Peter on cholesterol….pt 2

Following on from last week…. and trying to summarise Peter Attia’s cholesterol talk at AHS12 to illustrate why the cholesterol reading you get from Medlab doesn’t give you a good indication of your risk of atherosclerosis and subsequent heart disease. Cholesterol. The internal regulatory process responsible for cholesterol involves both the production of cholesterol and absorption of it. There are a few reasons why some people have higher cholesterol levels, and broadly speaking there are people who are good at producing cholesterol, and people who are good at absorbing it. The absorption of cholesterol is governed by a receptor in the gut which is responsible for allowing the movement of sterols in and out of the gut. There is also a receptor in the gut that is responsible for getting rid of all unwanted sterols (and excess cholesterol) from the gut to be excreted (called ABCG5 and ABCG8). It’s only ‘free’ sterols that are able to get in – esterified cholesterol (i.e. that which is delivered through food) is not able to enter the gut. For this reason there is very little, if any, relationship between cholesterol in food choices and our total blood cholesterol level. Health professionals have been aware of this for a few years now, however the general public is still confused and I can’t tell you how often I get asked the question of whether there is a limit on eggs. However some may have a defect with the receptor in the gut letting too many of the sterols in, or a problem with the ABCG5/G8 getting rid of the unwanted sterols. The effect this has on overall cholesterol homeostasis is not clear at this stage.

 I can't get enough of eggs, even the grumpy ones. (image from chelseacrockett.com)

I can’t get enough of eggs. (image from chelseacrockett.com)

While we hear a lot about LDL-cholesterol, the lipoproteins responsible for carrying HDL and LDL also carry triglycerides and phospholipids. These are produced by the liver and are known as Apo-A (HDL cholesterol) and Apo-B (LDL cholesterol). Apo-B lipoproteins contain more triglycerides than Apo-A lipoproteins, and include very low density lipoprotein (VLDL), which (when it sheds its triglycerides and phospholipids) converts to IDL (intermediate density lipoprotein) and LDL. VLDL contains more triglycerides than cholesterol (5:1 ratio) compared to LDL which is more in the vicinity of 4:1. When the VLDL are transported from the liver they release triglycerides and phospholipids and triglycerides to be used for energy by the muscles or stored in the adipose tissue. In people that are metabolically healthy, the triglycerides are delivered to the muscles by VLDL to be used for energy – however in those that have metabolic health problems, the triglycerides are more likely to be stored as fat. In addition, as they contain a lot of triglycerides, when we have high levels of processed carbohydrate we are going to have a lot more VLDL in our bloodstream as these excess carbohydrates are converted to triglycerides and packed up in the VLDL. Research has shown that the number of VLDL particles increases risk of athleroschlerosis. In addition, there is a lipoprotein Apo-E which is found in Apolipoprotein E (ApoE) is a class of apolipoprotein found in the chylomicrons (carriers of dietary fat after we eat) and Intermediate-density lipoprotein (IDLs) that is essential for the normal breakdown  of triglyceride-rich lipoprotein constituents such as VLDL, and there exists three main forms – E2, E3 and E4. These differ in the position of certain amino acids in the structure, but alters the function of the Apo-E lipoprotein significantly. Those people with the E2/E2 and E4/E4 expression have been found to be at greater risk of atherosclerosis.

The whole cholesterol issue is confusing. I spent about 3 hours writing that last paragraph and its very rough and actually probably didn’t mention 18 other ‘must knows’ in order to understand it properly. However, I think that, really, the most important thing to understand is that JUST knowing your LDL number (or total cholesterol number) is not going to provide you with a good idea of your risk of atheroschlerosis. Firstly – in NZ we aren’t able to quantify LDL – instead it is a calculated number based on the direct measurement of total cholesterol and HDL cholesterol. That’s an issue. However, moreso, there are certain conditions which can increase risk associated with cholesterol. The Apo-B lipoproteins can get into the sub endothelial space in the artery wall and can spark an immune response, causing inflammation. This inflammation can then increase the number of particles being delivered to the site (as LDL is released in response to inflammation) thus further particles get into the artery wall. The Apo-A lipoproteins, responsible for delivering HDL don’t.

