Goodbye to Primalmeded

It is time. I have been putting this off for a while. You may (or may not) have noticed that Primalmeded has been in slumber for quite a while. After a year of big life changes, including moving countries, it is also time to move my digital home as well.

I have been incredibly humbled by the response I have received since the birth of this blog. I have created lifelong friendships and relationships. I have learned so much but also have become painfully aware of how much there is still to learn. It is a daunting never-ending task but some of us (stupidly) dive into this rabbit hole and never re-emerge.

Primalmeded was a good start. I will keep the posts available for a while still. I do not go back and edit my articles. It is tempting to correct all the old naive assumptions but that feels wrong. It’s like editing a journal. You cannot correct the past, make it shiny, and pretty, and error-free. Those flaws are precious in themselves, making life richer and more real. So if you are browsing through the archives, bear in mind that my thinking may have evolved since the time a particular post was written.

My new online home is shared with my partner Jamie. We have very different writing styles and, hopefully, this will make for some interesting reading. As usual, there will be no blatant self-promotion or advertising of any kind on that blog. The regular programming of musings, rants, science, and whatever else I am interested at any given time will continue.

See you at


I am so doomed

As the sunshine gets hotter on the Mid North Coast of NSW, Australia, we get more and more paranoid about it. I got a first hand experience of this paranoia this Monday morning when I showed up at work with my forearms pink from getting mildly burned (gasp!) while walking this weekend. Getting burned is something I diligently try to avoid but hey, it happens. Expecting a lecture on sun safety and attempting to avoid one, I wore a high neck top but my bare arms still showed the tell-tale signs of my weekend indiscretions. The practice nurse took one look, threw her hands in the air, did the tsk tsk tsk, demonstrated the sun damage on her legs while hysterically enumerating my future ails. My raised eyebrow did nothing to quell the outpouring of the well-wishing criticism: “These young people think they are invincible… Skin cancer… How could you… A smart doctor…”

Eventually we switched to the topic of her weekend which was marked by a birthday celebration. The nurse proudly announced that she “ate too much and drank too much” and is feeling decidedly sick this morning. It took all my willpower NOT to point out that a weekend of junk food and alcohol probably carries a higher risk burden to your health than a weekend of walking out in nature, even if accompanied by mild sunburn.

This incident really drives home how we see melanoma. We zero in on one risk factor (“it’s the Sun, stupid!”) and ignore all others. However, we seem to be a lot better at understanding that for other cancers a variety of genetic and environmental influences is at play.

Somehow I don’t think I will ever see this conversation:

– I had a lovely dinner last night: a delicious lamb roast and a glass of red wine.
– Oh my god, you should not have done that. Don’t you know that alcohol gives you breast cancer?
– But I just had one glass with dinner.
– Yeah, but alcohol is a risk factor for developing breast cancer.
– But surely, a risk factor is not the same thing as the cause.
– It totally is. It pretty much means that if you have alcohol you are a reckless ignorant individual willingly putting yourself in harm’s way.
– But I am aware of the risks and benefits of red wine consumption and I am also an adult. I think I can estimate my own risk and make a rational decision.
– No you can’t. Let me show you post mastectomy images to horrify you even further. These women had been thoughtless like you, exposing themselves to alcohol when they were young. And that’s how they got cancer.
– But aren’t there other risk factors?
– Don’t be ridiculous.
– Do I even know you?
– …..

Pretty sure somebody will get punch out in this scenario. But somehow it’s ok for total strangers to share their unasked opinion when it comes to melanoma. If you want to replicate this experience I recommend that you paint yourself red and then go to work, go shopping, go to a café or see your family. And note every time you get told off for your recklessness and your upcoming demise.



Following on from my previous post on the inanity of anti-sun public health campaigns, I wanted to discuss a few aspects of sunlight itself and pathophysiology of melanoma.

Here is the story so far:

– the relationship between sunlight and melanoma is complicated. Genes matter (your family history), your phenotype (skin and eye colour) can be a risk factor, but the environment also seems to play a large role.

– there is no linear relationship between exposure and melanoma. Zero exposure over a lifetime will probably guarantee no melanoma (I’ll leave it up to you if you would like to spend your life hidden inside because let’s face it, what could possibly go wrong?) But beyond that, the picture is sketchy. Less exposure does not mean less melanoma. Chronic UV exposure has been repeatedly shown to be protective.

– in spite of widespread and very successful health campaigns which focus on one single risk factor (sunlight) the incidence of melanoma is rising.

– while it is tempting to reduce exposure to minimum in an attempt to mitigate risk, the lack of sun exposure is a significant problem on its own. I won’t go into too much detail here, but vitamin D deficiency (which is estimated to affect 1/3 of Australians)  is only a part of the picture.

Sunlight is frequently referred to as some homogenous substance in the same way that all fat is apparently the same because each gram contains the same number of calories. However, just like lauric acid (a medium chain saturated fat) is processed in your body completely differently from palmitic (long chain saturated) or DHA (long chain omega-3), different wavelengths of solar spectrum have varying effects on our physiology.

UV radiation is only a part of solar spectrum, with wavelengths between those of X-rays and visible light. Its unique effect on biological systems stems from the ability of the photon  to break chemical bonds. UVR is further divided into UVA (the longest wavelength at 400 – 315 nm), UVB (315 – 280 nm) and UVC (280 – 100 nm). While the shorter wavelengths of UVC and UVB are most damaging to biological entities like human cells, they are also filtered by our ozone layer. In normal run of things UVC is completely blocked with none of it reaching the Earth’s surface. UVB is blocked partially with the rate of absorption proportional to the length the photon travels through the ozone layer. If you got a little lost in the last sentence here is the gist. If the sun was directly over your head and the sun rays were falling at 90 degrees to the surface of the Earth (this is considered Solar Zenith Angle of zero), photons would have to travel the shortest distance through the ozone layer and more UVB radiation would reach the surface. If the direction of the radiation is at 45 degrees to the surface, more ozone is encountered on the way and less UVB gets to the surface.

Ok, with maths out of the way let’s get to the nitty gritty of what is different between UVA and UVB.

skin penetrationWhile UVB is a stronger partner being able to cause direct damage to DNA, it is also the one that has less penetration. In fact, very little is able to penetrate down to the basal cell layer where melanocytes live.

UVAWhat is this “photoprotection” I am talking about? Amazingly enough, after millions of years under that yellow orb our bodies did not wait for the invention of sunscreens. Instead, we have evolved multiple ways to protect ourselves. Locally in the skin, there are two major mechanisms of photoprotection.

  1. Skin thickening. Sounds too simple to be effective but it does in fact work, especially in preventing UVB penetration. This effect is mediated most strongly by UVB itself and manifests in thickening of stratum corneum.
  2. Melanin production. Melanin is a substance produced by the melanocytes in the basal cell layer. It absorb UVR as it passes through the skin and prevents further damage. It is an excellent defender against both UVA and UVB rays. The initial DNA signal is required for the initiation of melanin production. Here is where the differences between UVA and UVB are most striking. Even though the tan produced by UVA and UVB looks identical, its origins are different. UVA does not increase total content of melanin in the skin, it just releases pre-made melanin from the melanocytes and oxidises it. UVB, on the other hand, stimulates melanin production.

So if you predominantly expose your skin to UVA rather than UVB you may be getting sun damage without the benefit of innate skin protection.

