The Big Fat Fix features on Sky News no less...!

Nice interview on Sky News with Dr. Aseem Malhotra - now that's what I call primetime... :-)

Download and watch The Big Fat Fix today at - time running out for special price. The movie is visually sumptuous, whilst containing many of the key elements to avoid Heart Disease, Obesity and Diabetes. It also explains how that fella Ancel Keyes got things pretty screwed up. So many delicious foods you can observe and enjoy yourself, improving your health all the whiles. Watch it with your family...and you can all avoid that premature call from the reaper ! :-)

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Diabetes, Obesity and Heart Disease - let's talk LIVER !

Fat Emperor and his present wife have lunch in the Royal College of General Practitioners, London. Dr. David Unwin is their learned guest - along with Sam Feltham, head of the UK's Public Health Collaboration ( Primarily discussed is the pivotal nature of that crucial organ - the Liver. The Rosetta Stone of modern chronic disease, if you will. Oh, and we just coined the term CFLD (Carbohydrate Fatty Liver Disease) - remember that you heard it here first !!!

Also don't forget to download and watch (only £5 for 72 hours this weekend). A just-released classic, which entertainingly covers many home truths about heart disease risk... :-)

Note: go to - for the hard facts on cardiovascular disease identification !

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Sam Feltham with Fat Emperor in London ! #LCHF

Firstly, get to and download the new movie !

After the premiere of same, I got to 'Smash it Out' with Sam Feltham in London. We had a great chat on the dismal failure of existing dietary guidelines. And revealed the science-based ones you can download at Better still, £4 will get you a professionally bound copy through Amazon: ...and don't forget to buy one for your doctor too !

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Note: go to - for the hard facts on cardiovascular disease identification !

Dr David Unwin - at The Big Fat Fix premiere event London :-)

I finally got to meet Dr. David Unwin - and in the Houses of Parliament, no less! Don't forget to download and watch the just-premiered movie here - not only super entertainment, it'llclarify a lot of what Dr. Unwin is fighting for: 

For those of you who don't know, David has been pioneering the use of dietary interventions to treat/reverse diabetes and obesity in recent years. He is a key member of Sam Feltham's Public Health Collaboration ( ). These intrepid doctors and scientists are championing science-based food guidelines for the UK - and not a moment too late.
I have long admired David's work - especially as he explored the crucial nature of Liver biomarkers in tracking chronic disease risk. That's where I started my journey of discovery too!

He is also a rare gem in that he identified the liver enzyme GGT as a key marker for carb-induced fatty liver dysfunction (gamma glutamyl transferase). You may have heard me going on about GGT many times in the past! Most doctors only view GGT in the context of excessive alcohol intake. Big mistake. Rather it is an excellent marker for carb-sugar-induced liver dysfunction. (see also ). GGT is thus an excellent marker for overall mortality risk. It, like many other genuinely key biomarkers, makes a farce of the 'cholesterol capers'. In our brief interview here, David talks about the patient experiences that led him on his journey of discovery (one of his published papers: 2015 David Unwin - A Pilot Study Carbohydrate GGT HbA1c )

Go Dr. Unwin!

Note: go to - for the hard facts on cardiovascular disease identification !

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Wanna know how to collapse your heart disease risk? Ok then - you got it.

My recent talk at a large gathering of ambulance staff and paramedics in Dublin. Some new slides, new studies - and a rather special 'patient story' I recently dealt with. Wanna know how to address the root causes of Cardiovascular Disease? OK, you got it.   Please subscribe at - always free content - always !

Note: go to - for the hard facts on cardiovascular disease identification !

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A MUST-WATCH: The Big Fat Fix movie is nearly here !

Following the first two excellent Cereal Killers movies, we are about to see the big enchilada. Number three from Donal O'Neill will be very special - and not just because Aseem Malhotra is the leading man !

The Big Fat Fix will explore the real root causes of heart disease. And yes, your dietary choices will play a BIG role - in deciding who goes down with the big one.

A certain member of petty (adipose?) royalty happens to be an associate producer of this fine production - and will be attending the premieres in London and New York. Of course I'll report back on the shenanigans that Donal and Aseem get up to there...