Of course, inflammation is not just caused by one factor – and I bang on about this a lot in pretty much every health related post I write here and on my facebook page. The oxidation and glycation (binding of a glucose molecule to a protein) of the particles can change the functionality of the lipoproteins which causes them to damage the endothelial cells I mentioned above. These processes are caused by an overload of stress in the system: dietary, activity, toxins and the like. Result? Increased likelihood of atherosclerosis. Oxidised LDL can’t be measured in New Zealand but people can send their results to a laboratory in Australia to get this measured.

Another important factor is the size and the number of LDL particles in our system. There are two different patterns – and those with fluffy LDL particles (bigger) are less likely to get stuck in the artery all compared to the smaller (pattern B) particles, which are more atherogenic. It’s not just size that matters, though – it’s overall particle number. And when the size of the LDL particles have been controlled for, it suggests that overall the number of particles is more important. The greater the number of particles, the less able they are to move efficiently around the bloodstream, the more likelihood of being oxidised and subsequent inflammation.

Also important to consider that LDL cholesterol is used as a patch to help with inflammation in the body – if you have high LDL then that could very well be indicative of an underlying issue that needs to be addressed. Interestingly, while we’ve understood that a high HDL is a good thing and the higher the better, in fact a high HDL is not a get out of jail free card either. Indeed, trials that increase HDL levels through therapeutic means have been stopped before their planned end dates due to the lack of clinical benefit in people who have established cardiovascular disease. If HDL is high, then there may well be a reason outside of just eating a good quality diet. There are different forms of HDL and, its primary role is a carrier to remove excess cholesterol away from the blood vessel wall to be excreted, if it is not functioning correctly then that in itself can increase risk of heart disease (depending on other risk factors). If we use the car analogy (as people tend to do when it comes to cholesterol, quite useful), then if the car breaks down, then the cholesterol is not going anywhere – this is double-whammy bad actually, as it is unable to break down the plaque at the artery wall and in itself can cause inflammation.

Yeah. Cholesterol. So how useful are your own cholesterol readings? First – there are a couple of good ‘proxy’ measures that can be gleaned from your results to give you an idea of risk. Triglyceride/HDL can give you an indication of particle size. The smaller the ratio, the larger the particle size, the less risk. You need to calculate this as it’s not given to you. However, this may not be as important as total cholesterol/HDL, which can give you an indication of particle number. The smaller the ratio better and this is likely to be a better indicator of overall risk. Finally, and most importantly, is the context. As I said last week, our cholesterol readings are nowhere near as important as we once thought with regards to atherosclerosis and heart disease – and can’t be looked at in isolation of other risk factors. The context matters, so evaluate them in light of your current lifestyle to get a better understanding of their usefulness.

Peter on cholesterol…. pt 1

As I was scrolling through the Ancestral Health Society youtube channel (have you been? You need to!) I came across Peter Attia’s Straight Dope on Cholesterol presentation from AHS12. That would have been a great one to see in person, as he explains succinctly his understanding of cholesterol in light of the current view on its importance in health outcomes.  Over the last year or so this controversial topic has hit the media (including the Catalyst documentary investigating the use of statin medication for lowering cholesterol – a report on the resulting controversy can be found here), resulting in more people being confused about their own cholesterol readings. There is no dispute that your blood cholesterol increases with an increasing intake of fat; the real question is whether this might, over the long term, affect overall health outcomes. When looking more closely at the literature it would seem that, for the most part, messages around cholesterol and heart disease risk have largely been inflated over the years – driven by a misinterpretation or a misrepresentation of the available data. Indeed, when you look at the relationship between cholesterol levels and heart disease, around half of those who have heart related incidents have low blood cholesterol (see this summary from Chris Kresser). Does this mean that a low cholesterol level is as problematic for heart conditions as a high cholesterol level? That’s the wrong question to ask I think. The more important question is around context. It’s potentially quite different for someone with high cholesterol who has all of their health risk factors dialled in (are active, eat a minimally processed diet, manage their stress appropriately, have achieved work/life balance… I know what you’re thinking: who is this mythical creature??) However if someone is inactive, eats a poor diet, is highly stressed and doesn’t sleep, then potentially the amount of cholesterol in the bloodstream could become a main player.