UVB used to get a lot of bad rap. And who could blame the scientists doing in vitro experiments and seeing DNA molecules unravel, the sequence misread, uncontrolled proliferation initiated – all in response to UVB. In fact, we have done everything we could to eliminate our exposure to UVB rays full stop. SPF rating of sunscreen applies to its ability to prevent erythema, aka burn. Therefore it reflects how much UVB it can block (UVB being the erythematogenic partner).

UVA remained under the radar for a while. Solariums used to be advertised as “safer than the sun” because UVA was predominantly used. Now UVA is coming more under suspicion for being the culprit behind melanoma. How to tease out which is which? For starters, scientists like to use some poor animals to prove their theories.

It is hard to believe but we haven’t got very decent animal models of melanoma. Well, there is this fish which got melanoma after being irradiated with UVA.

…an alternate action spectrum that is more heavily weighted to the longer wavelengths, including UVA and visible light, has been found in the platyfish-swordtail hybryd model of melanoma, which suggests that UVA is a much more potent inducer of melanoma, relative to UVB, than it is of tanning. The relevance of this animal model to human melanoma is uncertain but cannot be completely discounted because of its particular characteristics and phylogenetic distance; development of mammalian models will be particularly informative in this regard.
Weinstock (1996) Controversies in the Role of Sunlight in the Pathogenesis of Cutaneous Melanoma. Photochemistry and Photobiology, 63(4) 407

And there is this knockout mouse which got melanoma after being irradiated with UVB.

These data show that in this albino mouse model UVB is responsible for the induction of melanoma, whereas UVA is ineffective even at doses considered physiologically relevant.
Ha L. et al (2005) Animal Models of Melanoma. Journal of Investigative Dermatology Symposium Proceedings, 10, 86–88;

Go figure. I would not be relying on the evidence from a fish and a GMO mouse as yet. Give me some humans. Well, actually, you can infer some information on which wavelength initiated melanoma by looking at what mutations are associated with this cancer in humans. As you remember (scroll up to the graphic if you don’t), UVB causes CPD and 6-PP product formation. UVA is the initiator of free radical formation. After going through the known signature mutations in humans, Lund et al concluded:

Thus it can be seen that, although not yet incontrovertible, the available evidence points away from pyrimidine dimer formation by UVB and toward oxidative stress damage caused by longer wavelengths [UVA].
L.P. Lund, G.S. Timmins (2007) Melanoma, long wavelength ultraviolet and sunscreens: Controversies and potential resolutions. Pharmacology & Therapeutics, 114: 198–207 (my square brackets)

The As have it?

Another crucial component to add to the mix is Vitamin D. Without going to far into this massive topic, I will just mention that it is one of our main immunomodulators, both preventing DNA damage and initiating repair and/or apoptosis (programmed cell death) when necessary. Its active form, 1.25(OH)2D, is protective against UVR-induced photocarcinogenesis. In diagnosed melanoma, Vitamin D levels and pre-cancer skin exposure are predictive of survival. Not forgetting that UVA does not lead to vitamin D synthesis. In fact, it can break it down when it is attached to the vitamin D receptor (VDR). You need UVB in order to synthesise Vitamin D in your skin.

So here you go. When it comes to sunlight, things are not always what they seem. Focusing our full attention to blocking ALL sunlight to protect ourselves, we may have unwittingly increased our UVA to UVB ratio.

UVA and UVB imbalance is a neat hypothesis. It resolves some of the apparent paradoxes relating to sunlight and melanoma, the paradoxes that conventional wisdom desperately tries to ignore.

To summarise: what are the effects of receiving too much UVA and not enough UVB?

  • Reduced propensity to sunburn
  • Reduced melanin production – > reduced photoprotection
  • Reduced Vitamin D production
  • Increased Vitamin D breakdown

And how to you ensure you upset this balance in favour of UVA?

  1. Wear sunscreen that predominantly filters UVB
  2. Consequently stay out in the sun too long because your sunscreen prevents you from burning so you continue to receive UVA without a burning signal to get your ass in the shade
  3. Go out in the sun early in the morning and late in the afternoon and avoid midday hours (when you actually get some UVB exposure)
  4. Get a “safe tan” in the solarium
  5. Stay indoors and get all your sunlight through the window (UVA gets through the glass, UVB doesn’t).

Sounds like something we have been doing for the last 30 years.

So do we still think that there is not such thing as safe tan? Or that sunscreens will save us all?



Shonky pseudoscience by NZ Herald

bang_headOccasionally I read stuff that makes me angry. Really angry. Moronic popular media pseudoscientific articles “debunking”, “educating” and “linking nutrient x with disease z” normally fall into this category. The award for the popular media article with the dumbest headline and the most questionable content of the month goes to NZ Herald article “Researchers write off benefits of vitamin D“.

Researchers who have debunked one of the claimed benefits of vitamin D capsules are sceptical of the links that have been made to a much wider range of medical conditions.

Auckland University physician Professor Ian Reid and colleagues concluded after studying 23 trials that most healthy adults need not take vitamin D supplements for the prevention of the bone-weakening condition osteoporosis.

Let’s start with the headline. The researchers DID NOT “write off the benefits of vitamin D”! The article relates to vitamin D SUPPLEMENTATION. Unfortunately we use the term “vitamin D” interchangeably with the pro-hormone 25(OH)D that we synthesise in our own bodies and with the white pill that you can take orally to supplement your serum levels of this. Still, shouting out “there are no benefits to vitamin D” is extremely stupid and deceptive. All vertebrates have to synthesise vitamin D to survive, and have been doing so for over 350 million years.

I have not got access to the actual study (only the abstract) so I will reserve the judgement on the paper. Let’s have a deeper look into this NZ article instead (it may very well be that it doesn’t fully reflect the authors’ conclusions).

Love this sentence:

Use is said to be very high among patients of GPs in wealthier areas.

That, I assume, either implies that GP are trying to scam their more affluent patients into buying a totally unnecessary supplement, or that health-conscious and gullible wealthy worried-well are using vitamin D in addition to their chiropractic appointments, yoga retreats, and other voodoo. Both are pretty insulting implications.

They have become something of a cure-all – or prevent-all – with low blood levels having been linked to multiple sclerosis, winter colds, heart disease, cancer, mental illness and numerous other medical conditions. Professor Reid has found reports of links to 53 conditions.

‘When you get 53 different diseases associated with low vitamin D levels and when those diseases are incredibly disparate … it’s pretty hard to see a common biological explanation for those associations except the fact that people don’t go outside and lie around in the sun [when they are sick].’

Hmmm. 53 “incredibly disparate” conditions linked to low vitamin D levels. That does sound rather suss. That’s, like, this is miracle vitamin, or something. What could possibly all these conditions have in common???

Erm. I assume Professor Reid has heard of inflammation. And I hope that Professor Reid is familiar with the extensive body of research looking at vitamin D as much more than just a “bone-building vitamin” but a powerful immunomodulator. Its method of action is so broad that vitamin D receptor (VDR) is expressed by the cells in most organs of the body: intestines, bone, kidney, skin, brain, heart, breast, parathyroid glands and gonads.

This from the Scandinavian Journal of Clinical and Laboratory Investigation (Reichrath et al, Hope and challenge: The importance of ultraviolet (UV) radiation for cutaneous Vitamin D synthesis and skin cancer, 2012)

Of high importance was the discovery that in contrast to earlier assumptions, skin, prostate, colon, breast, and many other human tissues not only express the vitamin D receptor (VDR) but also express the key enzyme (vitamin D-1 α OHase, CYP27B1) to convert 25(OH)D to its biologically active form, 1,25(OH) 2 D [1,2,6]. This active vitamin D metabolite is considered as an not exclusively calciotropic hormone, but additionally as a locally produced potent secosteroid hormone regulating various cellular functions including cell growth and differentiation.

