Malhotra and Dr. David Unwin:


Hope to see you there...register at:  http://www.bacpr.com/pages/news_box.asp?NewsID=19495696 !

Also for cardiovascular prevention strategies, don't forget to subscribe for free at WWW.THEFATEMPEROR.COM/SUBSCRIBE

Supported by www.IHDA.ie - the Irish source for crucial information...on identifying Heart Disease early enough to prevent Heart Attacks

Just back from #PHCManc2017. Time to progress #PHCIreland...!

Jason, Jeff and I had a fantastic weekend at the www.phcuk.org conference in Manchester. We enjoyed giving our talks, but more importantly mixing with so many exceptional and dedicated people. The event was packed with nutritionally-astute GP's. It was really quite extraordinary - and has the makings of a revolution: www.phcuk.org/conference

Something's also been brewing in the auld emerald isle. You guessed it - the embryonic www.phcireland.org is in gestation. We suspect that a Canadian entity will be coming to term by 2018... ;-)

We had the honour of hosting Dr. Jason Fung, his wife Mina and Dr. Jeff Gerber on Tuesday night (in Shanahan's on the Green). See Jason's fantastic resource at https://intensivedietarymanagement.com/

 David Bobbett and www.IHDA.ie brought us all together for an excellent discussion. Strategy will be imperative in tackling our epidemic of chronic disease - there are so many headwinds. The use of excellent diagnostic technology like the CAC scan will also be required, to identify those with severe but hidden disease. The latter folks will require well-formulated #LCHF as a minimum intervention.

Thanks to Dr. Gearoid O'Laoi for the photos:

We will start off with just MD's and consultants until we are ready to expand. The structure will be extended in late 2017 / early 2018. In the initial grouping we have some seasoned #LCHF GP's and surgeons, a pathologist and a psychiatrist. This is the first time we have all met in one place. The group will grow. In the past day or two we have been approached by a highly experienced #LCHF endocrinologist - and a hugely accomplished vascular surgeon. We expect many more from the medical community to come forth.

We will defer to the excellent leadership of Sam Feltham and the PHCUK organisation. But we will create an affiliate in Ireland to focus the effort that will be required. Recruitment to the group will continue over the next six months until we are ready to open for members.

The talking heads currently blame the victims. We blame the bad nutritional science that has been foisted on the people. Ireland is on a collision course for diabesity Armageddon. Someone has to do something about it: http://www.ipcra.org/ireland-leads-the-obesity-epidemic-in-europe 

Note: we apologize to Jason and Mina for such a sudden exposure to the fiery passion of the Irish crew (just like for the drug trials, they perhaps should have been afforded a "run in period"... :-)

Diabetes Unpacked - support The Noakes Foundation and help all with #Diabetes

Jeff and I had the privilege of writing a chapter for the new book on diabetes from the Noakes Foundation. It is packed with valuable information on the science of diabetes - our modern health epidemic. Most importantly it elucidates on how this epidemic can be halted through understanding its root causes. Appropriately it is dedicated to all diabetics - those who have suffered through the bad science of the past decades. The bad, bad science which underpins their condition.

The book is available at http://diabetesunpacked.com/ - all proceeds go to The Noakes Foundation. Please show your support for the hundreds of millions of diabetics in our world today - and buy a copy to help save them from quasi-exploitation.

Dr. Gerber has finally made it to Ireland and sits here on my deck in Dublin - "warming his arse" as we say... :-)

Denver's Diet Doctor gets published - #Insulin and #CRP Revelations !

Well lookie here, what have we got? Looks like the inflammatory marker of CRP is intimately related to elevated Insulin. Can't say I'm surprised - but super job to Dr. June S Yang and Dr. Jeffry Gerber to extract the reality from the data. But what about the amazing LDL? Surely it too correlated with CRP? Given the enormous focus on LDL for several decades?

Eh, no. As usual when you look closely...LDL sneaks away in shame.