Mythical Creature. Thanks, www.giantbomb.com

Mythical Creature. Thanks, giantbomb.com

Hmm. Complex, huh? Peter Attia explains cholesterol far better than I have heard anyone else do it – so I thought I’d shamelessly borrow from him (with full disclosure) to provide a synopsis of his explanation in a couple of blog posts.

Firstly – atherosclerosis – what even is it? Atherosclerosis is the thickening of an artery wall leading the the heart due to the build-up of plaque. This narrowing of the artery wall increases the risk of a heart attack. What causes atherosclerosis? Many things – cholesterol, the metabolic syndrome (cluster of risk factors), smoking, triglycerides… these are all related, however, atherosclerosis is the presence of a sterol in an arterial wall macrophage. Everything else aside – if you do not have this, then you do not have atherosclerosis. A sterol is not just that which is found in animal based sources (cholesterol) but also in plant based sources (phytosterols). These are different in structure but both have the potential to be involved in the development of atherosclerosis (see the picture below).

Different... but the same... Stolen from eurheartj.oxfordjournals.org (but not illegally - available to download

Stolen from eurheartj.oxfordjournals.org (but not illegally – available to download

When people talk about cholesterol they often refer to them as ‘good’ or ‘bad’ – like us kiwi’s pronouncing ‘Nestles’ as it is written, it’s all in how it’s been sold to us over the years. Cholesterol is essential. Without cholesterol we can suffer major health problems – the causes of which include genetic, however more interesting from a population standpoint to my mind is the link between low cholesterol and depression. Anyway). It’s involved in many processes in the body – while I won’t detail them all here, of note is its role in hormone production. Cholesterol is a precursor for sex hormones testosterone and oestrogen, also for cortisol and aldosterone. Another role is in the creation of a bilayer within virtually every cell, and holds proteins within them. Without this, we wouldn’t have the necessary fluidity that allows cells to move or interact with each other.

Cholesterol comes from both the food we eat and what our body produces – the difference is in the amounts. We consume approximately 300-500mg/d – and in New Zealand there is no longer a recommended maximum limit. Endogenously, we produce around three times that much – around 800-1200mg/d. The liver is largely responsible for this and if it gets messages that there is not enough cholesterol available, it will product more. Virtually all cells in the body are responsible for producing enough cholesterol to be sufficient for life, other than the adrenal cortex and the gonad two important exceptions given the importance of cholesterol for the function of these (the hormones I mentioned earlier).

Along with the production of cholesterol, the liver collects it there also. It is deposited into bile salts (which couldn’t be produced without cholesterol) and gets delivered through the biliary system into the gastrointestinal system. Our gut regulates how much cholesterol gets reabsorbed in the body, and most of this cholesterol is either that which is recycled or produced by the body – the rest comes from our diet. Overall, we have 40-50 grams of cholesterol in our body – so the 300-1200mg is really a drop in the ocean compared to actual cholesterol content in the body. Thus, it is a highly regulated process. While many people believe these small amounts trickling in and out of the system have influenced the action of cholesterol (and subsequently its importance in terms of overall health risk) Peter argues that it’s much more likely that any ‘abnormal’ reaction to cholesterol is in fact regulated by the internal system.

AHS14 Pt 2: quick debrief

Wow, what a whirlwind 12 days. I arrived home this morning from LA at 5.45am with an additional suitcase and minus $85 for the 10kg it was carrying. I’m just thankful that I checked the luggage restrictions before heading to the airport or it could have been a lot worse. I am glad to be on home soil, not least because I think I averaged about 6h sleep a night for the time I was overseas. Now don’t go thinking it was because I was hitting any kind of night scene in a ‘bright lights, big city’ kind of way. Unless your version of that includes a cup of tea then you’re bang on. It was really that Caryn and I had so many things we wanted to see that sleep didn’t take priority. Thankfully, real life resumes and that will be rectified in the next week.

Of course, regular followers of my blog may be expecting a synopsis of the talks from the remaining two days of the conference, but I’ve been pipped at the post by the Ancestral Health Society which is brilliant – they’ve already uploaded a number of the talks and you can find them here. Which is great as the simultaneous streams meant that I was unable to see a number of talks I was interested in, so I’ll be able to catch up with them too. It also means I’ll be able to jot down a few take homes from the overall experience rather than focus on the talks. Both Caryn and I really enjoyed the conference as it was largely nutrition, largely paleo-based (unsurprisingly) and largely low carb too. Obviously there were a number of talks around the other tenets of ancestral health – but such a big part of it is around food (or how lifestyle interacts with nutrition) that we both agreed it was one of the most relevant conferences we’ve attended. Equally, we enjoyed that the conference was attended by people from such diverse backgrounds. While we all converged upon the University of Berkley because of our interest in evolutionary health – we mixed with personal trainers, researchers, academics, nurses, IT specialists, functional medicine practitioners…. Most conferences we’ve attended have largely been with others in our field, so it was a good opportunity to mingle with others on the basis of what they value more than what they have studied or teach in. As Caryn and I stayed in the dorms at Berkely we had an opportunity to mingle more than we would have with others, and enjoyed the company of Tim (who we met initially through Jamie and Anastasia), Darcie, Dana and Sarah either through bumping into them at breakfast or in the dorm rooms and all of whom we may see again next year in Boulder, Colorado for AHS15.

An obvious highlight of the trip was to meet in person those people I’ve either followed on Twitter, or that I’ve read their book or blog, or that I listen when I tune into their podcast. There were a number of ‘big hitters’ in the ancestral health space. It was such a pleasure to meet them and to not be disappointed. At the presenters dinner we sat down with Jamie and Anastasia and were joined with Michelle from Nom Nom Paleo, Steph from Stupid Easy Paleo and Dallas, half of the original Whole 9. I regularly direct people to these sites for recipe inspiration or information and it was great to recognise that they were people genuinely interested in helping others rather than only being motivated by making money. I also had a good chat to Dr Cate Shanahan – the LA Laker’s nutritionist and author of Deep Nutrition, and Caryn and I discussed Spartan events with Ben Greenfield and saturated fat and cholesterol over breakfast with Paul Jaminet, creator of the Perfect Health Diet. I also met Jimmy Moore, podcast host of Livin La Viva Low Carb, author of Cholesterol Clarity and Keto Clarity (which I’m reading right now – it is a brilliant guide for anyone interested in ketogenic diets). A further bonus was being invited to dine with Jeffry Geber (Denver’s Diet Doctor) and his family – along with Gary Taubes. We discussed bad science and what to do with it, and at the end of the conference we came away from dinner not feeling in awe of the company that we had kept but more inspired by the work that is going on to help spread the ancestral health message.

Importantly, though, the conference was a great chance to strengthen the ties with the NZ contingent of the ancestral health conference. I’m someone who values relationships over and above most things, and to be surrounded by like minded people is something that makes me feel energised and inspired. We made the most of being in one place to share meals, debrief the day’s events and get to know each other better. It also gave us the opportunity to discuss how the first bigger symposium of AHSNZ may look next year (as we’ve got another mini symposium organised for Labour weekend in Wanaka – more details to come.) I’m sure that Caryn and I weren’t the only ones to come away feeling that the work we are doing as practitioners and also at AUT is strengthening the ancestral health message.