Cell growth and differentiation: that may have something to do with all those cancers, huh?


No, there is no plausible biological explanation at all.


Not sure why Professor Reid mentions any of these conditions at all since his paper actually only looked at the effect of vitamin D supplementation and the risk of osteoporosis. I am going to take a stab in the dark and say that osteoporosis is a multifactorial disease. From the abstract it transpires that 10 of the studies analysed use such piddly doses of vitamin D as 800IU. I wonder why they even bothered. For the populations in question the typical doses of 600IU to 1000IU of cholecalciferol barely going to maintain their levels, let alone increase them significantly. Compare this to 10,000IU your body can potentially synthesise from 30 minutes of direct sunlight.

Most healthy adults in New Zealand got enough vitamin D from the sun, said Professor Reid.

Riiiight. This may indeed be the case in sunny tropical New Zealand but here in Australia we have a few issues with vitamin D deficiency.

Research by Deakin University found that one third of Australians is now vitamin D deficient. The authors of this 2009 paper were quite alarmed by this fact, seeing it as a “major health problem worldwide”:

Low levels of vitamin D can contribute to a number of serious, potentially life-threatening, conditions such as softened bones; diseases that cause progressive muscle weakness leading to an increased risk of falls, osteoporosis, cardiovascular disease, certain types of cancer and type 2 diabetes.

One thing on which I will agree with Professor Reid. Popping vitamin D pills is not the answer. Some the links between vitamin D deficiency and various conditions are undoubtedly related to changes in our lifestyle. Going out for a walk in nature will not only top up your vitamin D levels but will boost your cardiovascular fitness, strength, circulation, and promote overall mental health and wellbeing. The whole is always more the sum of its parts. And this is supported in the literature. This systematic review, for example, concludes that cancer prevention related to sunlight, cannot be fully explained by the vitamin D effects alone. Just like with our diet, we should aim to receive all the necessary nutrients naturally. Ideally we will get most of our vitamin D through sunlight exposure and, to a much smaller extent, diet. However many of us work indoors from 9am to 5pm without ever seeing sunlight. Supplementation is sometimes necessary.

Irresponsible reporting such as this can cost somebody their health.



The Dark Side of Anti-Sun Campaigns

AHS13 has been and gone. Hideous trans-Pacific jetlag is now over. I am off Twitter and other social media, apart from our Whole9 South Pacific page as part of our Personal Growth September (Jamie calls it the Antisocial Media September). I will write a post on it another day to explain why we decided to surrender to our antisocial introverted selves. The main benefit of not spending wasting time scrolling through a Twitter feed is time to think and time to write. I have come to the conclusion that my 20 minute presentation on melanoma at AHS was grossly inadequate to explain my thoughts and conclusions regarding sunlight and melanoma.

I first became interested in sunlight when I was preparing an Honours project on Vitamin D and Multiple Sclerosis in medical school. I never published but I kept the research, as well as the overall feeling that sunlight is good, is necessary, and is sometimes healing. This is in contrast to what I can only describe is the state of fear when it comes to the UV radiation in Australia. This paranoia is incredibly pervasive*. Those of you who do not live Down Under might not appreciate its true extent. Otherwise sensible adults get a look of panic in their eyes when melanoma is mentioned. Children at school are not allowed outside into the sun at recess or lunch unless they wear a wide-brimmed hat. Those whose irresponsible parents dare to forget one, stay in the shade, unable to play. Every preschool and school excursion involves long sleeved rasher shirts, tubs of sunscreen applied liberally on each child and, again, hats.

*I am not talking about whether this is clinically justified as yet, merely describing the situation.

The public awareness campaigns are omnipresent. The iconic Slip!Slop!Slap! campaign launched in 1981 is widely touted as one of the most successful campaigns in the Australian history. From the SunSmart website:

Cancer Council believes its Slip! Slop! Slap! campaign has played a key role in the dramatic shift in sun protection attitudes and behaviour over the past two decades.

Wow! That’s fantastic. That campaign must have saved thousands of lives and stopped cancer in its tracks! From Melanoma Institute Australia website:

Melanoma rates have doubled in the 20 years from 1986–2006.


It is quite fascinating that most people in Australia like to talk quite expertly on the topic of melanoma. We are so well “educated” by various health campaigns that any self-respecting TV owning Aussie off the street will tell you that sunlight causes melanoma. Total strangers will point out that the visible burn on your nose from the weekend SUP adventures is practically cancer waiting to happen. And heaven forbid you mention you had blister burns in childhood. People just shake their heads and look away, as if you are not long for this world.

I like to compare that unshakeable assurance to the society’s view on saturated fat. Your Auntie Madge just KNOWS that butter on your broccoli will clog up your arteries (while she is completely safe with her low fat banana bread) and cause a heart attack. Just like she KNOWS that going out in the sun without sunscreen will result in your untimely death.

Researchers in dermatology may argue about photocarcinogenesis for another 20 years. As far as the  public goes, the sun has already been condemned.

For those of us who have come to question and ultimately reject the conventional wisdom as it relates to the diet-heart hypothesis, it is almost too easy to reject this other “undisputed truth”.

It doesn’t help the cause of the sunlight fighters that they use emotional blackmail and scare tactics to “warn” the population about the dangers of that bright orb in the sky. Let me give you an example. For those of you living in Australia this will be very familiar as you have no doubt seen these “health announcements” on TV multiple times.

The self-professed aim of these campaigns is to discourage the pro-tanning attitude of the younger generation. I don’t know about you, but I feel quite uncomfortable about the imagery used in this commercial. A healthy cell transforms into a black tentacled monster which burrows its way into a blood vessel and multiplies, seeding the body with its progeny. Children will have nightmares. I realise this is a pictorial representation but this is not what happens. Hard-hitting messages are sometimes necessary but you need to be absolutely sure that your message is 100% backed up by solid evidence.

And this is where we hit a little snag.

This particular commercial seems to imply that tanning increases the risk of melanoma. Let’s examine this assertion in a little more detail.

1. Having a tan is generally associated with chronic sun exposure. Chronic (occupational) sun exposure has been repeatedly shown to be protective against melanoma (Elwood and Jopson, 1997).

2. Tanning and sunburn are two different things. The evidence on sunburn and melanoma is not foolproof but there seems to be a slightly increased risk.

3. The ability to tan is first and foremost influenced by your skin phenotype which is genetically predetermined. When it comes to melanoma, your skin phenotype is one of the recognised risk factors. In other words, those who are able to tan are at less risk than those (unfortunate redheads) whose skin seems to go from “pale blue” to “scorched red” to “ginger peel” with not a hint of a healthy glow. So the very fact that you are turning a nice chocolatey brown the minute you expose an inch of flesh may indicate that you have a favourable phenotype. But, of course, not everyone with skin type I develops melanoma either!

4. All tan is not the same. Although they look identical, skin tans induced by different UV wavelengths have different mechanisms. UVB-induced tan causes dramatic increases in melanin synthesis. In contrast, UVA has no effect on melanin content. The tan produced by UVA is due to the distribution and oxidation of pre-existing melanin precursors. (Miyamura et al (2011) The deceptive nature of UVA-tanning versus the modest protective effects of UVB-tanning on human skin, Pigment Cell Melanoma Res). Melanin = photoprotection. Hence UVA and UVB have totally different protective qualities.