This is a very well-written and accessible paper, with very significant implications indeed. Please share it far and wide ! Link to full paper below:



Fasting Insulin and CRP below - impressive OR's :

LDL and CRP below - big fat nothing :

And of course Trig/HDL and CRP below - impressive OR's again:

...and don't forget to go to www.thefatemperor.com/subscribe for free updates supporting the science !

Gut MIcrobiome, Dysbiosis - and the pandemic of Insulin Resistance...

Hi all - I've been becoming more and more interested in the linkages between the gut microbiome / dysbiosis and the disease-driving curse of Insulin Resistance. Bad nutritional inputs directly lead to gut issues and potential permeability. These problems in turn have been shown to drive insulin resistance and through inflammatory pathways. To compound things, the bad nutritional inputs also directly drive insulin dysregulation through yet more pathways. The adipose tissue occupies a central mechanistic place in the disaster. Do you see a perfect storm forming here? Yep - right. Let's take a closer look:

Drew Duglan has done a lovely piece of study tying together some of the threads in this complex web of interaction. I've reproduced this below with his permission - enjoy !

(Don't forget to subscribe for free at www.thefatemperor.com/subscribe ! )

Drew Duglan May 17th 2017

(Drew is a post-doctoral researcher at The Scripps Research Institute, currently working in the areas of metabolism and circadian rhythms.) 

Insulin resistance and the (mal)adaptive immune system

A convincing case has been made that the development of type 2 diabetes has its origins in adipose tissue dysfunction, leading to uncontrolled lipolysis and the precipitation of full blown systemic insulin resistance (IR). As many intelligent folks here have pointed out (Gabor, Ivor and others), individuals that have the capacity to store excess nutrients by making new adipocytes (hyperplasia) can remain insulin sensitive and are metabolically healthy in their obesity (1). It is instead the enlargement of existing adipocytes (hypertrophy) which is the red flag; under these conditions there is a greater propensity for adipocyte cell death, stimulating the infiltration of immune cells that can induce a damaging pro-inflammatory cascade (2). An initial trigger for much of this may be a process called endoplasmic reticulum (ER) stress. The ER is an intracellular organelle which is critical for things like nutrient metabolism, calcium storage and protein folding. With an imbalance between protein load of the ER and its folding capacity, misfolded/unfolded proteins accumulate, leading to a stress response. Perhaps unsurprisingly, some of the major initiators of ER stress are nutrient overload (or deficiency), hyperglycemia and dyslipidemia; some of the major consequences are oxidative stress, insulin resistance and the activation of the adaptive immune system (3).

T-cells run wild

Obesity-related insulin resistance in both animals and humans demonstrates an influx of adaptive immune cells into adipose tissue, particularly in the visceral fat regions, usually located around the abdomen. Key players in this process are T-cells, and more specifically, certain subsets: cytotoxic T-cells, T-Helper type 1 (TH1) and type 17 (TH17). These effector cells release different cytokines such as IFN-γ and IL-17, which both directly disrupt insulin signaling in the adipocyte and invite other innate immune cells to the inflammatory house party (4, 5). Macrophages (but also neutrophils) readily accept the invitation and become differentiated into their pro-inflammatory state (M­1), secreting their own cytokines in the process. These chemical factors, such as TNF-α and IL-6, further impair glucose uptake, reduce normal lipid storage and only reinforce the inflammatory positive feedback loop. The negative arm of this process would normally include T-Helper type 2 (TH2) cells and the regulatory T cells (­Tregs), which are anti-inflammatory and help dampen the hostility of the immune system, in an effort to avoid potential autoimmune responses. However, during IR these immune buffering tactics are compromised; the adipose tissue shows reduced populations of these modulatory cells and the careful balance shifts towards the pro-inflammatory state (6).