We also got an opportunity to see what is on offer in the US market in the way of paleo-style snacks and supplements. A favourite for me was the Epic Bar – not for everyone, this meat and fruit based protein bar is not unlike jerkey with a softer texture. It really hit the spot one morning when a sit down breakfast wasn’t going to happen. Equally the Exo bar was another eye opener – a protein bar made with crickets as opposed to whey protein – yep, not a typo. It was delicious but, then, anything that includes cacao powder and dates can probably cover up any questionable flavour that a crushed insect might taste like. I am unsure if either of these ship to NZ, but like most things I am sure that something similar will likely be available at some point. Of course in amongst the more ‘real food’ like options were the paleo treats (almond flour cupcake mixture, anyone?) however I would say there is always a place for these items and to give these smaller companies exposure at a conference with 500 attendees is a win-win. They directly target those who will be interested in purchasing, and the AHS is able to raise funds to run the conference. And those Hail Merry Macaroons are super tasty and deserve the exposure they get.

And, with that – I’m done. It is 6pm NZ time, 11pm LA time, I’m exhausted and I’ve managed to get through about 1/8th of what I wanted to share. Not particularly informative in itself, the main purpose of this is to link to other sites which can help inspire and inform as much as to give you my impression of the conference. I’m already planning on attending next year in Boulder, but more importantly, I’m just excited to be part of the AHSNZ team. For those who are interested in being involved, it’s not too long before general membership will be open. The more people we get involved, the further the ancestral health message will spread. In the meantime, get your tickets for the symposium in Wanaka on Labour weekend at Rippon Valley winery here.

Ancestral Health Symposium 2014: Part 1

So I’m writing this from San Francisco. Berkley to be exact. It is 5.24pm and Caryn and I have made it back to our dorm rooms at the end of the Ancestral Health Symposium and taking some down time before heading out to dinner with the rest of the NZ contingent to have a debrief over dinner and a well deserved glass of wine. I had prepared two blog posts actually – to put up on line that were somewhat related to the AHS (as in, they are a summary of an excellent talk given by Peter Attia on cholesterol that he gave at the AHS in 2012). However, given I have half an hour in between now and dinner I thought I would quickly jot down some highlights of the trip so far. As you know, I’m neither systematic nor logical in how I collect my thoughts, and this blog post will reflect that. These are merely some of the many things that have piqued my interest.

Some key take home points from three of the first speakers on Day one of the conference:

Dan Pardi – creator of Dan’s Plan talked about the integration of technology to help people stay motivated in their health and wellbeing goals. Now, this concept is nothing new – anyone with a pedometer or fitbit (or anyone that tracks…anything) will be familiar with these tools – however, for some, the idea that we can use technology as a way to advance health through an evolutionary health model seems somewhat contrary to the goal of getting back to basics that many advocate. this talk was a good reminder that ancestral health is not about trying to emulate the environment of our ancestors and eschewing technology – it’s about finding ways of enabling us to meet these health goals.

Grace Liu, a researcher in the gut health area talked about how our changing environment has affected the diversity of the bacteria in our gut and how this has impacted on health.  Some challenges included:

  • the introduction of agriculture;
  • our decreased exposure to mud and manure;
  • electricity and the invention of refrigeration eliminating the need to ferment our food in order to preserve it;
  • using antibiotics to to fatten livestock; and for infants
  • being born by caesarean and the increasing use of formula all presenting challenges for the growth of that bacteria.

Grace’s recommendations for people who want to help preserve gut health by increasing the diversity of the bacteria were to:

  1. Include fermented foods
  2. Include resistant starch (a type of starch that is used as a fuel for the bacteria in our gut, and found either in strains of fibre or particular foods such as potatoes and unripe bananas)
  3. Exercise
  4. Lifestyle (manage stress, make time for meditation, minimise environmental toxins in all forms)

Denise Minger, known predominantly for her critique of the China Study and author of Death by Food Pyramid (a great read of the history of the dietary guidelines) gave a somewhat surprising talk regarding the plant based versus a carnivore diet for overall health outcomes. Most people would have expected the obvious outcome that anyone improving their diet will experience health benefits because the baseline diet was so bad. Not so. In fact, what Denise found was the the very antithesis of the paleo approach to diet was very successful at improving health outcomes for people that were long lasting and sustainable. She first investigated Walter Kempner’s work on the Rice Diet. A typical day’s intake looking something like this:
Breakfast: 1 c brown rice, 1 small glass of orange juice, 2 figs and unsweetened coffee
Lunch: 1c brown rice, 1 c stewed tomatoes, raw carrots and 1 glass skimmed milk
Dinner: 1.5 c Russian Pilaf, 1 bowl mixed carrots, cabbage, cucumber, ½ c fresh fruit cocktail

Based on 2400 Cal per day, 350g rice, unlimited juice and fruit and totaling between 100-400g/d of sugar, this diet was successful in reversing kidney disease and enabling people to regenerate insulin production. An analysis of the Pritikin diet illustrated that it was useful in reducing tissue attoxia (lack of oxygen in the tissue) and finally Esselstyn, famous for the diet that helped reverse heart disease in a small group of patients that had suffered a coronary event, has very recently published a trial that found heart disease symptoms reversed in 198 patients following the diet for three years. I’ve tried to find the corresponding research but have only found this white paper. Further, though one may argue that no one could stay on these diet plans for the rest of their life (and, indeed, Kempner – it was revealed – used to whip his clients if they fell off the diet bandwagon) both the Esselstyn and the Kempner diet’s appear to enable people to reverse their health issues for the long term – even when returning to a more sustainable diet. Denise points out that the health benefits seen on a very low fat diet (both of these were 10% of their calories coming from fat) are very much the same as those on a very high fat diet (80% fat) and that low fat studies (at around 30%) aren’t low fat enough to show the actual health benefits. While this is all very well and good – what is the point of following such an extreme diet approach if it isn’t something that can be followed in the long term? Or even in the short term? I don’t know if the corporal punishment approach would go down that well with my clients. But, then, I’ve not tried it. At any rate, this certainly provided food for thought – even if that food is rather bland and wholly unsatisfying.

And – dinner time. Short and sweet (well, shorter by about 200 words), you can see from the little I’ve provided you with, that there is undoubtedly more to follow to debrief you on the latest research going on in the ancestral health field. Not only that, but I will have to post a blog about the food experience to date on the trip also as Caryn and I make our way from San Fran to LA. That in itself is as interesting as the conference for the likes of Caryn and I.

A foodie's delight. Not necessarily that new. Or that different, but just... in a different location. Though have to say, the fruit is massive here.

A foodie’s delight. Not necessarily that new. Or that different, but just… in a different location. Though have to say, the fruit is massive here.

Raise your glass: a toast to Dry July.

Well, we’ve made it. It’s 2/3 of the way through calendar winter and, for Auckland at least, the climate starts to feel a lot more like spring (despite the deluge of rain this morning). Along with that, we can all raise a glass to those who participated in Dry July. A month without a drop of alcohol is, for some, a big deal. Earlier in the month there was an opinion piece in the Herald regarding Dry July, questioning the utility of it – asking what the point of going one month alcohol free when actually people should look to having a few alcohol free nights per week instead. For those who follow my Facebook page, you’d have seen my initial comments about it. There’s no dispute that choosing to drink moderately throughout the week and including alcohol free nights per week is important; certainly the toxic effects of excess alcohol consumption on inflammation and our organs that contribute to chronic disease are well established. But to my mind, the editorial missed the point. Yes, Dry July is an exercise in abstinence that isn’t a long term approach to alcohol consumption for most. However some people who undertake the challenge, sponsored or not, choose to do it because they are curious as to the impact that not drinking will have on their wellbeing. And these aren’t people who you might consider would ‘need’ it.

A client of mine is just that person. She wasn’t close to the maximum of two standard drinks per day, 14 in total across a week. She enjoyed just one on most nights throughout the week, perhaps two at the most on the weekend. The last time she drank what she would consider ‘too much’ was back in 2008 on a girls night out. And it wasn’t that one drink made her feel drunk – or feel anything other than relaxed – however there was a nagging thought in the back of her mind that the attachment to the glass of wine wasn’t a good thing. She didn’t hang out for the wine from 8am in the morning but it was a little oasis of relaxation in an otherwise busy day that started before 5am with an ironman training session, to move swiftly into her role in a busy insurance firm to another training session to finally arrive home for dinner at around 8pm. It was the only thing that helped her wind down and there was nothing she enjoyed more than that glass of wine as she prepared dinner. We had a discussion about this. While she enjoyed the glass of wine with her partner, she would also take pleasure in drinking it by herself. Her main fear centred less around the physical damage of her drinking but the psychological pull. Her parents are heavy drinkers and have been for years, so alcoholism is something that runs in her family. For her, going alcohol free was as big a deal as the person who has a drink or three after work and then one with dinner four or five nights a week.

What she noticed across the course of the month was interesting. As she reflected back to me this week, she said that the first week was eye opening. She realised that she had been waking up feeling slightly groggy and dehydrated for years without realising it. It wasn’t until she decided to go cold turkey that she discovered it wasn’t a natural state for her to be in. Even the seemingly small amount that she drunk had that effect on her. While the first week was a little strange – as the habit of a glass of wine after work has been ingrained for years – it became easier across the course of the month to go without. In fact, by the end of week four, with just a few days remaining, she realised the main issue for her giving up the wine was the question as to whether or not she would go back to drinking it. The exercise in abstinence proved that she could go without – however to reintroduce it suddenly put her in a conundrum. Would that attachment still be there? Yes, likely – it’s only been a month. The question of whether or not she should drink alone also came up. For some, this type of drinking is a red flag for a more serious drinking problem. However, this isn’t the case for everyone, and I didn’t see it as an issue with this client particularly. The association of guilt here is a lot like guilt around food – I think that in itself can be problematic. If you feel guilty for the drink that you have, you are more likely to drink quickly (almost like it didn’t happen) and not enjoy it. For some, this could also increase the amount being consumed as ‘this is the last time I’ll have a drink by myself.’

The thoughts going around her head were largely related to her family history – which is why she decided to do Dry July in the first place. The one thing she was most concerned about was the possibility that the first drink could open the flood gates and she would be on a slippery slope from one drink a night to two bottles of wine. You’d probably agree this seemed extremely unlikely. She’d been drinking this way for at least 10 years and it hadn’t cascaded into more problematic behaviour. We bandied about ideas that could help her enjoy her wine without the associated (and unnecessary) guilt – but this put rules on it which also didn’t make her feel comfortable. In the end we decided that, if she felt like a glass of wine, she would first have a sparkling water to satiate her thirst, then pour a glass if she felt like it. This solution may mean the end result wouldn’t look any different from what she was doing before Dry July, but it might at least offset the dehydration she felt. Also, for anyone who drinks, this is a good way to slow down how quickly you consume alcohol, especially those who neck the first drink due to thirst. I also always recommend to clients they back up every alcoholic drink with a non-alcoholic, sugar free option. That way they would drink only half as much as they would normally. I’d say I have about a 30% hit rate with that little gem. Those who do it though report feeling a lot better the next day, heavy drinkers or not.

So, raise your glass (of your drink of choice – alcoholic or not) to Dry July, as it creates an awareness around drinking behaviour – for heavy and light drinkers alike. Cheers.