Maybe to be on the safe side we should stay indoors and avoid the sun altogether. But it seems that those who work indoors and bask under the cool office lights are, in fact, at higher risk of melanoma.

Godar et al (2009) Increased UVA exposures and decreased cutaneous Vitamin D3 levels may be responsible for the increasing incidence of melanoma. Medical Hypotheses 72:434-443

“Paradoxically, although outdoor workers get much higher outdoor solar UV doses than indoor workers get, only the indoor workers’ incidence of cutaneous malignant melanoma (CMM) has been increasing at a steady exponential rate since before 1940.”

“In fact, outdoor workers have a lower incidence of CMM compared to indoor workers”

In diagnosed melanoma cases, previous exposure, intermittent or chronic, is associated with lower mortality. Which seems to make no sense at all if you subscribe fully to “sunlight causes melanoma” argument.

Rosso et al (2008) Sun exposure prior to diagnosis is associated with improved survival in melanoma patients: results from a long term follow up study of Italian patients. European Journal of Cancer 1275-1281

“Time spend on the beach during adulthood (on average 3 weeks/years for 19 years) was inversely associated with the risk of death…”

There are plenty of grey areas in the UV-melanoma story but tanning is certainly not one of them. I would love sending a public message to the organisation who sponsored the ad, requesting to show a single study linking suntan with melanoma.

Here is my new anti-Sun campaign suggestion. I think we are not far off that.



AHS 13 – moving forward.

I am not sure that I am at all able to sit down and write something remotely coherent about the Ancestral Health Symposium 2013. I feel like my jetlagged brain will struggle to sort through the blur of those 3 days but I shall do my best.


Physicians in evolutionary medicine panel

Physicians in evolutionary medicine panel


I was really impressed with the talks this year. Overall I felt that the spread was really even between more popularised topics and hard-hitting science. AHS12 seemed a bit hit and miss, as if the presenters haven’t quite decided whether they were delivering content to laypersons or presenting at a scientific gathering. This year we struck a really good balance. The quality of the talks was also more even, unlike last year when I actually walked out on a couple of talks with a WTF expression on my face. For those of you watching the action at home here are the ones I found interesting:

1. Nassim Taleb – if you haven’t read the book “Antifragile” (and you absolutely must) you are going to think that his presentation is wordy, baffling and incoherent. If you are a fan you will nod fervently at every sentence. A few of us had a quick conversation with Nassim just before his talk. That is to say, Nassim was talking and I was trying (and failing) to look as intelligent as possible. One for the fans, for sure.

2. Gad Saad (“The Consuming Instinct: What Juicy Burgers, Ferraris, Pornography and Gift Giving Reveal About Human Nature”) had a really relaxed engaging style. He presented great arguments for why our penchant for symmetrical face, big booty, junk food and red sports cars may be evolutionarily driven. I was quite befuddled to hear that evolutionary psychology is still considered a bit “woo” in academic circles. But then I had a recent conversation with a paediatrician about evolutionary medicine and she shocked me by asking innocently: “Isn’t evolutionary biology a bit alternative and unscientific?”

3. Esther Gokhale (“Walk the Talk”)- I was determined not to miss this talk like I did last year. Esther share more of her insights on what constitutes a good posture and why the traditional view of S-shaped spine is not it. She managed to conjure up a real-life baby to assist with her demonstration of traditional baby-carrying style. The baby cried when she handed him back to the parent. I enjoyed browsing through her very well-illustrated book.

4. Victoria Prince (“Fatty Liver – Is It the Fat’s Fault?”) presented a great talk on non-alcoholic fatty liver disease. Alcoholic liver disease was the topic of her PhD thesis so this girl knows a lot about liver (and I hear she likes eating it too!) She went through the evidence on dietary fat as a contributor to NAFLD and most of the readers here will not be surprised to hear that all fat ain’t the same. I think we all walked away giving ourselves a firm permission to drink piña coladas.

Keith Norris certainly looks interested

Keith Norris certainly looks interested

5. Jamie Scott (“Are Your Sprint Intervals HIITing You in the ANS?”) – ok, ok, I am biased. But it was a great presentation even though Jamie was accosted by a whole group of Crossfitters at the end, and I had to be on standby to prevent any possible bloodshed. Everyone knows, Crossfitters go nuts when told that maybe smashing yourself to the ground 6 days a week is not a great idea. (Just kidding, they were very polite and inquisitive).

6. Whole9 Seasonal Model Workshop – I have watched this idea develop between the brains of Dallas Hartwig and Jamie for over 1.5 years now. Dallas presented the much under appreciated Seasonal Model poster at last year’s AHS but this year they decided to make it into a 2 hour workshop. I think we need presentations like this at AHS: new untested ideas, untapped frameworks (after all, Paleo is a framework too!) which encourage people to look beyond rigid programming for each of their 3 meals a day from now to the day they kick the bucket. I also like the idea of seasonal approach because it brings us, humans, back into the fold of natural environment. We need a reminder that we are a part of the natural world. I cringe whenever I hear anthropocentric ideas still thrown around even in the ancestral community (“Humans are the only animals with a capacity to play” – WTF?). Anyone who is interested in moving beyond the dietary principles should watch this talk.

photo 4I was very pleased that the conference has moved away from pure focus on diet and weight loss. The diversity of topics is very very welcome because after all, people need to realise that while it starts with food, it certainly doesn’t end there. Sleep was the topic du jour with many post-conferences tweeps confessing they have been guilted into getting their zzzzz.


photo 1While we tried to attend the talks we were interested in we certainly did not travel halfway around the world just for those. We feel very privileged to be able to present our topics at the conference but our primary aim is always to catch up with “our people”. Living on the bottom of the planet is awesome when it comes to good food availability (sorry, US food just doesn’t cut it) but it sucks when it comes to Socialisation. We cherish the opportunity to talk in person with like-minded people and this trip was totally worth the big bucks it cost us for that fact alone.

I was going to say thank you to a few people but I don’t want to leave anyone out. Many have become close personal friends and goodbyes were really heartbreaking. I cannot wait to see them all again, either in the US, or Down Under. You know who you are, and you have an open invitation at our place.


I thought there was some really good vibe this year. There was no nit-picking, no whispers in the corner, no petty arguments. It was just a bunch of people who came together to talk about their passion to make a difference. The academic disagreements were polite and civil, and there was (to me) a general feeling of mutual respect. The word “community” kept coming to the front of my mind. “Community” does not mean “cult”. I think “community” means “a tribe”. It is still totally amazing to me that a misanthropic introvert like myself can mingle, and socialise, and chat for hours to total strangers. That’s how you know that you are among “your people”.

When you have a case of warm’n’fuzzies about where we are as a movement it is really disheartening to see the usual characters come out of the woodworks to trash Paleo from the safety of their computer keyboards. It was entirely laughable to read a few tweets commenting on body shapes of the participants or the interpretation of the scientific merit of the conference based of 140 characters. My diagnosis for these keyboard warriors is the severe case of the sulks on the background of desperate attention-seeking. I have no time for that.

Once again, warm thank you to the Ancestry Foundation, to Katherine Morrison for looking her radiant cheerful self while dealing with all kinds of shitstorms, which seem to be a part and parcel of a huge event like this, and to Aaron Blaisdell for his superb organising skills and for being so gracious and welcoming.


Some of the presentations are already up on slide share. Here is my presentation. I have been told it was quite good.

Here is Jamie’s.

The videos are still forthcoming. Of course I am not going to watch mine as I will undoubtedly feel dejected about its imperfections.