Adipocytes increase demand but choke normal supply

At the same time, adipose tissue inflammation may also suppress the function of different lymphoid tissues elsewhere. Metabolic syndrome is associated with increased ectopic fat deposition in the bone marrow and thymus, areas that are critical for the generation and maturation of adaptive immune cells. This results in a less diverse population of T-cells, effectively restricting the range of invading pathogens to which our immune system can respond (7). So while the adipose tissue summons increasing numbers of pro-inflammatory leukocytes, it limits resources elsewhere, impairing normal immune surveillance. This may go some way to explaining why obesity and insulin resistant folks suffer more from common infections and respond less successfully to vaccinations (8). The hormone and lipid profile typical of IR will only make this situation worse: diminished responsiveness to insulin prevents the differentiation of anti-inflammatory T-helper cells (9); HDL is decreased, which normally neutralizes bacterial lipopolysaccharide; while elevated leptin and reduced adiponectin prevents appropriate modulation of the immune system (10, 11).

A self-reinforcing loop towards autoimmunity?

Aside from a hypervigilant immune system, autoimmunity is normally also characterized by autoantibodies directed at self-antigens i.e. elements of our own tissues. Not only do B lymphocytes directly activate pro-inflammatory T cells during IR, they can indeed produce pathogenic antibodies to certain host cell proteins. Screening of obese subjects has shown that IR is associated with a distinct circulating autoantibody profile, with some of the most abundant antigen targets being proteins in the Golgi apparatus or glial fibrillary proteins (12). It’s concerning that the bulk of these targets are intracellular proteins ubiquitously expressed in all manner of tissues, such as the nervous system, pancreas, liver, muscle and fat. It seems plausible that adipocyte cell death could initially release antigenic proteins that not only trigger an autoimmune response at the site of the adipose tissue, but also prime the adaptive immune system to eventually recognize those same proteins in other organs. Alternatively, these antigens may simply already be present due to other tissue inflammation and cell death, potentially in response to hyperglycemia or ectopic lipid deposition. Some of the most frequently detected autoantibodies in type 2 diabetic subjects are those directed at the pancreatic beta cells, which may be predictive of future beta cell burnout (13). These cells seem to be particularly vulnerable to hyperinsulinemia, lipotoxicity and inflammation, which is often occurring long before a standard diagnosis of type 2 diabetes (based on blood glucose) is ever made.

Inflammation inside and out

Admittedly, the chronic inflammation is being viewed here from an “inside-out” perspective, i.e. insulin resistance within the adipose tissue that then triggers metabolic and immune dysregulation in the periphery. It’s worth noting, however, that this downward spiral of IR may be sparked and/or perpetuated by more of an “outside-in” process, namely gut dysbiosis. The presence of intestinal permeability and altered gut microbiota can be observed in obese subjects, which opens the door to foreign particles that can induce an immune response and contribute directly to adipose tissue inflammation (14, 15, 16). For those folks who are metabolically very sick, it’s quite possible that both these mechanisms are at play. This 1-2 punch would see over-filled adipose stores switching on insulin resistance and heavily recruiting innate and adaptive immune cells, only to be joined by antigenic material that breaches a leaky gut during the continued ingestion of an inflammatory diet.


(1)    Heinonen et al. Adipocyte morphology and implications for metabolic derangements in acquired obesity. Int J Obes (Lond). 2014 Nov;38(11):1423-31.

(2)    Klӧting et al. Insulin-sensitive obesity. Am J Physiol Endocrinol Metab. 2010 Sep;299(3):E506-15.

(3)    Tripathi et al. Obesity and endoplasmic reticulum stress. Front Immunol. 2012; 3: 240.

(4)    Nishimura et al. CD8+ effector T cells contribute to macrophage recruitment and adipose tissue inflammation in obesity. Nat Med. 2009 Aug;15(8):914-20.

(5)    McLaughlin et al. T-Cell Profile in Adipose Tissue is Associated with Insulin Resistance and Systemic Inflammation in Humans. Arterioscler Thromb Vasc Biol. 2014 Dec; 34(12): 2637–2643.

(6)    Feuerer et al. Lean, but not obese, fat is enriched for a unique population of regulatory T cells that affect metabolic parameters. Nat Med. 2009 Aug;15(8):930-9. doi: 10.1038/nm.2002.

(7)    Andersen et al. Impact of Obesity and Metabolic Syndrome on Immunity. Adv Nutr. 2016 Jan 15;7(1):66-75.

(8)    Painter et al. The weight of obesity on the human immune response to vaccination. Vaccine. 2015 Aug 26; 33(36): 4422–4429.

(9)    Viardot et al. Potential antiinflammatory role of insulin via the preferential polarization of effector T cells toward a T helper 2 phenotype. Endocrinology. 2007 Jan;148(1):346-53.

(10) Loffreda et al. Leptin regulates proinflammatory immune responses. FASEB J. 1998 Jan;12(1):57-65.

(11) Tsang et al. Novel immunomodulatory effects of adiponectin on dendritic cell functions. Int Immunopharmacol. 2011 May;11(5):604-9.

(12) Winer et al. B cells promote insulin resistance through modulation of T cells and production of pathogenic IgG antibodies. Nat Med. 2011 May;17(5):610-7.

(13) Turner et al. UKPDS 25: autoantibodies to islet-cell cytoplasm and glutamic acid decarboxylase for prediction of insulin requirement in type 2 diabetes. UK Prospective Diabetes Study Group. Lancet. 1997 Nov 1;350(9087):1288-93.

(14) Veilleux et al. Altered intestinal functions and increased local inflammation in insulin-resistant obese subjects: a gene-expression profile analysis. BMC Gastroenterol. 2015 Sep 16;15:119.

(15) Sato et al. Gut Dysbiosis and Detection of “Live Gut Bacteria” in Blood of Japanese Patients With Type 2 Diabetes. Diabetes Care. 2014 Aug;37(8):2343-50.

(16) Tsai et al. Are obesity-related insulin resistance and type 2 diabetes autoimmune diseases? Diabetes 2015 Jun;64(6):1886-97.

The Empire Strikes Back. Low-Carb & Keto Attacked by...Advertising People?

I received a most excellent cook book from my friend Patricia Daly last year "The Ketogenic Kitchen". It had delicious and nutritious low-carb recipes by the dozen. It also gave a very good overview of the emerging science behind low carb / keto as a healthy and highly nutrient-dense lifestyle. Probably even more so for people suffering from afflictions such as cancer. Low carb would make a lot of sense here - for example see this clip from head of cancer research facility Sloane Kettering Memorial:

So what's the problem? Well apparently some are not happy with sharing scientific progress in interesting new areas. And an advertising agency is taking upon itself the significant task of decoding complex metabolic science. Have a look at this latest shenanigans and judge for yourself - link below:


For a good overview of keto and cancer from real experts, see my interviews with Dominic D'Agostino PhD and Angela Poff PhD below - very balanced I thought:

Aseem Malhotra on SKY News - Some real Root Causes of Heart Disease :-)

Aseem Malhotra getting the message out again on SKY News - we've been hoodwinked for generations. Time to redress the balance....!

The recent paper published by Aseem et al here: http://bjsm.bmj.com/content/early/2017/03/31/bjsports-2016-097285

Even the Oirish media are covering it... :-)  http://www.thejournal.ie/saturated-fat-study-medical-journal-3358588-Apr2017/?utm_source=shortlink

Fat Emperor at Weston Price Limerick - a Root Cause Talk #cholesterol #diabetes

Had a great time a few weeks ago at Weston Price Munster event in Limerick, Ireland (www.wapfmunster.com/). Amazing crowd of smart people there - all learning about how a return to "wise traditions" could transform the health of the nation. And the world of course. Big thanks to Anne Maher and the team (Brendan, Deirdre et al) for inviting me down ! Thanks also to Fergal and the guys at Curragh Sound and Vision Studios for recording & expediting the video file to me... www.csvslimerick.com :-) 

In this talk there is some new material, particularly in the first 20 minutes. For the first time at a public forum I share the story of how I got into the health arena. What do YOU know about the blood markers serum ferritin and GGT? Probably about as much as I did in early 2013. If so, prepare to learn a whole lot more....

Supported by www.IHDA.ie - for heart attack prevention awareness

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Here's me, Anne Maher and the team afterwards on the hallowed turf of Thomond Park (Sam Feltham dropped in from the UK too...!)

Atherosclerosis and Calcification - Important Paper to Review !

I've posted before on some complicated concepts around atherosclerosis progression and calcification. This one is certainly not populist pap for everyone, but crucial for those who wish to understand the deeper mechanisms. Today's paper is from Dr. Scott Murray, a research cardiologist currently operating out of Royal Liverpool University Hospital (the paper is down bottom of the post, after some of my preamble).

First here is a blog post of Scott's which gives an introduction to the value of calcification:  http://www.invasivecardiology.com/blog/Vascular-Calcification-Friend-or-Foe

Here is another post which highlights the problem of assuming we know the mechanisms underlying acute coronary events:  http://www.invasivecardiology.com/blog/unveiling-evanescent-chameleon-%E2%80%94-true-risk-coronary-plaque-can-only-be-determined-prospectively

However, the primary paper for atherosclerosis and plaque property insight is linked at the end. It greatly improved my understanding of what is really happening in "vulnerable plaque". And how calcification metrics play into it. Scott and the team used vascular ultrasound to scrutinize the plaque properties in detail. They then created new mathematical constructs to quantify "vulnerability level" of the plaque. To say that it resonates with me is an understatement. Also, it explains why the "density versus volume" part of the CAC score (from a simple CT scan) can be so important to analyse.

To grossly simplify, a person who has high density for a given plaque volume in the CAC, would likely on average get a desirable score in Scott's modeled variables of vulnerability. They would likely have a higher plaque calcification equipoise (PCE) and a lower calcified interface area (CIA) in general. Thus Scott's work may bridge the local mechanistic physics of vulnerable plaque, to the prognostic power of the CAC score - especially when the latter is examined for the interplay of both density and volume.

Confused? That's ok - read the below paper again, and link the insights to what I've discussed before here:   http://www.thefatemperor.com/blog/2017/3/3/dr-mike-eades-important-note-on-calcification-volume-vs-density-cac .

Really confused? Don't worry - just ping Scott, Mike Eades, Jeff Gerber or Gearoid O'Laoi - and they'll explain it all to you ! But first internalise Scott's fascinating paper at the link below !!

Site-specific intravascular ultrasound analysis of remodelling index and calcified necrosis patterns reveals... 

Gallup Strengthsfinder - A seminar to help you identify your strengths ;-)

And now for something completely different. It's true that #LCHF, fasting and good nutrition will enhance your overall and indeed career performance. But there are other tools too. If you are interested in maximizing your personal strengths, here's a seminar I gave recently on the topic. Gallup Strengthsfinder is a powerful tool. You can take the survey and access some excellent analysis at:  https://www.gallupstrengthscenter.com/
Over 15 million people have taken part. I highly recommend it for personal self-awareness - and career optimization !
Note 1: I have no connection to Gallup, and no financial interest in this matter. I may however be available to give similar seminars, if the incentive was appropriate...  :-)  Note 2: The sound is poor for the audience inputs - didn't have a dedicated mic... :-(

Ireland National Wellbeing Day 31st March - what are they telling us? #LCHF?

Ok you couldn't make it up. So I didn't. National Workplace Wellbeing Day arrives on March 31st. What will stem the enormous tide of diabetic dysfunction based on previous dietary advice? Well let's take a look. 

Document can be downloaded here:  HEALTHY KIDS DIETARY GUIDE

Some excerpts below. Carb-up with insulinogenic Holegrains? and decimate the healthy evolutionary fats in our diet? Perfect fuel to prime the pump...for a metabolic syndrome future. The pyramid first - as for the past 40 years, so it continues:

...and it appears that our children have transmuted into little horses:

...looks like they are certainly not a species descended directly and proximately from hunter-gatherer tribes:

Just in case you inexplicably didn't get the main message:

For correctly interpreted science updates, subscribe for free at:


Fat Emperor and Weston Price's Anne Maher on Limerick 95FM Radio #LCHF

Nice little chat this morning on Limerick's finest radio station - myself and Anne covered ancestral foods, what to eat, what NOT to eat - and a few more interesting things. I'll be speaking at this year's Weston Price event at the weekend with many others - Oirish peeps would do well to come along! The interview:


The upcoming event - get in there! : https://wapfmunster.com/

The interview here also in case above link doesn't work across the world:

Fat Emperor Limerick 95FM

Cardiovascular Discussion - and Debate - in London October 2017 #LCHF

A most interesting and prestigious event will be taking place in London later in the year. It is being run by the British Association for Cardiovascular Prevention and Rehabilitation (BACPR). Welcome will be cardiologists, doctors, nurses, nutritionists and even knowledgeable members of the public. Link below:


Interestingly, a debate has also been mooted, relating to some element of cardiovascular or obesity treatment controversy.

The "Pro" side will have representation from the UK's medical establishment. And it appears that the "Con" side has also been chosen I believe. This person would want to be sure of the science, if going against the accepted orthodox approach. That would be a minimum requirement, wouldn't it?

I wonder who this person might be?

The 2017 conference sessions will include many fantastic speakers, some of whom will be familiar to many LCHF people across the world:

·         Dr Aseem Malhotra: Choosing Wisely

·         Dr David Unwin: Revolutionizing Diabetes Care

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Supported by www.IHDA.ie - the Irish source for crucial information...on identifying Heart Disease early enough to prevent Heart Attacks

Excellent Metabolic Science Podcasts from Gabor Erdosi and Raphi Sirt #Diabetes

UPDATE 12th March: Episodes 2 to 6 now released!






Gabor Erdosi has a masters in molecular biology. Raphi Sirt is also a biochemistry graduate. Importantly, they are expert problem-solvers, with engineering brains. They can decode the complexity - and get to the inner workings of the human machine: Diabetes. Fatty Acid and Glucose metabolism. Insulin Resistance and Hyperinsulinemia. And the rest.

Warning: these podcasts are superb discussions, each centring on a particular scientific study of great interest. But in fairness they are not really intended for the layperson. However, they are excellent for the more biochemically-versed individuals - who wish to understand how it REALLY works ! Chat to them by joining the Lower Insulin Facebook group:  https://www.facebook.com/lowerinsulin/

...and don't forget to subscribe to www.thefatemperor.com/subscribe !

Please access these and more excellent podcasts by clicking below image:

The RCT's said PUFA was NOT better than SAT Fat. And so they buried the results...

Polyunsaturated oils lower your "cholesterol" - true. And this supposedly should lower your heart disease and death rate? Oops - false. Rather embarrassing for the defenders of the risible Diet-Heart Hypothesis.

And the early Randomized Control Trials (RCT's) that showed up this sweaty naked "cholesterol" emperor for what he really was? They disproved the rsilly hypothesis. So they had to bury the results, didn't they. How naughty - even before they could think up a reason for the failure. Lies of omission, lots of them.

The morons of course then retreated into the grossly misleading epidemiological junk-science. We've seen mountains of this stinking manure, desperately propping up a rubbish hypothesis. These nefarious efforts have doomed the population to continued ingestion of the revolting seed-oils. Have they no shame? Have a read of this 2016 article here, which summarizes the debacle (click the image below for paper): 

Subscribe to www.thefatemperor.com/subscribe - for real science, not fake epidemiological claptrap.

Oh, and below is the master Masterjohn on the topic: