11 things you may not know about perimenopause (and 10 things you can do about those symptoms).

I know what you’re thinking. She’s too young to be writing about perimenopause, right?! Actually, no. I might feel 24 years old, but it only takes being around younger age groups to remember I’m not! Despite the ‘M’ word being almost a taboo, unwanted phase of life that some women fear (and men too!) it is a natural part of our lifecycle. What isn’t natural are the symptoms associated with menopause. Like premenstrual symptoms, the discomfort experienced through perimenopause may be common, but it’s not normal. This was reaffirmed in my mind when I listened to a fabulous interview with Lara Briden (naturopath who works with women with hormone imbalances, based in Sydney and Christchurch). A wealth of information who had some great information around why we can experience symptoms and (importantly) what we can do about them.

  1. Defined as 10 years before going through menopause, practitioners often view this as highly variable, with women from 35 years to 55 years in this perimenopausal state. The average time spent here is around 4 years. Though, as with any ‘average’ this might not reflect your experience!
  2. All hormone levels change during perimenopause. There is first a decrease in progesterone, which changes the balance of progesterone to oestrogen (some describe this as ‘oestrogen dominance’, though not all practitioners like using this term). Testosterone also declines, and this is an important hormone for sex drive. Finally oestrogen drops – and while we will continue to produce oestrogen (as this occurs not only by the ovaries but by the liver, breasts, adrenal glands and by fat tissue, it is at amounts of around 30-60% lower.
  3. Oestrogen is a major regulator of a number of processes in the body, and the sex hormones and our glucocorticoid hormones (the most ‘known’ one, cortisol) are controlled by the hypothalamus -the part of our brain who is also the controller of our sex hormone regulation – therefore it makes sense that a change in one will result in a change in all of them.
  4. Some of the main symptoms of perimenopause are
    1. Heavy periods
    2. Hot flashes
    3. Breast tenderness
    4. Worsening of premenstrual symptoms
    5. Lower sex drive
    6. Headaches or migraines (due to sudden removal/reduction of oestrogen)
    7. Fatigue
    8. Decreased sense of wellbeing (research shows that extended periods of low oestrogen, fluctuating levels of oestrogen and sudden withdrawal of oestrogen – via surgery or stopping oral contraceptive pill – is affected with lower mood)
    9. Irregular periods
    10. Brain fog and memory – oestrogen helps consolidate both episodic and spatial memory in the brain, and protects against cognitive decline as we age.
    11. Vaginal dryness; discomfort during sex
    12. Urine leakagewhen coughing or sneezing and an urgent need to urinate more frequently – due to oestrogen’s role in maintaining the vascular mucosa folds in the vagina, acting as a watertight seal.
    13. Mood swings (via fluctuating levels of hormones)
    14. Trouble sleeping
  5. Some women are ABSOLUTELY FINE and sail through perimenopause. Generally, though, those that have been on the oral contraceptive pill are more likely to experience symptoms than those that haven’t. This may be due to the difference in the hormonal balance once the pill is removed. The pill provides large amounts of synthetic hormones, and it is a huge adjustment to go back to the normal (lower) levels of hormones. Approximately 147,000 women in New Zealand take the oral contraceptive pill, of which 80% of them are on a combined pill, delivering oestrogen and progesterone.
  6. The types of hormones in the pill are synthetic and are not ‘bioidentical’ – meaning that the amounts are higher than what the body would produce AND they are in a form that the body can’t use. The pill doesn’t regulate hormones, it shuts them off.
  7. During perimenopause, women can have fluctuating oestrogen levels due to variable concentrations of FSH (released by our pituitary gland in response to a low oestrogen environment – it isn’t necessarily all low oestrogen. This could also be a result of an inability to detoxify and clear out oestrogen metabolites.
  8. A well-functioning liver is required to remove oestrogen from our body and prevent build up and associated symptoms. Our liver packages up oestrogen metabolites and removes it through our detoxification pathways. We need our inbuilt antioxidants to be firing, along with certain nutrients (selenium, B vitamins and glycine (not present in large amounts in the standard diet) to do this.
  9. Many women going into perimenopause are insulin resistant (oestrogen has an insulin-sensitising role in the body and influences glucose uptake) – this partially explains the increase in body fat (particularly around the middle) that many women experience as they progress through. This makes it harder for their body to metabolise and use carbohydrate effectively
  10. Many women going into perimenopause have a low thyroid function due to age-related changes in thyroid physiology. These include a reduction of thyroid iodine uptake, synthesis of free thyroxine (FT4) and free triiodothyronine (FT3) and the conversion of FT4 to reverse triiodothyronine (rT3). TSH levels may be slightly elevated. Luteal-phase spotting, or lumpy breasts may indicate this.
  11. Your gut? SUPER IMPORTANT!!! The oestrogen might get detoxified (packaged up ready for removal) via pathways in your liver only to be unpackaged (deconjugated) again by nasty gut bacteria which pushes it back out into the blood stream as more toxic forms of oestrogen.

These 11 points may or may not have been news to you – certainly probably not to those experiencing some of the symptoms, or who have dug a bit deeper to determine the cause of the symptoms. This wasn’t a post for you to sigh in resignation and decide there is nothing you can do. Yes these symptoms and health outcomes are common – but (as stated earlier) they are not normal. Like many things, we normalise a lot of health issues because so many people experience them. We just think they are an inevitable process in ageing and moving into a different phase of life. Certainly (I gotta say), some health professionals don’t suggest otherwise so it’s no surprise many are led to believe this.

Some awesome tips from Lara as to how to start the process of mitigating symptoms – some are great DIY ones that you can put into action immediately; others will likely require the help of a practitioner who has a solid understanding of how our hormones interact – this may be your open-minded doctor, which is excellent – or naturopath, nutritionist or dietitian.

  1. Limit alcohol consumption – it impairs oestrogen clearance rates from the liver and may be one of the influencing factors in the relationship between alcohol and breast cancer risk
  2. Limit or omit dairy –dairy can increase oestrogen in the body, increase insulin release and the A1 caesin in dairy is pro-inflammatory and increases gastrointestinal inflammation (which could then push inflammation out to rest of your body).
  3. Ensure adequate vitamin D status – optimal is around 100-150nmol/L which is required for the production of all hormones, and related to other hormonal issues such as endometriosis
  4. Reduce intake of carbohydrate if following a higher carbohydrate approach, and get rid of processed, refined foods and sugar.
  5. Eat your brassicas: broccoli, Brussel sprouts, cauliflower, cabbage – all provide di-indolylmethane (DIM) which targets certain proteins in our body that help reduce inflammation and balance hormones (particularly detoxifying oestrogen). Supplementing with this is also really helpful, but only once you establish that oestrogen clearance is an issue for you – super unhelpful otherwise (a practitioner can help you find this out – and there is a test I’ve started using with clients called the D.U.T.C.H test which is able to measure each hormone and it’s metabolites in much more comprehensive detail than a blood test alone.
  6. Ensure a healthy gut: bloating, excessive gas, cramps and diarrhoea or constipation are not the normal consequence of eating (though they are extremely common). Keep a food diary to establish what might be causing your digestive upset by connecting your symptoms to your food intake. Work with a health practitioner experienced in the ‘real food’ digestive health to help not only heal your gut, but seal it too.
  7. Turmeric in therapeutic doses (more than you can get from food) helps reduce oestrogen related oxidative stress, reduce prostaglandins (inflammatory biomarkers) – opt for one that is also combined with bioperine (to make it more bioavailable) such as this Good Health 15800 Turmeric complex. The alternative is one that says it is formulated to have smaller, more bioavailable particles, and the Meriva formulated varieties have this.
  8. Iodine: low dose supplementation can be extremely helpful in supporting the pathways associated with thyroid hormone production which in turn affects the sex hormone production pathways. Again, talking to a practitioner is a good idea to establish your own requirement. However, 150 micrograms per day (and having 2-3 brazil nuts to balance this with selenium) is a safe amount.
  9. SLEEP. Hands down, the most often overlooked yet important restorative, nourishing thing you can do to support your hormone health.
  10. Meditation. Journalling. Yoga. Diaphragmatic and full belly breathing. Slowing down. Yep – stress reduction.

Regardless of if you are pre, peri or post menopausal, I think there is some excellent information here that will be helpful for hormones in general actually, and if you are experiencing some of the unwanted (and unnecessary in most cases) symptoms of hormone balance, this may give you some pointers as to how to combat them. Definitely check out Lara’s site for accessible and informative hormone related content.

PC www.gazetteinterviews.com

Let this not be you. Or your mum. Or your wife. PC http://www.gazetteinterviews.com.

 

Like what you read? For more, check out mikkiwilliden.com for individualised nutrition plans, or sign up now for online nutrition coaching and meal plans.

The Gout: what you need to know and 7 things you can do about it.

  1. Gout is an auto-inflammatory disease caused by a disorder in purine metabolism and the resulted chronic elevation of blood (serum) uric acid (i.e., hyperuricemia)
  2. Men have a higher risk of gout at a lower given blood level of uric acid, and at a lower age than women – generally 10 years earlier.
  3. Women who go through early menopause, or have estrogen deficiency are at higher risk than women who progress through menopause at a normal age, due to oestrogen’s role in increasing uric acid excretion.
  4. Insulin resistance increases risk of gout, as insulin reduces uric acid secretion. The relationship between insulin resistance and gout is more pronounced in women than in men.
  5. There is a bi-directional relationship between high blood pressure and gout: ie if you have high blood pressure, your risk of gout goes up (independent of diuretic medication that is taken), and if you have gout, your risk of developing high blood pressure also increases. High blood pressure can result in damage to kidney and a reduction in uric acid excretion, and the inflammation associated with gout can stiffen and damage arterial walls, and reduces production of nitric oxide – which helps widen arteries.
  6. Genetics play a role in determining risk associated with gout – and people with a particular genetic profile (such as those of European descent with the SNP sequence SLC2A9 as an example) have an increased risk, as do those with ABCG2 rs2231142. However, as with any genetic risk factor, lifestyle determines if these genes are switched on or off, so while this information could be useful (and more people are starting to find out their genetic profile and determine what it means for their health), it is your lifestyle habits predominately regulate overall risk
  7. Triglycerides increase in the bloodstream when people overeat refined carbohydrate foods, and recent research suggests a reduction in serum uric acid occurs when triglycerides decrease.
  8. Alcohol intake is associated with an increased risk of gout – beer more so than wine.
  9. Overall fructose load in the diet is the only type of carbohydrate that is known to increase uric acid levels, potentially because when metabolised, it depletes phosphate and therefore doesn’t help produce ATP (energy) in the body and instead increases uric acid production. Fructose from processed food (and particularly sugary sweetened beverages) can elevate insulin levels and increase risk of insulin resistance. There may be a genetic element to this also, with people who have polymorphisms in SLCA9 and ABCG2 genes responding unfavourably to a load of fructose.
  10. A large cross sectional survey found that people following a vegan diet had the highest serum uric acid concentrations compared to fish eaters, meat eaters and vegetarians, independent of smoking status or alcohol intake.
  11. While seafood is often cautioned against for people who experience gout due to its purine content, a number of studies have failed to find a relationship between seafood intake and serum uric acid levels. Those that have found a relationship may not have adjusted for body mass index (BMI), which can confound the relationship as it did in this study. Indeed, those populations who are at greater risk today (such as Maori and Pacific among New Zealand population) enjoyed a traditional diet of predominantly seafood, vegetation, tubers and gout was non-existent.

What to do?

  1. Look after your gut. Bacteroides caccae and Bacteroides xylanisolvens are increased, and Faecalibacterium prausnitzii and Bifidobacterium pseudocatenulatum depleted in the gut of people who experience gout, suggesting a strong correlation with the presence of gout. F prausnitzii is one of the most abundant bacterium in the gut of a healthy individual, helping produce short chain fatty acids butyrate, which is fuel for our gut bacteria, and the provision of B pseudocatenulatum improves markers of gut wall integrity. So these are pretty important! While this doesn’t necessarily mean that the provision of certain bacteria through probiotics will reduce gout attacks, it does suggest that inflammatory processes of the gut play a role in the presentation of gout and provides further evidence of the importance of a diverse population of bacteria in the gut for overall health.
  2. Supplementing with 1500mg vitamin C reduces serum uric acid and its antioxidant functions may also help kidney function by reducing inflammation.
  3. Like your coffee? You don’t have to go without if you have gout and in fact, 4-5 cups per day have found to decrease serum uric acid that isn’t seen with green or black tea, or total caffeine intake. Decaffeinated coffee has afforded similar benefits, leading investigators to suggest the phenol content (phytochemicals) might increase insulin sensitivity and decrease serum insulin, as discussed above insulin levels have a positive correlation with uric acid due to decreased renal excretion. Furthermore, xanthines, either in caffeine or in coffee itself, could inhibit xanthine oxidase – an enzyme that increases reactive oxygen species (and inflammation).
  4. Magnesium intake is associated with a decreased serum uric acid level in males, and marginal intakes is associated with higher levels of markers in the body indicative of inflammation. Magnesium is low in soil which makes dietary sources of the micronutrient not as high as they once were, therefore supplementing with magnesium of 300-600mg/day (depending on bowel tolerance) is likely a good idea. (To be honest, I’m a big fan of magnesium supplementation for pretty much anyone male or female, given it’s a co-factor in over 300 processes in the body).
  5. Tart cherry extract – not just useful for sleep – is found to reduce the prevalence of gout flare ups in cross sectional studies, potentially due to the presence of polyphenols including anthocyanins, and vitamin C found in the fruit, which have anti-inflammatory and antioxidant affects.
  6. The consumption of low fat dairy products is linked to a lower risk of gout in larger population studies.*
  7. Anecdotally (as in, I didn’t find any study on pubmed to support this), baking soda is used to increase pH level of the blood (¼ teaspoon in water), thus making uric acid in the blood able to be excreted. If you know of any studies around this that I’ve missed, let me know!)

The take-home?

While a low purine diet is often recommended as a dietary prescription for people with gout, many purine-containing foods (such as seafood and vegetables) do not contribute to hyperuricemia or gout and may in fact be protective. The effects of red meat consumption on serum acid levels are arguably hard to disentangle from other elements of the modern dietary pattern, and are often in conjunction with higher alcohol intake, lower fruit and vegetable consumption and higher fast-food intake – all contributors to inflammation in the body. In addition, the agricultural practices of the cattle industry in countries such as the US where many of the epidemiological studies that associate red meat with poor health (including higher serum uric acid levels) include the use of antibiotics, poor farming practices and animals that are grain and not grass fed, altering the fatty acid profile of the meat to be higher in omega 6, pro-inflammatory fats. Furthermore, processed and fresh meat is often grouped together – thus a steak is viewed the same as a hamburger from a fast-food outlet – the latter often being in the company of a bun, fries, mayonnaise made with industrial seed oils and a sugar sweetened beverage – the adverse effects which many, myself included, argue cannot be adjusted away by a statistician when determining risk.

*I don’t think you need to start consuming low fat dairy if right now you’re enjoying the benefits of full-fat dairy in the context of an awesome diet. I think this could well be indicative of overall lifestyle patterns. I’d be surprised if there were studies showing that risk of gout is increased in a diet that is whole food, minimally processed, an abundance of vegetables that also incorporated full-fat dairy products.

 

14 reasons to ditch the toast and jam (and 7 key tips to help you do this).

After feeling like I’d taken a trip back to 2003 with some of the sports nutrition posts and articles I’d been reading lately, I got tagged in a cool picture from a listener of our Fitter Radio podcast  – a triathlete who has switched from the traditional higher carb, lower fat diet approach to eating lower carb, higher fat, real food whilst training and commented she ‘didn’t know her 41 year old body could be the best body I have ever had’ (Woot! high fives all around!!) This coincided with finishing Mark Sisson’s Primal Endurance book.

Mark outlines 115 reasons why athletes should train and eat the Primal Endurance way. I concurred with pretty much all of them. I have added my own 2c worth, added some literature below (and cut it down to 21 for brevity’s sake). While geared towards athletes, hands down this is applicable to everyone. Everyone.

So if you’re currently eating toast and jam pre OR post training (or in general), I’ve outlined the 14 reasons why you need to ditch that junk and become a fat burning beast, and 7 key tips to help you get there.

  1. Western diet is based on excess grains and sugars (and low fibre) which stimulates excess insulin production, leading to lifelong insidious weight gain, chronic inflammation and elevated disease risk factors.
  2. A high carb, grain-based diet can leave endurance athletes nutrient deficient (due to phytic acid effects on minerals), inflamed and more susceptible to the oxidative damage of the stress of training, general life and poor nutrition.
  3. The way that most people consume modern grains (cereals, breads, pasta) ends up being a cheap source of calories which are immediately turned into glucose upon ingestion and offer minimal nutritional value. There are no good reasons to consume these types of grains and many good reasons not to, especially for those who are sensitive to gluten and other anti-nutrients found in wheat.
  4. Everyone is sensitive to the health compromising effects of grains at some level, especially the pro-inflammatory effects of gluten and the propensity for the lectins in grains to cause leaky gut syndrome.
  5. Even lean people suffer from the consequences of carbohydrate dependency, such as chronic inflammation, oxidative damage, and accelerated ageing and disease risk factors.
  6. Carrying excess body fat despite careful attention to diet and a high training load is largely due to carbohydrate dependency caused by a grain-based diet and chronic training patterns.
  7. Carbohydrate dependency cycle looks like this: consume a high carbohydrate meal – elevate bloods sugar – stimulate an insulin response – shut off fat metabolism and promote fat storage – experience fatigue and sugar cravings – low blood sugar elicits stress response and we consume more carbohydrates – stimulate the fight or flight response to regulate blood sugar – dysregulate and exhaust assorted hormonal processes, and end up in burnout and weight gain (potentially lifelong)
  8. Weight loss through portion control, low fat foods and calorie burning is ineffective long term. And while we think calories burned through exercise stimulate a corresponding increase in appetite – research might not back this up. I tend to think that people are more likely to eat more because they ‘reward’ themselves OR the long slow training allows increased opportunity to eat sports ‘junk food’ and the amount of calories burnt through training is far less than you think – and overestimated more so in females in certain instances. At any rate, the secret to weight loss is hormone optimisation, primarily through moderating excess insulin production.
  9. Endurance athletes can begin to dial in to their optimal carbohydrate intake by asking themselves the question ‘do I carry excess body fat?’ Any excess body fat calls for a reduction in dietary carbohydrate intake to accelerate fat burning.
  10. Endurance athletes who already have an optimal body composition but are looking to optimise training and recovery should choose high nutrient value carbohydrates. These include a high volume of vegetables, a moderate fruit intake, kumara/potatoes and other starchy tubers, dairy for those that tolerate, wild rice, quinoa and small amounts of dark chocolate.
  11. Endurance athletes with high calorie needs who also have an optimal body composition can enjoy occasional treats, but the habit of unbridled intake of nutrient-deficient carbohydrates should be eliminated in the interest of health and performance.
  12. Primal style eating (or eating minimally processed foods) is fractal and intuitive, and when escaping carbohydrate dependency and becoming fat adapted, you don’t have to rely on ingested carbs for energy. Eating patterns can be driven by hunger, pleasure and maximal nutritional benefit.
  13. Escaping sugar dependency and becoming fat adapted gives you a cleaner burning engine, since glucose burning promotes inflammation and increased oxidative stress
  14. Ketones are an internally generated, energy rich by-product of fat metabolism in the liver when blood glucose and insulin levels are low due to carbohydrate restriction in the diet. Ketones are burned efficiently by the brain, heart and skeletal tissue in the same manner as glucose. You do not need to be on a ketogenic diet to upregulate your ability to produce ketones – you can do this via a lower carbohydrate approach.

HOW TO DO THIS: 7 KEY TIPS

  1. Step one: omit sugars, grains, industrial seed oils for 21 days. Step two: emphasis highly nutritious foods such as meat, poultry, vegetables, eggs, nuts, fish, fruits, some full fat dairy, seeds, and kumara/potato.
  2. 100g or less of carbohydrate promotes fat loss, 150g is around maintenance level and over this could promote lifelong weight gain and over 300g could promote disease patterns.
  3. While transitioning to primal there are some struggles initially due to lifelong carbohydrate dependency and the addictive (for some) properties of sugar and excess grains and wheat. Headaches, dehydration, lower blood pressure and ‘dead legs’ are all initial side effects when removing processed food. Trust me – this too will pass.
  4. To minimise side effects, start the transition in a base-training phase of your training where training occurs at an easy pace. The transition phase can take anywhere from 2-12 weeks initially.
  5. Consume salt. Don’t underestimate the importance of this! Lower circulating insulin affects your body’s ability to retain sodium (and other electrolytes) – so we need more, particularly as processed food (of which you are no longer basing your diet around) is where you got around 70% of your sodium from.
  6. You can accelerate the process of fat adaptation by instigating some of the tactics used by athletes who opt to ‘train low’ – i.e. in a low glycogen training state. Some of these are naturally undertaken if you train without eating in the morning, or work out after dinner in the evening and don’t consume anything post-workout. If you’re new to this, have a read through to establish which might suit you best, and start instigating 1-2 x per week. Don’t undertake all of them as this aggressive approach could cause too much additional stress, derailing your plans to become a fat-burning beast.
  7. The FASTER study and Peter Attia, Sami Inkinen suggests any endurance athlete can become fat adapted and deliver performances that may be superior to carb-fuelled efforts all of the way up to anaerobic intensity. This is a new and growing research space, one AUT is testing, among other Universities around the globe.
Strong, lean and awesome at 41y.

Strong, lean and awesome at 41y.

 

PS What the Fat Sports Performance – currently an ebook, about to be published is one I can’t WAIT to read as well – sure to be a goody.

Could your gut health be responsible for your high cholesterol?

You are probably aware if you have been reading my blog for a while and following likeminded people that it’s not as black or white as whether or not your high cholesterol level is a problem. Much as I get a bit on edge when I see plates of food without any colourful vegetables (I’m not going to lie to you!), I get a little bit twitchy when I see it professed everywhere that it’s no longer a problem to have a high cholesterol level. Not true. Now cholesterol is essential to life. Without it, we wouldn’t be able to make hormones, repair cell membranes and do 68 other things that require cholesterol. Your body makes 85% of the cholesterol circulating in your bloodstream even, meaning that, for most people, the cholesterol eaten by way of animal products (animal protein, eggs, cream, butter, cheese) will have very little impact on their overall cholesterol level in the body.

One of the main factors that can cause high cholesterol levels is not the cholesterol that you eat (and you’ll be aware that in New Zealand we’ve not had a recommendation around reducing cholesterol containing foods for a while – though the rumour of the egg just will not die). It’s also not just about the fat that you eat. While scientists were busy trying to prove the diet-heart-hypothesis correct over the last 50 years (you know, the one that has pretty much governed our public health nutrition messages and is still today being pushed by nutrition authorities, despite the failure of aforementioned scientists to do so), the powerhouses of the food industry were busy manufacturing and marketing those low fat, processed, refined carbohydrate-based foods that contribute to an inflammatory state which underpins all chronic disease – including heart disease and high cholesterol levels. That is something I have understood well. However after listening to that brainiac Robb Wolf discuss cholesterol with Dr Rhonda Patrick on a recent podcast about cell metabolism the role that the gut plays in both the inflammatory state and our cholesterol levels which could determine whether or not we should be concerned was touched on. One of these was through increasing insulin resistance (IR; and inflammation) at the local level of the gut, and the other was the inflammation that occurs through gastrointestinal or gut issues which may include this IR, but also any challenge which stimulates an immune response.

We know that IR is caused by high circulating blood sugar levels requiring a constant response from our pancreas to produce the hormone insulin to ferret that glucose to where it’s required (working muscle tissue, our carbohydrate stores, red blood cells and retina, brain and excess converted to triglycerides in the liver). Constant and chronic high blood sugar levels and subsequent insulin release causes the pancreas to work overtime which, over time and in some situations, our body is unable to read appropriately or respond effectively – our cells become immune to the insulin trying to deliver glucose and glucose and insulin hang around our blood system causing glycation of proteins, cell damage, oxidation and inflammation. The IR causes systemic inflammation which further drives insulin resistance, higher blood triglycerides, lower HDL cholesterol and weight gain, specifically central weight gain which creates even more inflammation. A bit of a cascade which, if not managed, leads to type 2 diabetes (one of the major ‘end points’ of insulin resistance, if you like). Further, those with type 2 diabetes tend to have higher cholesterol levels. Well, what if this also starts in the gut?

Dr Rhonda Patrick spoke of a paper she read in Nature* that reported on research that showed chronic over consumption of processed refined carbohydrates can cause epithelial cells of the gut to become insulin resistant and unable to take up the sugar. We get IR in the local level of the digestive tract and this is pushed out to the rest of the tissues because of the inherent systemic features of the inflammation. Meanwhile, the bacterial cells that are present in our gut are getting all of the glucose that they want and thriving*. Because the IR means our gut cells aren’t able to take the glucose up, the goblet cells in our gut (the ones responsible for secreting mucus to protect our gut wall) aren’t getting the substrate required for them to make energy and produce the mucus to protect our gut intestinal lining. Over time, with no energy, the gut barrier will begin to break down.

Now – this is where the quality of the carbohydrate matters. Dense carbohydrates such as potatoes, sweet potatoes and minimally processed grains tend not to be metabolised in the upper portion of the small intestine and tend to provide more fermentable substrate that feeds our gut and supports our gut health (for an excellent paper by Dr Ian Spreadbury – incidentally one of the speakers at the upcoming Ancestral Health Society conference in Queenstown in October, click here). This means that these types of carbohydrate are not going to create the inflammation in the way that those refined grains do – the ones that we base our public health recommendations on (cereal, wholegrain bread, pasta and the like).

So, that inflammatory state that is started locally at the gut level is another mechanism that explains how the state of our gut can determine whether your high cholesterol level could be a problem.

The other one more directly affects the LDL cholesterol circulating the body.

FACT: the gut is the nexus to health – it has the largest concentration of immune cells as it is exposed to the external environment (food). Those immune cells are there to fight off things which are pathogenic.  The gut also it has the highest concentration of bacterial cells, and immune cells and bacteria together are NOT a good thing, particularly when they come into contact – that’s why we have that epithelial barrier that protects the immune cells.  As soon as that barrier breaks down, the immune cells come into contact with the bacteria cells and it’s all on, they start firing off these pro-inflammatory cytokines to kill off the bacteria. This results in the bacteria releasing off endotoxin – which is where some of the problem relating to LDL cholesterol can originate.

Bacteria in the gut have a cell wall called lipopolysaccharide which holds endotoxins –it gets released into the circulation when the bacteria are dying (which is why anyone who is undergoing diet or supplemental changes to change the bacteria in the gut might experience initial discomfort as the bad bacteria die off). This increases production of very low density lipoprotein (and LDL eventually) because these bind endotoxins – they soak it up like a sponge. However, instead of being delivered back to the liver to be recycled it remains in circulation as the endotoxin binds to the LDL receptor on this particle and prevents it from being taken back up by the liver. This will increase the likelihood of the LDL particle being oxidised – a major risk factor for cardiovascular disease. You know it’s not about LDL cholesterol or total cholesterol, it is to do (in part) to particle size –the small dense particles have been associated with heart disease.

Now the problem with these LDL particles that have an endotoxin attached is that they are the smaller, denser LDL particles. These particles, already a risk factor for heart disease now have a bacterial signal floating around the blood stream. This causes your immune cells to suddenly be on high alert. The macrophages that come to kill off the bacteria are attacking the LDL and endotoxin and the subsequent action of the immune system starts a cascade of events which over time will lead to the stiffening and narrowing of the artery as it gets stuck there.

Is your head spinning? Tell me about it. And I’m not a brainiac and suspect this could have been explained far more simply by someone far more intelligent than I. However, the main take home from this is that if you are someone that leads a lifestyle which promotes inflammation (high intake of processed carbohydrates and vegetable oils, little to no vegetable fibre, no exercise, lack of sleep, too much exercise, smoking, high consumption of alcohol…) then your high cholesterol reading could be a problem. That, for most people, should by now be a no-brainer.

However, if you are someone who has these factors dialled in and still has a high cholesterol reading, perhaps it wouldn’t hurt to consider the health of your gut.

*try as I might, I couldn’t find this paper. Let me know if you can as I’m interested to read it. Thanks George.

(Not me, though I'm as cute as this dude IMO) - and thanks to http://mrmenoc.wikia.com/wiki/Mr._Brainiac for image.

(Not me, though I’m as cute as this dude IMO) – and thanks to http://mrmenoc.wikia.com/wiki/Mr._Brainiac for image.

Spice it up

One of the benefits of eating real food is that it minimises the amount of processed refined foods that drive the inflammation pathways in the body which, as you know, is the underlying cause of modern chronic disease. From a general health perspective, this is awesome. From an athlete perspective it is even more so – given that the training derived oxidative stress causes cell damage and breakdown, increasing recovery time from sessions. Anything that impedes recovery is not going to allow you to make the fitness gains you are looking for. Of course, it’s more than just diet you have to consider.  I’m three weeks post-marathon and am up to running around 50 minutes every 2-3 days, with calf and foot niggles making me more cautious that what I’ve needed to be in the past. It’s frustrating for me to tell you the truth; yes I enjoy gym work and swimming, but there is nothing I love more than running and when the weather is blossoming into summer and the choice is between a Smith squat machine or Auckland Domain, I’d know where I’d rather be. Worse is that I really only have myself to blame. I’ve pretty much got my diet dialled in (as to be expected – though, no, it’s not perfect as I am human 😉 ) and I honestly have been taking the return to running seriously and listening to both Coach and osteo advice to ease into it. But it’s slower than what I would have imagined. Where I fall down is the recovery out of training – you know, the wind down time, getting enough sleep – that kind of thing. Hence I’ve been making a real effort this week to get to bed early, to practice diaphragmatic breathing whilst driving and to invert my legs up onto the wall at the end of the day and just ‘be’. So it got me thinking about additional ways to support the body outside of the diet, exercise and lifestyle. What other dietary factors can help support the anti-inflammatory pathways in the body outside of a reduction of processed food and the free-radical scavenging properties of fruits, vegetables, animal protein and eggs?

A lot of athletes are heading into heavier schedules with the Christmas holidays allowing for some block training to occur. This is (for some) combined with the increased indulgences of additional alcohol at end-of year drinks and caffeine to get through the day. In combination with late nights and early starts, it’s no wonder that we hang out for December 23 as this time of year can wreak havoc on the body. It’s too easy to think you can pop a Voltaren or Neurofen tablet before going out and training (or at the end of a hard session) to mitigate the niggles and strains you feel that come from a lack of recovery. This might not seem like a big deal at the time but it really does more damage than what you think. I know – I used to be blasé about these things too – I had a ‘stomach of steel’ that was Impenetrable to even the most harshest of substances (there’s few things harder on the stomach than a mixing bowls worth of green gooseberries that I’ve successfully put this away with no ill effect in my younger years). But the older I’ve become, the more digestive issues I’ve struggled with around training, the more aware I’ve become of the impact that anti-inflammatory pharmaceuticals can have on the gut and subsequent health. Training in itself has been found to increase gut permeability. The decreased blood flow to the gut through even moderate steady-state exercise has resulted in intestinal injury and elevated liver enzyme parameters – and that’s an acute effect of just 60 minutes training. You can imagine what your normal high intensity effort or Sunday bunch ride does in relation to tearing up your insides?*  This increased gut permeability is a big deal. The once tight junctures that should not allow foreign matter to travel through are now not-so-tight. When we have foreign bodies allowed into our system this sparks an auto-immune response. Inflammation is one of the body’s first line of defence against injury, and over time this acute inflammatory response can become chronic which leads to deleterious health effects moreso than just impaired recovery. So the training in itself loosens the guts main defence against foreign proteins, which can increase inflammation – and when you throw ibuprofen on top of that, the effects on the gut and inflammation over time are even worse. It’s an easy thing to do, certainly, and a lot of people do it – however over time this can cause sensitivities to foods that you once had no problem digesting. Think grains, milk, certain types of carbohydrates in the FODMAP spectrum. Our gut has just one cell thickness protecting it from the outside environment. It doesn’t take a lot to upset the balance.

Of course, I’m speaking mechanistically here and everyone is different – some people will go through their athletic career and not have an issue at all despite a regular habit of popping vitamin V; others though, will notice that their tolerance to certain foods is now lower, the time taken to recover from training sessions is greater, and they are not able to get as fit as fast as they used to be able to. Is it an age thing? Sure. You’re not as bulletproof as you were in your 20s. But it could be more than that.

So I thought I’d mention some spices that can help support the anti-inflammatory pathways in the body. This isn’t going to dive into the ins and outs of that information – this post is already verging on being too long.

Tumeric (active ingredient curcumin): (particularly in the presence of fat to help absorption) – my friend Chris loves eggs with a heaped teaspoon or two of turmeric, and avocado and butter in the morning.

Ginger (I love ginger tea, just grating it fresh into hot water) and in green smoothies with lemon.

Cinammon: known for helping blood sugar control and also for its anti-inflammatory properties – I always like to include this in my breakfast meals, as a sweetener for baked rhubarb (no sugar required), in a slow cooked meat recipe or mince.

Garlic a member of the sulfur family, a well known anti-inflammatory compound.(okay, not a spice, but worth a mention)

Cayenne and chilli (active compound capsaicin) – chilli flakes and cayenne pepper are great on eggs, in salad and have you tried chilli chocolate? it is Christmas after all.

The beauty of these spices is that they are cheap, readily available and complement perfectly your real food lifestyle. This post is not prescribing anything more than the liberal inclusion of them in your everyday food. Every real food pantry should regularly utilise these in cooking, baking and barbequing. They are not a panacea to burning the candle at both ends – but it is worth your while to spice things up a little bit in the kitchen if you’re not already doing so.

Gallstones and your gall bladder 101: what, why, who (and generally speaking) what to do?

Until this week I had no idea how prevalent gall bladder inflammation (cholecystitis) and gallstones were. And in who. A lovely client of mine had experienced cholecystitis for years. She was actually none the wiser as equally suffered from irritable bowel syndrome too so had lumped the symptoms (upper abdominal pain, particularly after a fatty meal) into the same category as ‘digestive issues’ which we had been working on (and she had been having success with) over the last few months. It wasn’t until this week that she called me to say she was diagnosed with gallstones and was going in for emergency surgery to remove it that I thought – hmm, is that unusual? Turns out it’s not.

The gall bladder is required to store the bile that is required for fat digestion. If a person is experiencing inflammation (systemic or local) this can irritate the gallbladder and cause significant abdominal pain after eating which usually subsides in the hours that follow. Gallstones are a result of reduced gallbladder function, where the bile isn’t released as it should be and can become thick and sticky, forming stones that can be the size of pebbles to the size of golf balls. There are three types of stones; black pigment stones (related to cirrhosis – scar tissue build up in the liver – or haemolytic disorders – breakdown of red blood cells); brown pigment stones (related to an infection in the gall bladder) but overwhelmingly in the western world, the prevalence of the third type of stone – a cholesterol rich one – is increasing, accounting for around 70% of gallstones. Pain occurs if one of these get stuck in the bile duct – this may also subside. However if you experience continual pain, or begin to have more frequent attacks, then it is generally recommended that something needs to be done.

I had always associated gallstones with people of an older age bracket, but that was just because I’d never had a reason to look into it at all. In fact, this week I was bombarded by young, fit women who responded to a post I put on my Facebook page related to cholecystitis and gallstones that had all experienced problems and subsequently had their gallbladders removed. Now not all people suffering from cholecystitis have gallstones, and not everybody with gallstones experience pain – indeed some remain asymptomatic for most of the time. However, there is a surprisingly high number of people that experience problems with either condition and in New Zealand it’s estimated that 20% of people aged 30y – 75y will be affected. Now that is a LOT of people who may be having problems with either cholecystitis or gallstones and potentially not even know it. The pain experienced in an attack may be in isolation of other symptoms, or put down to ‘normal digestive issues’.

The formation of gallstones and cholecystitis is (like most things) possibly due to an interaction between both genetic and environmental factors. Genetically, a mutation in a protein that may be responsible for the delivery of phospholipids and bile from the liver will increase the risk, as will having a genetic predisposition – the latter increasing your risk four-fold. In addition – and this is what sparked my attention from the Facebook posts – the presence of an autoimmune disorder (Crohns disease, celiac disease) or even a sensitivity to gluten increases risk. The first possible reason for this could be from increased inflammation due to the nutrient malabsorption, or a defect in the gallbladder ability to empty – both resulting in a reduction in gallbladder function. Alternatively, it could be that the gallbladder disease is the result of the same immune system attacks that occur with an autoimmune condition. Regardless of the mechanism, there is a very real relationship here.

Other factors that increase the risk of gallstones are taking an oral contraceptive pill, being pregnant, or having had multiple pregnancies. The increased oestrogen levels affect gallbladder motility (delaying bile release from the gallbladder) and increase cholesterol saturation of bile (cholesterol is the backbone of our sex hormones). A high carbohydrate intake in pregnant women (particularly fructose) is also associated with increased incidence, and there is a link between pregnancy, pancreatitis and gallstone risk. Weight loss, weight cycling or fasting can also increase risk of gallstones as fat is being rapidly broken down and there is increased secretion of cholesterol into bile. With these factors in mind, it is no wonder women are at greater risk (two-thirds of those in the US with gallbladder disease are women). Equally a diet that is higher in processed refined food and calories increases the risk with higher circulating insulin and triglycerides as a consequence of the standard western diet. People who are overweight or obese, or have risk factors associated with the metabolic syndrome are at an increased risk – now this may well be due to the previous point, however this has also been found independent of diet; those with a fat deposition around the middle are more likely to experience problems. Indeed this type of fat patterning is related to reduced function of the liver (and non-alcoholic fatty liver disease) which may result in fat build up and cirrhosis also related to gallbladder function.

A question that arose on my Facebook page was whether athletes were at greater risk compared to the general population.I had a good look around the literature and only came across a couple of studies that related a high training load to problems with the gallbladder. As athletes we place ourselves under a lot of training stress – chronically this leads to increased inflammation. Haemolysis can also occur in susceptible athletes who heavily exert themselves which again impacts on inflammatory pathways. This inflammation is in the absence of gallstones but may well lead to gallstone formation as it reduces gallbladder function. If you combine this with an intolerance to certain food (as a number of endurance athletes also experience), then there are certainly links between the two despite an absence of academic literature out there. Changes to liver enzymes after an extreme endurance event may place an athlete at risk, and interestingly, this case study illustrated how inflammation due to higher intensity training led to a thickening of the gallbladder tissue and an increased tension in the absence of stones or bile buildup (‘sludge’). The removal of the gallbladder stopped this tension and the athlete was pain-free. In this instance, surgery was potentially the only route as it wasn’t related to stones. But if you do suffer from gallbladder problems with or without gallstones and don’t want to go down the surgical route, what are your other options?

For those with problematic gallstones, a first approach may be sound wave therapy to break down stones so they can move down the intestine and be excreted without the risk of getting stuck. Similarly, ingesting a naturally occurring bile (in the form of ursodeoxycholic acid) may also gradually break down the stones. However many people continue to suffer symptoms associated with gallstone attacks after these treatments. Though not in the academic/medical literature, I’ve read a lot of people do an olive oil/lemon juice protocol which (it appears) involves fasting/apple juice/anywhere from 1 cup to 3 cups olive oil and lemon juice/sleeping then warm water. I’ve actually just lumped a lot of different components of these protocols to give you an idea of what you can find if you can go searching… not to recommend you try it (it’s not my place to do that!)

For those with problems related to inflammation of the gallbladder, or with gallstones that are symptomatic, an anti-inflammatory diet is the way to go – removal of grains, dairy, legumes, refined processed food and a focus on fruits, vegetables and animal protein. These foods are rich sources of antioxidants and are not going to cause stress on the digestive system, thereby they are your best line of defense. For some, following an auto-immune protocol that also removes eggs, nightshade vegetables, nuts and seeds initially may be required, with further supplementation to help heal the gut. If you have neither of the above and are currently losing weight, research suggests that following a higher fat diet for weight loss is protective against developing gallstones when compared to a lower fat diet. Further, there is limited research that vitamin C supplementation can prevent gallstones by promoting the conversion of cholesterol to bile salts in the gall bladder.

And what if you have the surgery to remove your gallbladder? Is it low fat foods from here on in? This seems to vary a LOT from person to person. Some people can continue to include good amounts of healthy fat in their diet with no noticeable digestive issues. While some notice a vast improvement with the addition of digestive enzymes, others don’t notice any change. It’s best not to drink fluid around meals so you don’t dilute your stomach acid and obviously try to eat as ‘clean’ as possible –following a paleo approach will ensure nutrient intake is optimal.

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.