AHS14, we will be there.


Resistant starch: the missing ingredient? Part 1

Just when you think you have everything in your diet dialed in, something new comes along and upsets your carefully constructed nutrition knowledge applecart. This particular compound has been getting nutritionists a little giddy with excitement for a while, and now it is receiving more and more media exposure causing everyday folk scratch their heads at the new wonder boy. It’s hard not to get swept away in general enthusiasm when our popular morning TV show touts Resistant Starch (RS) as a “sneaky fat fighter”.

Remember when things were simple and we were told to just eat more fibre? Well, that is so 1990s. CSIRO in Australia note that while Aussies eat more fibre than many other Western countries we still have the highest incidence of bowel cancer in the world. They call it ‘the Australian paradox’ (what number paradox is it now? I lose track). So looks like adding more fibre in form of All-Bran and bran muffins into our diet has done bugger all to keep those pesky intestinal cells from going bananas and turning into some evil little suckers. All hail resistant starch.

However, as most of you know, I am naturally a fairly skeptical person when it comes to dietary ‘miracles’, especially when the recommendations to increase RS in our diet from the above mentioned morning program look like this:

  • Eat more canned or soaked legumes such as kidney beans, chickpeas and butter beans.
  • Include more intact wholegrains, seeds and cereals, in your diet e.g. oats, barley corn and linseeds.
  • Eat fruit such as bananas before it’s ripe.
  • Eat salads that have been cooked and cooled, such as potato salad, rice salad and pasta salad.
  • Look for breads and cereals with added resistant starch

So what the hell is it? And are you missing out on this miracle food substance?

The official website named Resistantstarch.comAn Information Portal for Health Professionals (don’t you wish that broccoli had an official website?), gives us this definition:

”Resistant starch is the sum of starch and products of starch digestion not absorbed in the small intestine of healthy individuals”

It is also classified as the third type of fibre (together with soluble and insoluble) by several health agencies, including Food Standards Australia and New Zealand, and its MO is to bypass the normal absorption process in the small intestine straight to the colon where it is fermented by colonic bacteria (which also makes it a “prebiotic”).

There are plenty of resistant polysaccharides (starches) that you won’t find in your average shopping trolley and this is reflected in 4 types of RS. Here is a handy table from one of the published reviews (1) on RS (click for better resolution):

Source: Nugent 2005

Source: Nugent 2005

Kind of makes you wonder whether you should start munching on raw potatoes in spite of what Momma always told you and inflict your bean-eating habits on your nearest and dearest for the sake of digestive health. Or should you just trust the clever scientists who conveniently altered the chemical structure of polysaccharides via esterification in order to escape your digestive enzymes? Why are we doing this again?

Oh yes, the claims. I will be relying on the enthusiastic RS article (2) by an Australian dietician Robert Landon written for the official Resistant Starch website to provide the claims to benefits. My facetious comments will follow for your reading pleasure.

Satiety, metabolic health and obesity

I’ll start with this one because clearly this is the stuff that makes big headlines.

“Recent breakthrough research has linked the fermentation of resistant starch with increased levels of gut hormones (PYY and GLP-1) that play a role in satiety and potentially, long-term energy balance.”

“We believe the fermentation of resistant starch may be an effective, natural approach to the treatment of obesity.” says Dr Keenan, the study author.

You can read the study in question here (3) and decide for yourself if feeding 30 rats a carefully engineered concoction of corn oil, methylcellulose or high-amylose corn starch is applicable to human metabolism or behaviour around food. And more importantly, does the release of those “satiety” hormones correspond with actual satiety? Sadly, the previously mentioned (1) 2005 British Nutrition Foundation review by Nugent (peer-reviewed) mentions that the studies which looked at satiety as the end point appeared “to show a weak or no association between RS and satiety over the course of several hours or an entire day.”

Incidentally, I know of a way to increase GLP-1 and PYY levels in humans in a real world which does correspond with satiety: feed them a high protein diet.

This excerpt from the 2013 review on RS (4) made me laugh:

“The physiological effects of resistant starch make it extremely difficult to assess its impact on weight. Resistant starch increases stool bulk, luminal thickness, and bacterial numbers in the colon. These factors add to overall body weight, perhaps masking any differences that do exist due to resistant starch ingestion”

You know you need a new weight loss strategy if your current progress is easily masked by the weight of your poo. Just sayin’.

And I love it when researchers get excited about postprandial glucose and insulin levels. Sounds like this stuff is pretty important, eh?

“… a number of human studies have demonstrated the capacity for Hi-maize® resistant starch to elicit a positive impact on both postprandial glucose levels as well as insulin response.
Most recently, a human trial with maize-based resistant starch incorporated into test beverages showed effective reductions in the relative glycaemic response without any change in palatability”.

Again,  the review by Nugent is a little more cautious:

“There is a lack of consensus regarding the precise effects of RS on insulin and glucose responses: 15 studies have reported an improvement in these measures following the consumption of a RS-rich test-meal, while 10 have showed no, or a physiologically irrelevant effect. It is noteworthy that, to date, there are no reports of RS worsening insulin and glucose responses.”

Phew, it’s nice to know that at least this stuff doesn’t make our blood sugar go through the roof!

Several more recent studies looked at insulin sensitivity in men and women with slightly better results which were obtained by very high intakes of RS: up to 40-50g a day. A paper of note is by K.Maki et al published in the Journal of Nutrition in 2012 (5). The study subjects this time were human overweight and obese men and women broken into 3 groups: control group who received a digestible starch meal and 2 intervention groups, one with 15g of RS a day and the other with 30g of RS. They had to add the products to their usual daily meals for 4 weeks, followed by a 3 week wash out period and then a swap. They underwent a glucose tolerance test at the end of the study.

Insulin sensitivity between 3 groups. Source: Maki et al, 2012

Insulin sensitivity between 3 groups. Source: Maki et al, 2012

The reason why this study caused a bit more of a stir is because it showed better insulin sensitivity in men with a more achievable dose of RS: 15g/day than in men who consumed starches (do you see a little problem here?). Interestingly, there was no effect in women and there was no effect with higher doses. The big problem of this and other similar studies in my opinion is that their control (the column in black) was digestible starch. So in fact,  any difference in insulin sensitivity was relative to the equivalent in starch consumption in people who already have poor glucose tolerance judging by their abdominal girth.

But seriously, can we come up with a plausible explanation why RS starch may improve markers of glucose metabolism? Sure! It reduces the amount of absorbed glucose. This wasn’t too hard, was it? It’s a bit like comparing nicotine levels in full strength vs half strength cigarette smokers. If you smoke low nicotine cigarettes your nicotine levels will be lower. Hooray! We found a measurable improvement! Ahem, you could just stop smoking, of course.

[To all my sweet potato-loving friends, I am not suggesting that you stop eating carbohydrates. Just pointing out that if the only goal is to reduce glycaemic response one might decide to reduce dietary glycaemic input. Or add more protein. Or fat. And by the way, I consume large amounts of this orangy goodness on a daily basis.]

If you demolish your timber dining chair to shreds and sprinkle it onto your Coco-pops, it will also reduce your postprandial glucose levels. Don’t try this at home, kids.

And since we are trying to keep your family physician happy, how about that pesky cholesterol? While early animal studies were quite promising with significant reductions in triglycerides and total cholesterol, these were not replicated in human subjects. 13 human studies showed that RS had no effect on lipid metabolism (1). Sometimes we need a reminder that we are not rats in cages fed laboratory produced chow. Hang on…

So all in all, I wouldn’t be hanging your hat on RS as a shortcut to winning the obesity battle on a global or individual scale as yet. In my next post I will address the evidence behind RS effect on digestive health and, specifically, colorectal cancer. In the meantime, don’t go crazy with that potato starch.


1. Nugent, A. P. (2005), Health properties of resistant starch. Nutrition Bulletin, 30: 27–54. doi: 10.1111/j.1467-3010.2005.00481.x

2. Landon S, Resistant Starch Review published for

3. Keenan et al (2006), Effects of resistant starch, a non-digestible fermentable fiber, on reduction in body fat. Obesity, 14(9): 1523-34

4. Higgins J, Brown I (2013), Resistant starch: a promising dietary agent for the prevention/treatment of inflammatory bowel disease and bowel cancer. Current Opinion in Gastroenterology, 29(2):190-194

5. Maki et al (2012), Resistant starch from high-amylose maize increases insulin sensitivity in overweight and obese men. The Journal of Nutrition, 142(4):717-723

P.S. I will keep the comment section closed at this stage as I will probably address some of the questions and comments in my next post.



Evolution of Reading

Most of you are incapable of reading this post attentively from start to finish. In fact, you will probably just skim the first paragraph, then quickly scroll down, your eyes will skip to the text in bold for a fraction of a second, then you will hover of the picture, and then, convincing yourself that you got the general gist, you will speed off to click on the next tab on your screen.

photoYep, this is the stunning conclusion that Nicholas Carr comes to in his book ‘The Shallows: What the Internet is Doing to Our Brains’. One damning fact at a time he builds a case proving that the Internet is not just a mindless database of knowledge, passively waiting to be accessed and researched. It is an active medium which has the ability to change the very way we think, structure our ideas, the way we learn and the way we communicate.

Hang on, you say. Isn’t that taking this whole ancestral thing a little too far? Am I firmly on the path of giving up on smartphone and flush toilets to live in a hippie paleo commune on a Pacific island, farm coconuts and wipe with a leaf? (in the words of the timeless King Julien: ‘Who wipes??’). Bear with me for a little while.

I used to be an avid reader. I discovered books at a tender age of 3 and started reading ferociously. My mother used to joke that I swallowed books whole and it was not that far from the truth. Written (or rather printed) word had such power of me that when I did not have a fresh fiction text I would read an encyclopaedia. Fiction had the ability to keep me enthralled to the point of danger. I distinctly remember the night when I was supposed to “watch over the stove” while my mother went to see our neighbour. The 8 year old me was engrossed in “Jane Eyre” and only vaguely registered my Mum’s screams at the room full of smoke and the stove on fire on her return. I was in another world, oblivious.

My eyesight started failing early. Blaming my reading obsession, my parents waged war on books, sneaking up on me in the middle of the night (and taking away the torch from underneath my pillow), locking the crime book cupboards when I needed to study, even checking my school bag in the morning for stealthy novels between textbooks.

I continued to read books when I came to Australia but the love somewhat lessened. The language barrier made it more exhausting initially, then I didn’t really know any good authors, and then I needed to work and study. Fiction reading became a rare indulgence. Non-fiction reading was a necessary chore.

In my first degree I owned a little laptop which I used purely for document editing purposes. My knowledge base was still acquired from a printed text. The massive (and expensive) tomes on microbiology, biochemistry, anatomy and physiology were covered in multi-coloured bookmarks with text underlined in pencil. (Yes, in case you haven’t figured it out, I am a nerd). I memorised anatomy structures by drawing them with pencils (multi-coloured, of course) and writing sheets and sheets of text next to the diagrams. I still remember what a writer’s cramp feels like although I haven’t had it for years.

My computer use stepped up a level in medical school. Buying textbooks for a huge variety of subjects was not feasible plus the underground student online book share was supplying me well. I struggled initially reading textbooks online. My eyes would get tired quicker, attention waver at the slightest provocation, I missed my coloured pencils and bookmarks, I missed being able to curl up on the couch with a cup of tea.

At least this last problem was resolved when I got an iPad. Man, I love(d) this thing. My own personal window to everywhere. Not a bulky laptop with a charger, 5 minutes wind up time and somewhat disturbing warmth radiating to my groin. Coupled with a snazzy blood-red cover, this thing was the shiz.

Word processing to emails, to world wide web, to online learning, to blogging, to social media – I am amazed at how quickly my reading and Internet habits changed. I have found the world of Ancestral Health, although the search was initially triggered by a book (Gary Taubes ‘Good Calories Bad Calories’), this world would be unknown to me if it was not for blogs and social media. I have so much to be grateful for: meeting like minds like Dallas and Melissa, and being able to take our combined knowledge to the people in my part of the world. Heck, I would have never met this awesome guy if it wasn’t for the Internet.

However, recently I have been noticing some things that started to concern me. Far from being engrossed by books, I have become inattentive and distractable. Instead of looking forward to a blissful escape, picking up an old-fashioned printed book seems a chore to my concentration. When I click on a new promising link posted by someone on Twitter I skim it quickly. If scrolling down reveals a huge document I get inwardly annoyed. Frequently I get caught in the comments to the blog post, rather than the blog post itself, clicking on more links and letting my opened tabs multiply. My reading in general has become less reflective and more reactive. My interaction with those “like minds” has reduced to 140 character snippets, not the long intellectual discussions.

As for research, it’s getting harder and harder. One search on Pubmed opens you to a spiderweb of articles. One wrong turn, one wrong click – and you are caught in a labyrinth. My innate curiosity encouraged by an easy availability of information leads me away to the point where I forget what it is that I was looking for in the first place. The sheer volume of information is overwhelming. Every study on the benefits of fibre is counteracted by the study deeming it useless. If I feel lost and confused at times, what of the people who rely on popular media for their health advice?

And there is the interwebz conflicts. You never have as many opponents in your real life as you will have on the Internet. When every snippet is available for judgement, when people do not know you as a person, when your printed word is not accompanied by your tone or body language, it is all too easy to wilfully/accidentally misinterpret and cast your vote. I watch the deterioration of a healthy discussion on Facebook into crazytown bitchfest and want to go away to that Pacific island. The reality is, you wouldn’t say half of this to a person to their face, but the ability to instantly type up a knee-jerk reaction in a witty response is hard to pass.

My escape plan

My escape plan

‘The Shallows’ could not have come at a better time for me. Exhausted from meaningless internet jibes, wary of loss of own concentration and feeling the lack of intellectual stimulation, I wanted to understand what was happening. I don’t blame the Internet (neither does the author). I merely concede that to sharpen the signal I need to reduce the noise. I already keep my Twitter account private but I think it is time to take a holiday altogether. I would like to close the comments on this blog. Not because I don’t value my readers or their opinions – far from it. But I would like to concentrate my time and energy on the work that requires a 100% of me. For those who would like to stay in contact – feel free to email me. Those whose opinions I value and cherish (you know who you are) I want to stay more connected, I want to give our interaction more than just a cursory glance on my phone screen. Let’s chat, let’s exchange papers, let’s Skype. Let’s use this powerful force to what it can be – bringing minds and passions together. I am done with wasting time on anything less than that.