Click below to see details - and get to watch the Cereal Killers 2 movie for free !

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Note: Go to - for the hard facts on cardiovascular disease identification !

Recent Study on Fat Metabolism Behaviour of Brain Cancer? Clarification.

Ok I got a lot of queries about Fat driving Glioma-type brain cancers. Example:

As always, the fat implicated in cancer will be omega 6 oils (see my previous posts). Anyway, I held my counsel and waited for Andrew Scarborough to do a piece on it. He has. I'll leave it at that for the moment, except for one thing. The press releases for these studies are more interesting for what they DON'T say, rather than what they do. Click on pic below for Andrew's post:

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The Power of Calcium Score. Because it SEES the Disease.

Ok not much text here - hopefully the diagram is self-explanatory. Pretty much nothing touches CAC. The only questions is how often you need to do it. To keep safe.

Yep - CAC is the way to assess your atherosclerotic burden, and whether the cliff is near. Period.

Yep - CAC is the way to assess your atherosclerotic burden, and whether the cliff is near. Period.

And want to see a sample of the raw reality? Sure why not - the mathematics speaks:

Go figure....but if you like seeing the data, please subscribe for free to !

Go figure....but if you like seeing the data, please subscribe for free to !

#Atherosclerosis High Level Root Cause. The ApoB/LDLp Question.

Before we start, if you want to help move the science forward, please subscribe for free to ! That said, let's get on with it:

Been a bit of fun lately on the old web, what with talk of native, non-damaged LDLp's burrowing into a single-cell endothelium's and wreaking havoc with the help of our native immune system. Well it's an easy-to-grasp theory, I gotta hand it that. Let's take a look at the options, shall we?

We'll start with the established Insulin Resistance-centric driver for CVD. I haven't included everything in this schematic, but most of the big boys are at the party:

The common-or garden Insulin Resistance / Fatty Liver / Dyslipedemia / Met Syn Riff...

The common-or garden Insulin Resistance / Fatty Liver / Dyslipedemia / Met Syn Riff...

Ok, so not outrageously controversial I think, although there's more to it. But what are the <actionable> ROOT CAUSES of this nasty, self-reinforcing destructive feedback loopery? That's what we'd want to avoid - right? After all, we can't replace all our internal machinery - but we can certainly maintain it optimally (for a long service life ...). Let's take a look:

Now (in white) we see some things we can actually DO to help avoid the reaper...

Now (in white) we see some things we can actually DO to help avoid the reaper...

That's a bit better. Almost feeling empowered to make a difference here. Bet if I did all those white things right, we'd see some bloods getting way better - yep, think so. But wait - this selection of addressable root causes don't just address IR etc. In fact, this set has many connections to CVD that don't necessarily have IR as an intermediate deleterious process. So let's represent that here - in column of calamity down the left hand side:

Ah, there we are. The addressable root causes do more than just the old IR riff...!

Ah, there we are. The addressable root causes do more than just the old IR riff...!

Mmmnn...still not happy. LDLp/ApoB seems kinda...underemphasised here. I mean, it's VERY popular. We almost seem to imply here that its badness is only because it tracks with the IR / inflammatory milieu. it's not independently toxic. Ok then - let's give it a special seat at the root cause table. In yellow down the bottom left:

'Native/undamaged' LDLp / ApoB particles get their own special root-cause-driver status ! :-)

'Native/undamaged' LDLp / ApoB particles get their own special root-cause-driver status ! :-)

Mmmnn again. I think it's only fair to clarify the logic here though. You see, IR is a huge driver generally of high ApoB particle numbers - so the much-lauded correlation between ApoB and poor outcomes...could be mainly due to this aspect. Tricky that. Even after decades of research, I don't think there's any data available that tracks ApoB outcomes - specifically when all the other metrics are great. Isn't that weird? Oh well - I guess nobody cared enough to look. So let's break out the two routes to ApoB's being bad. A - Through oxidative damage etc. of the particles, and the strong associations with the other root causes that drive ApoB high. And then B - through ApoB particles just being inherently toxic when there's lots of 'em:

There. Separated those critters. ApoB is now a 'Janus' Lipoprotein !