One doctor’s take on Whole30: when the Magic doesn’t happen

I can’t take any credit for today’s post. Pam, a general practitioner from Wellington, NZ, has shared her recent Whole30 experience with Jamie and myself, and then kindly allowed me to make it public. We first got in contact with Pam via Twitter a few months ago. A New Zealand based doctor who is vocal about being anti-grain, anti-sugar and pro-real food? Yes, please, we are very interested! I don’t even know how she went from being from a voiceless Twitter handle to a huge part of our “kiwi Paleo gang” (not entirely sure how a Russian-born Australian got invited there either but they tell me it’s a privilege). Pam is 47 years young and her voice is loud and uncompromising. I have been greatly entertained and awestruck watching her take on conventional nutritionists, media and medical authorities, all in a 140 character format. When Jamie and I announced Whole9 South Pacific she became one of our most staunch supporters. It was only a matter of time before we convinced/coerced her into doing a Whole30. I found her insights particularly compelling because it was not all fireworks and champagne. Her motivation is to improve health, prevent becoming hypertensive and diabetic (yes, believe it or not, doctors worry about this too!). Here is her story.

My Whole30 roundup – When the Magic doesn’t happen

I am learning.  Learning to be patient. Learning to have realistic expectations. And learning to appreciate the value of small changes. I have learned that it’s ok not to experience the ‘magic’ that many other people do when they make purposeful changes to their lifestyles. It is hard not to feel disappointed or that you have been rather unsuccessful when you constantly read of these ‘magic’ stories and personal epiphanies. That is the nature of the beast. People crow unashamedly about their great achievements. And so they should. They have done the work. They should be proud of their achievements and we should share in their success. They inspire others to give change a go. I am happy for them. Really I am.

But what of those who put their very best efforts in and don’t experience that ‘magic’. I am sure there are as many or more who land up in this place. But they are not shouting from the ‘comments’ or ‘discussions’.  What happens to them?  I suspect many give up and slink quietly back to their old habits feeling as if they have failed yet again. I’ve been there. Many times.  Not any more. Part of the reason is that I have accepted reality. There is no ‘magic’ for most people. So, what would have been the ‘magic’ for me? Despite trying to convince myself otherwise, a dramatic weight loss would have been my magic. I didn’t start with health problems that others have had to suffer with. Gluten and dairy didn’t mess with me. I had no autoimmune issues. Just too much body fat. So I guess I could say I had /have hormonal issues! What I did learn was that even if there is no magic, there is hope. And there is certainty that you can become healthier.

My ‘aha’ moment occurred about 9 months ago. A chance comment at a random moment piqued my curiosity. With the world of information at my finger tips I could Google, follow links and find any information I wanted. I could formulate questions and find answers. I found the pathway to the truth about dieting, health and weight loss. I found amazing people and I also found out about the lies, politics, egos and money which have ruled the information about diet and health on which the average person relies on for better health. Information gives you knowledge. Knowledge is power.

So what the heck has all this got to do with Whole30? You may be wondering. It has everything to do with my Whole30. You own your own Whole30. I owned my Whole30 and because of this I got through the 30 days (and continuing on).

Whole30 was one of many plans/programs/guides that I came across. When Whole9SouthPacific put out the challenge and fronted the charge to lead by example, I made the decision to take up the challenge too. The time was right and the challenge was right. I had been eating pretty clean for 8 months. Too clean to bother with Whole30? Maybe, maybe not. In my head I decided to commit. Although the challenge was for January I made the decision to delay starting until after our holiday when I could be fully in control of my environment. We were going to stay with friends and I felt it would not be right to be too picky about everything I could and couldn’t eat ‘because it’s not Whole30’. That didn’t mean that I didn’t come pretty close to adhering most of the time.

Holiday over, time to start. My weight had not changed much for 2-3 months. Maybe up a kilo over Christmas/ New Year and holiday. I wasn’t expecting miracles but I was hoping for at least a small change in direction and getting off the stalled weight loss. In order to become totally Whole30 I needed to quit dairy (had already reduced a lot), no alcohol – not too difficult, no coke zero (a bit more challenging). I had already quit bread and wheat as well as other grains many months before. So that was the ‘leave out’ bit.

Whole30 was also about ‘adding in’ – more food and more meals. I was eating very low carb, not eating even starchy vegetables. I started adding in some pumpkin and sweet potato. I also added in occasional fruit as I had not been eating any for months. And it was berry season. I had to put more effort into having 3 meals a day. I was used to skipping breakfast at times. Sometimes because I just wasn’t hungry and other times just because I didn’t have time. My egg intake soared. Spinach became my ‘go to vegetable’ – I added it to everything where I needed more on my plate.

I didn’t find it particularly difficult to complete the Whole30. I made sure I wasn’t hungry. I also made sure I always had some compliant foods to grab if I was hungry coming home at meal times. A stash of ready boiled eggs, homemade mayo and salad greens made sure I had no excuse to eat the wrong things.

So what did I get from Whole30?

  • I lost about 3kg. I am sure that had I gone from SAD to Whole 30 directly I would have lost double that (the double bit being water loss). I think my clothes loosened fractionally.
  • I don’t miss my wine. I seldom really feel like my latte coffees. Black is fine (as long as it’s not too strong).
  • I am absolutely fine eating more vegetable sourced carbohydrates – very low carb is not necessary for me.
  • Bread does not have a hook out for me. The trick is not to be hungry – making sure I eat enough.
  • I think about sweet things less often and they are less tempting.

Perhaps a lot of this resilience to reverting to SAD food is pure willpower because I feel so strongly that I have to avoid unhealthy food to prevent future health problems. But maybe there is a biochemical change that has occurred and that I really have a true lessening of desire for those foods. Probably a bit of both.

The only Whole30 ‘rule’ I broke was the scales one. I make no apologies. This was MY Whole30 and I had to make it work for ME. I get why the rule is there but for me it wasn’t going to work. In the past when I have lost the scales it has started the slippery slope back to weight gain. I realised that I might not lose weight so I wasn’t too stressed about that. But there was no way I was going to contemplate gaining. I didn’t weigh myself every day. I weighed here and there, maybe 2-3 times a week and in a random fashion. It helped me knowing that despite eating well I was not creeping up the scales. After close tracking of weight for 8 months I can recognise the fact that weight loss is both slow and definitely not a straight-line graph. It is an alpine graph with lots of ups and downs but the overall gradient slopes downwards.

The direct and indirect support of the cyber-community has reinforced my awareness of why I need to stick to the plan. My own knowledge growth has made me realise that having knowledge is only part of the plan. It’s up to me to do the very best I can for my own health. Whole30 provides the rudder, its up to me to steer the ship. The pathway doesn’t have to be straight and narrow but if I lose the rudder, the ship will loose its way. The tighter I steer the more stable the ship.

My message: If you don’t feel the magic, don’t give up. Your health depends on following a real food template for the rest of your life. Give yourself years before you decide real food doesn’t make a difference. Your future health is not measured in days or months.

PS: there are no ‘before’ and ‘after’ photos. It’s not what you look like that tells you whether you are healthy or not. There is so much more to health than a picture. For me the pictures do not speak a thousand words.


A case for simplicity

Case 1. Bev

Bev is a jolly 63yo farmer who came in to the hospital after suffering a minor stroke. One quiet afternoon when I spot our medical student looking a bit out of place (well, even more so than usually) I take him to see Bev for a neurological exam practice. Bev looks flattered and obediently sits back in her bed, being the perfect patient. I remind the student that we start with a general observation of the patient,the side of bed assessment. He dutifully recites “alert, comfortable and in no respiratory distress”. I gently nudge him to describe the patient’s body habitus, the student gets instantly embarrassed and looks lost. How do you tell a patient she is fat? I explain while looking at Bev that her central obesity is an important risk factor which may be pertinent to diagnosis at hand. Bev chuckles good-naturedly: “I love me food, I’ve always been a good baker!”.

Most medical students hate the neuro exam: it’s tedious, long, complicated and seemingly impossible to make smooth. I don’t rush him and Bev seems happy with the attention. The student correctly identifies the weakness on the left side of Bev’s face. He asks Bev to blow up her cheeks, Bev makes a valiant attempt but ends up making a noise like letting out air of a balloon and promptly laughs. I hear laughs from the other side of the curtain: evidently this has been a source of amusement to other patients as well. Bev’s limb weakness is improving and we take her for a gait assessment. With her tiny feet, narrow shoulders, perfectly rotund middle and a wide crooked smile, she looks almost comically cute. The student summarises the findings of his examination and correctly identifies that Bev has likely suffered an ischaemic stroke in the area of a middle cerebral artery in the right brain hemisphere. I thank Bev for being the perfect model for us, she wisely nods:
– They all gotta learn somehow, don’t they? So you think it’s gonna get better for me, doc?
I point out that she already has made marked progress and then ask her how she feels about the future.
– Oh I know. I gotta watch that cholesterol, don’t I? No more fish’n’chips for this chickie! (laughs)
I tell her I’ll come back to chat to her about diet before her discharge, thinking I’ll get to her before she gets fed some pseudo-nutritional rubbish.

Two days later, on my day off, Bev suffered a major stroke. The nurse found her in the morning, stiff in her bed, unable to move, call out or ring the bell. The stroke affected the other side of her brain and left her completely paralysed on what just 2 days ago was her “good side”. I never got to see her again because she was transferred to another hospital to a dedicated stroke unit.

Case 2. John

I only find out about John at morning rounds as he was admitted last night. I barely have enough time to register “64yo male transferred post BKA” on my handover sheet as we enter his room. BKA stands for Below Knee Amputation. John has just had his second one. As I stand in the room while the consultant chats to John about his surgery my eyes keep drifting to an empty space below John’s knees. No matter how many times I have seen it, this sight still unnerves me.

I distinctly recollect one of my most distressing experiences in operating theatres when I was assisting in a BKA. My job was to stand at the bottom of the table and stabilise (a.k.a hold tightly) the foot and calf of the leg being amputated. I still remember own visceral startle when the toes suddenly started to move, as if in a mute protest, when the surgeon was severing the tendons at the knee. At some point through the cut the lower leg stopped being a part of the human being and became an object. As the last thread connecting it to the breathing body was dissected I was left holding that object in my hands, temporarily stunned, until the nurse offered a big bucket to deposit it in.

John is looking defiant. The consultant has just finished drawing a pretty bleak picture and suggesting a nursing home placement. I feel the hot wave of indignation at this seemingly cruel crushing of a patient’s determination to maintain independence and mobility. John repeats mulishly that he wants to have double prosthesis, he wants to walk again. Later that day I find out that my anger was misplaced. While his raging diabetes destroyed the small vessels in his feet and opened him up to ugly ulcers and gangrenous infections, John’s dementia caused him irretrievable short term memory loss and, consequently, an inability to learn new skills required for amputation rehab. He has been on insulin for years but has been steadily forgetting to inject himself in the evenings when he gets most confused.

Case 3. Pat

Pat is a 47 year old Indigenous woman who presented to our Emergency Department with chest pain. The ECG and cardiac markers do not show any signs of heart muscle damage but she is at high risk for coronary artery disease as she is a former heavy smoker and a diabetic. Routine nursing observations show that her average blood sugar has been between 25-30 mmol/L (450-540 mg/dL) over the last day. She normally takes metformin but it’s clearly not doing very much. Like many Indigenous patients she doesn’t look grossly overweight, with her skinny arms and legs sticking out of her hospital gown. The gown cannot fully hide her round belly though, and I have to double check the notes that she is not pregnant. No, she is not. I try to be gentle when I tell Pat that she is likely going to need “the needles”. Sometimes the mere mention of injecting insulin serves as a good wake up call and a good opener to the lifestyle modification conversation. Pat doesn’t seem phased: “Ok doc”. I feel a hint of frustration: the conversation is not going the way I planned. I try to bring it back to the diet, saying that stopping junk food may be an easier solution than injecting yourself every day. “I don’t eat junk food, doc! I didn’t have Maccas for yonks!” – she protests. I note a half empty 2 L apple juice bottle on her bedside table: “And what’s this? You can’t have that with your sugars!” She looks confused. I take a breath and start to rant about soft drinks and sugar but she has already turned off and when her mobile phone rings she picks it up leaving me with my mouth open mid-sentence. As she starts to chat, I walk away taking the juice bottle off her table and pouring it out into the nearest sink.


My other life, on this blog, as a part of Whole9, on social media, is like another world. Highly motivated people sharing their success stories, intelligent eyes watching our Whole9 South Pacific presentation, challenging questions being asked – I find my enthusiasm recharged and renewed. Although recently I see more and more splinters appear in the community.

Recently a video made rounds in “Paleosphere”. Some bloggers that I respect and follow found it offensive in its simplicity. I won’t comment on the video itself, I have a few minor quibbles with it myself, although I wouldn’t hesitate for a moment to show it to my average patient. I want to comment on the “It’s not that simple” critique. Maybe it’s not that the message is too simple, maybe we are trying to make it too complicated. We dissect this diet thing to its smallest constituents, calories vs grams vs ratios vs micronutrients vs cytokines vs endocannabinoids. Critical scientific discussion is enormously valuable and discourse should only be viewed as the way forward. But somehow discourse all too quickly  turns into a personal attack, a spiteful tweet or a post from the safety of a computer screen. And, sadly, some who used to offer valuable contribution to the body of knowledge now seem to offer nothing but negativity. Are we turning into the equivalent of elderly cranky academics arguing about the best fire-fighting methods while the room is engulfed in flames?

What about your average reader who has just googled Paleo or primal or ancestral health? Are we causing “paralysis by analysis” by not making it crystal clear what we actually all agree on? Even those firmly indoctrinated in beef broth/bacon/kale seem occasionally lost. Sometimes getting lost is easy if you are given a way out – maybe Lustig is wrong and sugar is ok? Maybe Taubes is delusional and it’s time to count calories again? Oh no, this thing is not simple at all! Let’s browse through some blogs, maybe we can catch the author out, find an error in the archives and pronounce the final judgment. It’s not exactly helpful for own health problems but sure is satisfying.

I did not choose the three cases for their dramatic value, I chose them because they are average. I see between 20 and 30 Bevs, Johns and Pats daily. Sure, I love reading the latest research papers in a search for truth but for these guys I want SIMPLE. I need a heuristic. If your goals are getting to a single percentage body fat, running a marathon or continue setting PBs by doing smashfit 5 days a week (hopefully not all at the same time!) you may need more tweaking but you are not exactly your Average Joe, are you? My favourite Internet testimonial this year is a 71 yo lady on a social security budget who reduced her HbA1C, came off insulin and halved her blood pressure medications, probably without giving a second thought to the latest blogosphere drama.

We are onto something good here. It’s real and, let me tell you, it may better than any expensive medication I can offer my patients. SIMPLE will get most people most of the way there. Here is my heuristic:

– eat meat/fish/eggs + vegetables (tubers, greens) three times a day to satiety and activity levels

– prioritise your sleep

– move in a way you enjoy

Do this every day for 3 months. Without dissecting, or philosophising, or looking for a loophole. This may just be enough to see change.