There. Separated those critters. ApoB is now a 'Janus' Lipoprotein !

Just one last thing. We need to take a quick look at the relative importance of each face of ApoB particles. Let's look a 'A' first - ApoB's simply caught up as 'substrate' in the inflammatory milieu, partaking in the damage-fest....because many other bad things are raging throughout your system:

Ok, lot going on in this CVD-driving scenario - including ApoB interacting in the mess...

Ok, lot going on in this CVD-driving scenario - including ApoB interacting in the mess...

We'll close with the other popular theory. That even without all the multifactorial mayhem of the above (or even the 'OTHER' drivers on the bottom right) - ApoB particles are innately, inherently, natively toxic. Mainly when there's more of them (remember simply more of them - it's cheating to blame ApoB if the 'more of them' or 'toxicity of them' is driven by another underlying problem). How would we depict this scenario in our final slide? Well how about this way: 

The 'ApoB is independently toxic' slide. That's all folks !

The 'ApoB is independently toxic' slide. That's all folks !

Well there we have it. Something seems not quite right, but I can't put my finger on it. Maybe it's getting my head around an evolutionarily selected physiologic component being inherently damaging? And remember, we are talking about this in the absence of something driving it to be so. If 'X' is driving the ApoB particles to be a problem - then 'X' is the root cause, not ApoB itself. We've just shown a big cluster of X's in that penultimate slide.

Dr. Steve Horvitz suggested two ideas: (a) that sustained high ApoB may in turn drive IR-milieu through other paths, thus making it self a problem - but this would not simply be 'ApoB hi is bad because it tunnels in the endo' - still it would make 'hi ApoB' a cause along the top row of white elements. So lowering it for this reason could help I guess?  Also (b) Receptor issues in genetic hyperlipidemia could be interactive/coupled with insulin system - hence conflating the two as cause of problems. This one I've mused on before, and is appealing. I'll add another one (c) that comes to mind (again for genetic receptor issues in say FH) - if receptors screwed then ApoB gets long residence time, exposing it to deleterious modification - here again it is damage to ApoB rather then simply 'ApoB bad because of tunneling'...

I can imagine a fusillade of irate replies, but I'll only answer one in advance. People may say "oh but in people with genetic glitch causing super-low ApoB, there is much lower heart disease". Quite. But ApoB is a part of the system, and stripping it right down may prevent the deleterious multiple CVD drivers from causing the usual level of damage. If you took all the fuel out of an aircraft, I dare say in a crash landing it would burn up the passengers less. But the kerosene still didn't cause the crash. And also there are plenty of studies where ApoB doesn't show up much - and plenty where ApoB/ApoA1 blows it away.

I often muse about high ApoB peeps (high risk?)  whose ApoB/ApoA1 -  a stronger marker - reflects low risk? Are they indeed low risk? I would say yes - go with the stronger marker. But...then their high ApoB was a very misleading marker indeed. Here is a report from Gabor Erdosi just now - consider it very CAREFULLY - consider the relative hazard ratios. Consider. Think on it before you run after ApoB willy-nilly:

Here's another from the Women's Health Study - on the right hand side I've taken out the log scale for a simpler compare - would you believe a high ApoB here (saying a person is at risk), when their ApoB/ApoA1 says the person is ok?

ApoB/ApoA1 encompasses so much more about the person's physiology and risk level...

ApoB/ApoA1 encompasses so much more about the person's physiology and risk level...

Of course, if something is causing your ApoB to be an issue, and you're not confident you can resolve this - well then it may be the best route to lower it anyway. But the general question stands, and should be answered. It must be answered. Or we are not doing ourselves justice at all. Here's my go-to post for those that are worried regardless - can play with ApoB levels nutritionally like Franziska did:

Great Discussion here also btw, in Peter's post and the comments following it:

And here is the fascinating piece of detective work, with Subbotin's paper linked at the end of this post:

p.s. the dogs in the street know that LDLc is a near-useless biomarker at this stage, so I don't even bother including it. Still, it dominated for decades (and still dominates) the orthodox world of CVD root cause. Funny old world that, isn't it? Wonder if ApoB turned out to be just an interacting component in CVD...would it still be seen as a primary cause...for decades more?

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Tim Noakes Short - by Low Carb USA San Diego. Changing the world...! #LCHF

Excellent short discussion here between Tim and Doug Reynolds of Low Carb USA. Touching on the core of our global health issues. And the solutions. Doug is attempting to gather forces from all the LCHF people around the world. About time I might say...  :-)

"Call us Legion, for we are many..." Mark 5:9 :-)

For those who know the background, I've linked to where the discussion really hits on path forward. My canny NY lawyer friend Antonio Martinez gets a mention too - he's gonna sort some of this sh"t out !

Everyone who can should be going to San Diego on the 29th July - history in the making...

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Eating more Pasta makes you SLIMMER ! Who are these guys? #LCHF

Oh God. Latest internet messing is this study, sent on to me by a few questioners. I don't have time to analyse these epidemiological bits of bias-fluff. What the hell though - I had a very quick look. Here is the study news bulletin:

Here's the epi-junk study itself:

Here's my 3-minute look at it:

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#ATHEROSCLEROSIS ILLUMINATED. Time to Progress. Even the Pigs Are.

UPDATE 7th July: The learned Peter Dobromylskyj of Hyperlipid has posted on this fascinating subject - ignore the cholesterol goons and get some education here :-)                            

What constitutes a valid, actionable 'Root Cause'? I have my definition, been good for over 25 years of problem-solving:

"When an Issue manifests itself, Root Cause is the interplay between (A) The most direct modifiable driver of the issue (usually situated early  in the root cause chain diagram), and (B) the most addressable factor to achieve acceptable solution (usually it will be the factor/input that has actually shifted and driven the problem itself"

  There may be multiple coincident factors that are implicated as worthy of Root Cause status by the way - especially in the nasty multi-factor issues. And Atherosclerosis is certainly one of those. Of course interaction and synergy is extremely important to decode - some 'causes' are only relevant when other real/driving ones are present - gotta tackle the latter.

I am happy with the dominant probable root causes of Atherosclerosis. These are excessive carbohydrate/sugar (Inflammatory/IR/multiple), low Sun/VitD (Inflammatory/IR/multiple), Low Omega3:6 ratio (Inflammatory/IR/multiple - esp. filthy veg oils), low Magnesium(multiple), bad sleep/stress (glycaemic/insulin/IR), low K2/C and a few other vitamins (multiple). Insulin Resistance is a no-brainer, hence the 'IR' thrown regularly in there. But I'm still more interested in what key factors gave you the IR of course(!). The pareto principle is useful here - focus on the 20% of factors that likely cause 80% of your issues. Why didn't I mention Gut Microbiome? Well until proven otherwise, I think it is often a outcome of the preceding RC list, which then in turn causes knock-on issues by all means. Why didn't I mention ApoB particles in the list? Well because they wouldn't meet my definition of root cause, would they? ApoB particles are physiologic - they are normal to have, almost regardless of their quantity. Of course if they were damaged ... or elevated due to a real 'root cause' (read IR etc.), then they get warmer. But even here they would be too far down the root cause chain for my liking - they would also be 'knock-on' drivers...

So, what have we got for you today? Well thanks to George Henderson,  a rather fascinating atherosclerosis experiment just published - that's what. ( ). And the effect-size seen was, well - impressive to say the least. These guys were not caught up in ApoB - they were switching on and off a real root cause - and it seems to have paid off. They gave very little Vitamin D to some pigs, and adequate amounts to others. They fed them all a horror-show junkfood diet to accelerate atherosclerosis, then killed them all after a year or so. (Diet of course had high sugar and chocolate etc. - they know what blows up IR & atherosclerotic fires). What did they see? Well get a load of this: 

Note that 'cholesterol' again shows itself up as the correlational junk science that it is. But let's look at an excerpt of their conclusions (my emphasis included). This is VERY interesting:

“Studies have shown that the administration of inflammatory mediators outside the arterial adventitia leads to immune cell invasion, increases in intimal thickness, and arterial remodeling (40,41) and increased coronary vasa vasorum neovascularization PRECEDES endothelial dysfunction in swine fed a high-cholesterol diet (42,43). These data suggest that local adipokines from EAT could diffuse into interstitial fluid across the adventitia into the vascular wall by paracrine factors or be directly transported into downstream coronary arteries by vasocrine factors (i.e. via the vasa vasorum). This hypothesis supports a notion of outside to inside signaling of atherosclerosis, in which the inflammatory milieu in EAT promotes the development and progression of CAD. Recently, in atherosclerotic swine, McKenney et al11 clearly showed that EAT excision attenuated the progression of CAD, but their observation did not have a clear mechanistic link. Here, we provide critical data on EAT signaling mechanisms underlying CAD.”

Interesting indeedy. Time is brief here so I'll give my top-level takeaways:

1. Vitamin D deficiency seems to has a dramatic effect on Atherosclerosis progression, like a 'root cause' should if it is valid (I have some quibbles that their diets do not seem to be identical outside of the D factor though)

2. They clearly provide support for Subbotin's hypothesis of vasa vasorum being pivotal in atherosclerosis progression - and add other 'outside-in' mechanisms of acceleration from the external surface of the arteries (i.e. NOT the endothelial-ingress concentration gradient stuff that many of us have struggled with)

3. They leave ApoB out of the discussion - fair enough. It's not a 'root cause' that can be changed in magnitude to assess its contribution. In it's native (non-damaged) self It's not really a 'cause' as such by my definition - even though it has mechs in the athero game, and it is supported by much 'correlational' data (although much of this correlation was likely gifted by the insulin resistance which drives both it and athero acceleration up together - sneaky stuff - see:

I'll also direct interested parties to this post, for further ruminations on ApoB as a 'cause'. Real 'causes' stand up to case-control and other scrutiny - but correlational ones don't:

...and of course an overview of Subbotin's atherosclerosis mechanisms paper - I am still waiting for anyone to give a reason or two why Subbotin may be incorrect. After this pig study, the reasons would want to be pretty solid indeed...

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LDLp and Lp(a) Black Swan Scenarios - got any more out there? #Cholesterol #Insulin

A few people have been sending me queries recently about ApoB - the so-called 'master-risk metric' from the NMR test. We must question whether high ApoB is a problem in its own right. If ApoB is above 'ideal' - should one strive to lower it regardless? Should we attempt to lower it...'blindly'?  Do we really believe that the Low Density Lipoproteins are inherently toxic to our bodies, regardless of the conditions in which they function? there a concern only when the ApoB particles have actually become compromised; for example, oxidised? Biq question that. Huge question in fact. Luckily there are a suite of measurements that may exonerate the high ApoB in any given case. But these don't seem to exert a hypnotic effect on the experts like ApoB does. Strange that - why place so much focus on ApoB as massively malign?

Well, here are a few links that question the universal evil of ApoB. We must ask has it EARNED it's broad-brush demonic status. Or is it yet nother associational interactor, problematic only when far more important causal issues. Should it never be judged alone, in other words? Anyway, here's a sample of the ApoB black flock to ponder on:

Another thing I find quite shocking is the practice of looking at ApoB, without a simultaneous focus on ApoA1. How on earth can one be used for risk...without considering the other?? First take a quick look at this study pic (Women's Health). On the right I've changed it from log scale to linear for clarity. Wow - ApoB on its own is kinda weak here, compared to other (better) measures. And many people who would appear high risk looking at APoB alone, would be low risk looking at their ApoB/ApoA1. So much for ApoB - major bum steer, eh? (some posts below addressing this also):

Finally, "say hello to my leetle friend"....El Pee Little Ay ( Lp(a) ). Apparently not such a clear-cut pantomime villain. It looks like high Lp(a)....just means you have to be even more careful to follow the  LCHF/D/w3/w6/Mg/K2 prescription. Is all. :

So it appears to me that a lot of support for ApoB and Lp(a) has been inherently associational. Sure, an enormous edifice of mechanistic discussion has been built to support them as universal bad-actors (especially the old ApoB). And sure they partake in key roles within CHD. But the black swans will have their say. Good hypotheses should be borne out in Case Control study outcomes. Failures like these demand revisiting the hypothesis. Especially when there are so many interactions, so many more causal drivers of greater importance. So how big is ApoB as a risk, IN AND OF ITSELF?  Without correcting for HDL/ApoA1/Insulin/glucose etc. etc.?

Well I for one wouldn't waste too much time on it. Far bigger root-cause fish to fry.

In closing, if one must pick a single thing to fixate on for CVD (not a good idea btw) - I certainly wouldn't have it be ApoB.

For those who still worry (with all-round good metrics but naturally high LDLp), Franziska has great discussion here:

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Dietdoctor interview with Fat Emperor #LCHF #FattyLiver #GGT

My short interview with Andreas Eenfeldt, the Dietdoctor himself. Experience the best Low Carb Website here - everything you need for superior health and weight control:

"Can an engineer know more about how to get healthy than his doctor, in fact more than his three doctors? When it comes to using nutrition, the answer is yes. Meet Ivor Cummins, who quickly had to become an expert to cure himself. Ivor Cummins is a well-trained problem solver. When blood tests showed liver problems – the very common issue fatty liver – Ivor set out to find the solution to the problem. He soon found it. Soon he had lost lots of weight and his liver problems were totally gone. It all begged the question – why did an engineer quickly understand how to cure himself using nutrition, when none of his doctors could help him?

I interviewed Ivor Cummins recently and it’s a truly interesting and insightful story. The full interview has only been available on our member site, but now everyone can watch it. Enjoy – and feel free to share it.

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#ATHEROSCLEROSIS - Vladimir Subbotin is Back ! Must-read for Athero Afficionados

UPDATE 24th July - Just found this paper, looks like a must-read for those interested in emerging hypotheses of atherosclerosis: Subbotin Support Paper

Ok I did a quick blog post in 2014 after reading one of Vladimir's papers. Well he's back - and with expanded scope. I'll update this post later with my review, but I don't think you should have to wait ! Here it is:

2016 Vladimir Subbotin Paper - Mechanisms of Atherosclerosis beyond the dogma

Big thanks to Kelly Trosper, for drawing my attention to this delicious read :-)

My original post concerning Vladimir:

Note 1 - familiarity with existing proposed mechanisms of athero is kinda required...

Note 2 - If he's not entirely correct, he's certainly pointing out major flaws in the orthodox athero dogma !

Weblink to paper:

A Passion to Save Lives: David Bobbett speaks to the people. Inspiring !

"This is not a percentage game - death is an individual game." - David Bobbett, entrepreneur and business leader.

What would you do if presented with a devastating diagnosis? A diagnosis revealed with a powerful test, a test that can clearly identify the world's biggest killer - raging in your body? Finally, what would you do when you discover that this test has been available for 30 years, and could save millions of lives - but no-one really knows about it? Welcome to the world of Calcium Scanning and the CAC Score. Suppressed and underused for decades based on politics/economics, and millions of people lost.

This is David Bobbett's inspiring story, delivered with an rare passion to save people from premature cardiac death. He has dedicated his life to saving others. Hear his story. And I certainly don't always ask this but....please share like hell ! Also please for more compelling content - always for free...

01:15David's Intro
02:50David's Inspirational Story
18:21Ivor reads two sample letters from the Saved
22:26David's closing comments - and an entreaty to the people !

Recorded at the May 2016 Dublin Cardiovascular Event, DCU.

David's background story here:

The movie: and trailer vid:

Visit for more details...and did I ask people to PLEASE SHARE ? :-)

#LCHF in the USA: Coming up fast: The Big San Diego Event !

I'm gonna be lazy 'cause it's late - and steal Jeff Gerber's fb post ! :-)

"Hot off the press: Low Carb USA Asks "Is Our Government's Dietary Advice Making Us Fatter and Sicker?"

Super Speaker Lineup:

See latest press release here:

Everyone's invited to this first-of-its-kind event being ...held in the US, including the general public and the scientific community. For healthcare professionals, application for CME credit has been filed with the American Academy of Family Physicians (AAFP). Determination of credit is pending.

We're looking forward to seeing you in San Diego. Use discount code 'IVOR' to receive $100 off the registration fee. Registration and conference details: