Six things I think you should know about LDL cholesterol

Does bacon deserve the health halo it now seems to have in light of what is becoming common knowledge about saturated fat? Mm. Good question, and it probably comes down to context. If we were to position bacon against Flora Proactive, then that changes the question somewhat: which is better for your health? I mean, one is designed specifically to lower low density lipoprotein (LDL), aka ‘bad’ cholesterol (something we’ve been told for years to strive for) and is ridiculously expensive; the other is … well, bacon. Due to its saturated fat content (or perceived saturated fat, it contains less than 50% of its fat from saturated sources), it is always the second food which people think of when it comes to elevating cholesterol levels and causing heart disease – the first being butter.

Many clients come into my clinic with a total cholesterol above 5 mmol/L and are told by their GP that they should bring their cholesterol level down by way of eating low saturated fat, low total fat and reducing animal protein in their diet. OR (worse) go on cholesterol lowering medication (why is medication worse? Check out here and here). There are many things contributing to a higher cholesterol level, and the risk this poses to you is based on many factors. I’ve covered some of these (and what you can do about it) previously.

Here are 6 things I found useful to know about LDL cholesterol. I’m not talking about particle size, particle number, patterning of particles or Apo A or B, reverse transport cholesterol etc. Keeping it kind of simple. If you know more than your average Joe about cholesterol this will likely be a bit elementary. Otherwise:

  1. Most studies and media reports that report a reduction of risk of heart disease when taking cholesterol lowering medication focus on the relative risk. Relative risk – takes a small effect and it amplifies it. This makes the medication look far more effective than it actually is. Let’s explore what this means:

If you have a clinical trial whereby 100 people are given a placebo drug* and 100 people are given the experimental drug, you might find that 2 people in the placebo group go on to have a heart attack (2%), 98 have no adverse events. In the drug-treated group, 1 person has a heart attack (1%), and 99 people have no adverse events. The difference is 1%, however the relative risk reduction is 50% and a much more impressive number, don’t you think? Those reporting in the media certainly do.

  1. We need cholesterol to synthesise naturally occurring steroids in our system. It is necessary for life. It is the substrate for every sex steroid, for vitamin D, to make new neurons and new synapses to consolidate memories. Many people think cholesterol is in our body solely to clog arteries, and the lower the better. This is not the case. For example, in some populations a low total and LDL cholesterol are linked to higher incidence of depressive symptoms. A low cholesterol level may also result in less synthesising of vitamin D in the body, lower hormone production and an impaired immune system.
  2. LDL is an innate part of the immune system. When there is damage to the artery, you have susceptibility to infection, and there is evidence of pathogens present in plaques. When there is damage to the artery and artery wall, resulting in atrophy, there is an infusion of white blood cells as well as LDL cholesterol which work together to promote inflammation (for healing purposes). Blaming LDL for creating damage is like blaming the fireman for creating a fire.
  3. There is NO level of LDL that is unhealthy. There is an assumption that LDL cholesterol is inherently atherogenic and that above a defined level it is dangerous – there is something about the LDL packaging of cholesterol that causes heart disease. That’s not the case, and some experts in the field believe there is no level of LDL that should be treated with a statin. Researchers reviewing the literature have found people with high LDL with no heart disease. The cut-off of 4mmol/L or 5mmol/L depending on your reference point is an artificial distinction that has been created to suggest LDL is inherently toxic to the heart and cardiovascular system. Now there are people who have a genetic predisposition to storing cholesterol, so they have an increased risk? Actually research looking at the lifespan of people with familial hypercholesterolemia (FH, a mutation in the LDL receptor whereby the end result is elevated LDL cholesterol) have found that, aside from a subsection of the population, there is normal lifespan, with just a small number of these people going on to develop heart disease. There are people who have other genetic variants which do result in build up of LDL cholesterol, and we don’t know enough to say that a very high LDL level is NOT dangerous – however the likelihood of harm will be increased with the presence of other risk factors for cardiovascular disease, such as high blood pressure or smoking.
  4. It is not LDL that is causing heart disease. Blood cholesterol (including LDL) is high in people consuming a higher fat diet. However, research shows that other biomarkers are not only fine, but can be improved when transitioning to a higher fat diet from the standard western diet. A recent paper found that people 60 years and older who have the highest LDL live as long or even longer than those with low LDL. They have lower rates of cancer and lower rates of infectious disease.
  5. If it’s not LDL cholesterol, then what is causing a heart attack? A critical trigger factor is coagulation. We rely on the coagulation factors in our bloodstream to create a clot when we become wounded and begin to bleed. However, our blood can clot without there being a wound. High stress, tobacco smoke, high blood sugar all trigger clotting mechanisms. It looks like this:
    1. In our artery wall, there are tiny arteries which feed to the inside of the artery (called vasovasorum).
    2. Vasovasorum are easily blocked or clogged by clots.
    3. If these can’t feed our artery wall, the wall essentially becomes hypoxic and the tissue dies.
    4. When the tissue dies, the LDL cholesterol comes in to repair it, and this happens repeatedly, causing the artery wall to become thicker and thicker until it chokes the artery.
    5. When you combine this thickening of the artery wall with something that might trigger clotting of the blood (such as high blood sugar, smoking or a stressful or emotional event etc), a clot will pass through the narrowed artery,
    6. The clot will eventually block the artery entirely and the result is a heart attack.
    7. None of this is caused by LDL cholesterol.

What really matters is keeping your clotting factors inactive until they are needed. Most people (unless they are haemorrhaging) don’t need their clotting factors on high alert all the time.

So, which is better for your health? IMO – while bacon may not be a health food, I’d choose it over the Flora (preferably free range, minimal added preservatives, along with an abundance of vegetables). Flora doesn’t have a lot going for it, TBH, and while it may lower your cholesterol level, how important is that really? If your cholesterol levels are high and you’re not sure of your risk, get in contact with someone like me who can work with you to address the lifestyle factors that might be driving up your cholesterol levels and contributing to health risk.

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This bacon isn’t preservative free, however it’s the only one I could see that had less preservatives and was free-farmed, so using it as an illustration. Henderson’s is free of preservatives but only select supermarkets carry their free-farmed variety FYI

 

LCHF…why isn’t it working for me? (Part 2)

Last week I posted three reasons why many people undertaking a LCHF diet stall with their success or never get it off the ground to begin with. The following delve a little deeper into the less obvious reasons why people struggle with their diet, and offer some options to help troubleshoot.

  1. Fat doesn’t fill you up. For some people, they don’t feel satisfied when swapping out their carbohydrate for more fat. If it takes a few handfuls of nuts or half a block of cheese to feel satisfied, then there can be some serious increase in calories that isn’t compensated for by an appropriate increase in satiety from the meal. Yes, cheese and nuts contain protein, but to be honest I treat them more as sources of fat than I do protein. If this is you, then.
    1. Increase the portion of protein you are consuming with your meals. I know many people are scared to consume more protein because protein can be broken down into glucose in the absence of carbohydrate, therefore pushing up their blood sugar levels. For people on a ketogenic diet (where 80% of their calories should come from fat), or those metabolically damaged (whereby there is a dramatic change in blood glucose response from a protein-rich meal), this may be a problem. For most people though? upping protein by 1/3 of a serve is no biggie. Still hungry? Up the protein some more.
    2. Drop out some fat –make room for the added protein by dropping out some of the fat – you could start with ½ – 1 serve and see how satisfied you feel when you do that. A serve of fat is typically 1 tablespoon of oil or butter, or ¼ avocado.
  2. You’re eating too much in one meal. A lot of people move from three meals a day, to two a day, to a ‘minimal food during the day’ approach, to sit down to a large meal at night, especially if they’ve been in the LCHF way of eating for a while and are further tweaking it. This may be awesome for some people, but not all. Eating most of your calories in one meal can, though, wreak havoc on your metabolic blood markers (such as blood glucose levels and insulin), increase fat gain, inflammation and reduce your day-to-day energy if this eating pattern doesn’t suit you. You’ll know if this is you, and if it is then:
    1. Spread your food intake out across 2-3 meals to lighten the caloric load and see if this makes a difference to your energy or other more objective markers mentioned above.
    2. Remember you’re still a rockstar even if you have to eat more often.
  3. You’ve got a high intake of dairy or nuts. Some, especially women, are not suited to high amounts of dairy or nuts, and when the begin to include more of these foods – ones they’ve avoided for years due to their fat content – they have a weight loss stall they can’t move past or, worse, they begin to store fat around their middle. While some suggest cheese is a food akin to crack, research investigating the addictive properties of the protein in cheese have not found this to be the case. Of course, if you personally can’t stop at one slice and find you’re eating the block, then perhaps it is for you. Nuts can also be trigger foods for some people, and they find it difficult to stop once they’ve started eating them. Ditto with a jar of peanut butter. What to do?
    1. Omit dairy for 30 days – sometimes it’s not the dairy per se, it’s the amounts that you’re eating it in that need to change. Removing it entirely will allow you to change your habits and then reintroduce it.
    2. Omit nuts and/or nut butter as per above in #6a.
    3. Swap snacks to those that are predominantly protein-based rather than fat based – despite the satiating effects of fat, for some, it’s just not like having protein. A hardboiled egg or some leftover chicken wrapped in lettuce or nori sheets (my current obsession) may satisfy you more.
  4. Genetically this isn’t the diet for you. If metabolic markers such as cholesterol, blood sugar or inflammatory factors go skewiff then it could be the LCHF approach doesn’t suit you. Genetic variation in the ApoE gene (ApoE4) is associated with LDL cholesterol not being recycled very well, and therefore it’s more likely to hang around the bloodstream and increase the chances of it becoming either oxidised or being transformed into smaller LDL particles, both highly atherogenic. Variants in the gene FTO can increase risk of obesity in the context of a high saturated fat and low polyunsaturated fat intake and may increase risk of high blood sugar and diabetes in individuals already overfat. The PPAR genes plays a role in ketogenesis (the oxidation of fat for energy) and storage of fat by activating genes associated with fatty acid transport and metabolism. Variants of this gene (particularly PPARa and PPARg ) are associated with increased risk of high triglycerides, total small dense LDL cholesterol and type 2 diabetes in the context of high saturated fat to polyunsaturated fat intake. Further, individual glycemic (blood sugar responses) vary considerably for the same amount of carbohydrate in food, suggesting there are a lot of factors to consider when determining the best diet for you (such as genetics, gut microbiome, activity level, stress etc), not just its macronutrient content. How to figure out if LCHF is not the diet for you? A few things to consider:
    1. Are you losing weight? If so, then wait until your weight stabilises and then retest your numbers – your body recycles triglycerides that are released from adipose (fat) tissue, therefore your triglyceride levels can appear high, but it is transient.
    2. Don’t get your cholesterol levels measured if injured, if you haven’t slept properly or you’ve been under significant stress. Cholesterol levels can change easily based on environmental triggers.
    3. Some people notice their cholesterol increases specifically in response to dairy fat, others to coconut fat – experiment for 6-12 weeks by dropping these out of your diet and get your cholesterol levels retested to see if this brings a drop in your numbers. Replace it with foods that have a more balanced fatty acid profile (such as lard or beef tallow) and foods high in monounsaturated fat or omega 3 fats, such as avocadoes, olive oil, nuts, seeds, salmon, mackerel, sardines.
    4. Here’s one I prepared earlier (and by ‘one’, I mean, ‘post on reducing your cholesterol naturally’. And by ‘naturally’ I mean ‘without Flora Pro Activ’).
    5. Get more in-depth testing of your cardiovascular disease risk profile – cholesterol is one measure and possibly not the most important one. CRP, fibrinogen, LDL particle size, number, oxidation and patterning can all give you more information than the run-of-the-mill lab test can. Contact me as I can help you arrange this testing which, for the most part, your doc might not even be aware of.
    6. Consider getting tested to find out your genetic predisposition (either through your doctor, or I can assist via Fitgenes gene testing).
    7. Consider dropping your fat intake, upping your protein intake and perhaps your carbohydrate intake too – ala the Zone diet approach. Despite its gimmicky name, it’s proven itself to be very effective for blood sugar stabilisation and blood cholesterol management. Some people just aren’t meant to eat a higher fat diet.
  5. You’ve got an intolerance you didn’t realise you had. Going LCHF means, for many, significantly increasing fat content in the diet from the obvious choices: cheese, nuts, seeds, avocados and coconut products. However, while these are awesome in terms of the nutrients they deliver, they can cause digestive issues in a number of people. Avocado, coconut, nuts and seeds are moderate-high in FODMAPs – a type of carbohydrate that can cause bloating, abdominal pain and other irritable bowel symptoms in many people. Further, the inclusion of larger amounts of cream, cheese or full fat yoghurt can be problematic due to an intolerance to the dairy protein or fat which can result in similar IBS in susceptible people. If you’ve been following a low-fat diet for many years, enzymes that help digest the fat and protein may be downregulated, so your body might not cope with the additional amounts. Sometimes it is a matter of backing down and building up, and sometimes it is that these foods just don’t agree with you. What to do? One of these tips may help:
    1. Follow a lower FODMAP approach to see if removing these foods settles down your discomfort. Doing this for at least 21 days and reintroducing a different food one at a time can pinpoint which one in particular might not agree with you.
    2. Introduce fermented foods as per #3e above to re-establish healthy bacteria in your gut.
    3. Replace dairy fat for alternative fat choices: nuts, seeds, avocado, coconut oil, beef tallow, lard.
    4. Ensure you chew your food properly at each meal to break it down, include lemon juice in water in the morning, and apple cider vinegar with meals to stimulate your digestive system, and consider ox bile supplement or a digestive enzyme that has lipase and/or pepsin enzymes to help you break down the fats and proteins.
  6. You’ve upped your alcohol intake because red wine and white spirits are “allowed” on LCHF. This might not even be intentional, but dropping your carbohydrate intake can lead to increased alcohol cravings, especially if your fat intake is too low, or your food intake is too low, or your stress levels are chronically too high. Or perhaps, you enjoy a moderate amount of alcohol but are continuing to gain weight on the LCHF diet.
    1. Be honest about how much you are drinking. Regularly consuming a ‘large’ as opposed to a ‘standard’ pour at the pub? Cracking open a bottle one night and then drinking to finish it off? Your plan to be alcohol free during the week has reduced to being alcohol free Monday – Wednesday? Evaluate if this is a problem for you … or not!
    2. Go alcohol free 5 nights a week, and enjoy a glass of whatever you fancy on the other nights. Ideally not those lolly water vodka mixes, but if you don’t like red wine, then choose something else. It’s not a deal breaker.
    3. Eat enough during the day so you’re not craving alcohol in the evening. This may mean including some additional starchy carbohydrate in your lunch meal – it doesn’t mean you’re not ‘low carb’ – as that in itself is a spectrum. This can really offset your cravings. Try it for 14 days to see if there is an effect.
    4. Lighten the load by choosing to have a low-fat meal if you drink. Old Skool 90s ‘dieting’ approach – those fat calories will only be missed by your adipose tissue, which is where they will be directed to when consumed with alcohol (which is processed first and foremost).
    5. Drink to ensure you are hydrated before you have your first alcoholic drink. This is like 101 really – we always drink more when we are thirsty, and then when we drink more, we become uninhibited and then all hell can break loose, right?
  7. Food timing: If you’re beginning your day with breakfast at 7am and winding down with a cup of tea and some dark chocolate at 10pm, you may be doing yourself a disservice. Eating over a time period of more than 12 hours can be deleterious to health. Recent research has found that restricting the eating period to 12 hours or less can improve insulin resistance and glucose tolerance, and reduce breast cancer risk even when the calories remain the same. Anything you consume that requires processing of any sort by the liver – including black coffee or herbal teas – will begin the metabolic process. When we eat is also important as our appetite hormones are on a circadian rhythm (food being an important signalling molecule for hormones), and eating late at night – even if overall eating window is short – can be problematic for your liver. The benefits derived from intermittent fasting (such as these) can still be realised if your version of fasting includes coffee in the morning, however it appears actual fasting (nothing but water) for at least 12 hours is most beneficial for metabolic health.
    1. Try to keep within a 12 hour window for consuming anything other than water. If you struggle with remembering to do this, there are apps that can help. It’s not as hard as it might seem – if you have breakfast at 7.30am and are done eating by 7.30pm then you’ve nailed it.
  8. You’ve focused entirely on diet without giving pause to consider other aspects of your lifestyle that contribute to your wellbeing. Lack of sleep, chronically elevated stress levels, over or under activity can all contribute to some of the common complaints people attribute to diet which have nothing to do with the food.
    1. Evaluate your sleep – are you getting to bed at a reasonable hour? Able to sleep through the night with ease? Feel refreshed waking up?
    2. Evaluate your physical activity – are you doing enough? Are you doing too much?
    3. Evaluate your stress levels – are you trying to do too much? Feeling overwhelmed? Or conversely is there not enough stress to keep you stimulated and motivated?

Of course these factors contribute to how your body responds to the food, but it isn’t the food per se. As I said last week, this isn’t a definitive list, however if any of these resonate with you then try some of the ideas I’ve listed, or enlist the help of someone like me to guide you to the best approach for you.

PS: I have organised a few talks over the next couple of months to talk about making a real food (aka LCHF) approach work for you. At the moment I have:

  • Takapuna 23 March @ Streetwise Organics, Byron Ave
  • Hawkes Bay 6 April – location TBC
  • Queenstown 25 May – location TBC

…with others to come, so watch this space 🙂

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Yes, I created this pic myself 🙂

 

10 ways to naturally reduce your cholesterol-related risk and save yourself $8.00

I was at the supermarket yesterday and just happened to be taking a picture of an iced coffee drink when someone came beside me to grab a couple for themselves and put them in their trolley alongside a pottle of Flora ProActiv margarine.

Heinous drink containing 75g sugar on the left, and overpriced margarine on the right. JICYWW.

Heinous drink containing 75g sugar on the left, and overpriced margarine on the right. JICYWW.

There’s a disconnect right there.

These margarines are not only ridiculously expensive and taste terrible (I suppose that’s the nature of margarine anyway), but consuming this spread in an effort to reduce cholesterol levels is totally misguided. Don’t get me wrong. They work. In fact, a good friend of mine did her Master’s project at the same time as I did to show their effect at lowering LDL cholesterol in a clinical trial. There have been more than a handful of randomised controlled trials that show plant sterols can inhibit cholesterol absorption and reduce LDL cholesterol.

The end goal, however, shouldn’t be about reducing your LDL cholesterol levels. You’re probably down with that anyway given you’re reading my blog. The end goal is about reducing your overall health risk, and these margarines have not been shown to do this, despite the Heart Foundation tick and the Health Star Rating. In fact, for a substantial proportion of the population, a lower cholesterol level increases the risk of heart disease (for more information, read this excellent blog post by Zoe Harcombe)

Interestingly, even the American Heart Association released a statement saying the use of sterol and stanol esters should be reserved for adults requiring LDL cholesterol lowering because of hypercholesterolemia, or as secondary prevention after an atherosclerotic event – and these have yet to be updated.

If you want the real benefits of cholesterol lowering foods, eat your plant sterols in the form that nature intended (i.e. plants), not a pharmaceutical company

Anyways.

Here are 10 ways to naturally reduce your risk related to cholesterol and save yourself $8.00

  1. Eat more vegetable fibre. Fibre is the ‘f’ word that is super important but doesn’t receive nearly as much press as the other ‘f’ word (fat). Current recommendations are 28g for females, and 34g for males and we are currently consuming an average of 20g per day. Fibre comes in a few different forms and while soluble fibre has been found to lower cholesterol absorption – this is not the most important aspect to my mind. A few people (who may have a genetic defect that makes them hyperabsorb fibre, or have a defect on their LDL cholesterol recpetors which limits their cholesterol uptake and removal) would benefit from this in particular. Moreso, eating more plant based fibre shifts us back to an eating pattern that, as Eaton & Cordain point out, we consumed for over 99% of human evolution. And while estimations of fibre intake of Hunter Gatherers vary (as pointed out by Steve in this excellent blog post), the point is: we don’t eat enough of these plant-based foods and we need to eat more AND more from the sources of foods which are as close to their natural form as they can be. You’ve heard of the 5 a day campaign? I say we should aim for 9 – and mostly vegetables. This is particularly true if you do have underlying inflammation that is driving up your cholesterol level. There different types of fibre and soluble fibre is known to absorb cholesterol and remove it from food you eat and your bloodstream. This level of detail is certainly useful if you have a genetic predisposition towards a high cholesterol level which places you at risk (i.e. familial hypercholesterolemia). However, to keep it brief: if you’re currently barely managing three serves of vegetables a day – work on increasing vegetables in general. Natural sources of fibre from plants will deliver soluble and insoluble fibre, along with resistant starch. This is a good place to start.
  2. Ditch processed food. Sounds dramatic I know – and it’s not realistic to ‘never eat anything in a packet’. However if most of your daily calories come with a nutrient information panel and an ingredient list, then you seriously need to reconsider what you are putting into your body. Processed food is devoid of nutrients in the forms your body requires, contains additives and preservatives, some of which have a dubious health profile and takes very little energy to digest. This leads to peaks and troughs in your blood sugar levels, poor appetite control and the potential to overeat.
  3. Ditch sugar. No surprises here. Sugar not only increases your risk of metabolic syndrome that can result in type 2 diabetes and increased cardiovascular disease risk, it drives almost all inflammatory pathways in the body. Thankfully though, if you try hard to stick to #2 above, you’ll do this by default. Do note though, minimising sugar includes all forms of sugar – including the ‘natural’ forms. If you’re unsure of what a sugar is, print out this PDF which tells you the 56 different names to burn into your brain for your supermarket shop.
  4. Lose weight. Or, more specifically, lose body fat. Being obese is an independent risk factor for cardiovascular disease, type 2 diabetes, neurological conditions and some cancers. Yes there are certainly limitations with how we define ‘overweight’ or ‘obese’, but you don’t have to rely on tools to establish whether or not you need to lose some additional fat around the middle. You know this yourself.
  5. Increase your intake of omega 3 fatty acid rich foods (think salmon, mackerel, herring and sardines) and consider an omega 3 supplement if you don’t eat fish. I know – you’re thinking ‘what about plant-based sources’? truth is, these don’t contain the type of long chain fatty acids that are most beneficial for reducing risk of chronic disease, and their conversion rate into those forms is quite poor. Eicosapentanoic acid (EPA) is the omega 3 that is involved in reducing inflammation, and if you do have high cholesterol and inflammation, then a supplement such as this Nordic Naturals could be worthwhile taking. While a very recent clinical trial failed to show improvements in total cholesterol with the addition of an omega 3 supplementation, it did show a reduction in fasting blood sugar, triglyceride levels and c-reactive protein (a marker of inflammation in the body). And as I said, your cholesterol level might not be the most important metabolic marker to focus on anyway. Vegetarians especially would benefit from supplementation, and an algae supplement would provide a similar benefit.
  6. Get out in the sun…. and get your vitamin D levels checked. There is an association between low vitamin D and poor metabolic health – studies have shown a link between high sunlight hours and lower cholesterol levels at a population levels. This is due to the exposure of skin to the UVB rays that uses cholesterol to create vitamin D. However, a large percentage of New Zealander’s are below adequate levels. For best and safe practice, sun exposure, minus the burning, for 10-15 minutes where parts of your skin not often seen by the sun (for maximum absorption) are exposed (think: armpits, abdomen – unless you’re young and gorgeous) is best. The thing is, though, the sun doesn’t hit the earth at the right latitude to get any of those rays to produce vitamin D in winter, so we can be lagging even more coming into spring. So supplementation could well be required. In addition to the mechanism above, studies (like this one) have shown that higher dose vitamin D supplementation can lower cholesterol and inflammatory markers in women. If supplementing, choose a supplement that also includes vitamin K2 to help vitamin D’s absorption such as this Clinicians one.
  7. Alpha-lipoic acid (along with other antioxidants vitamin C or E) can provide antioxidant support to help reduce your overall health risk associated with cholesterol levels (i.e. reduce inflammation and oxidative species) by increasing the activity of your body’s antioxidant defences. If you’re wanting to spend your money on actively lowering your cholesterol, these relatively safe supplement options are a better idea than margarine.
  8. Your thyroid, your gut, your genetic profile can all influence your cholesterol profile. If your cholesterol is more than a bit elevated, consider investigating other reasons for this. FYI it’s now easier to get your LDL cholesterol tested, rather than calculated, including those which are more atherogenic, such as VLDL, oxidised LDL if you do have concerns. You can work with a practitioner to do this.
  9. Exercise. Free and long known to improve metabolic health. The arguments for or against the benefit of exercise for losing weight are irrelevant. Mood, lean muscle mass, cardiovascular fitness and general all around awesomeness will increase. It doesn’t mean you have to slog it out in the gym. Body weight exercises and some short, sharp, intense exercise a couple of times a week – combined with walking and general movement as much as you can – is most effective for health and wellbeing. If you like to track your details then get a Fitbit or a Garmin or similar. If you obsess over numbers then don’t.
  10. Stress less. Sleep more. And if you are losing weight, and doing all of the above, wait for your weight to stabilise before worrying too much about your cholesterol levels, which can be elevated during this time.

 

Body weight exercises from the 7min workout - not a bad place to start. (http://well.blogs.nytimes.com/2013/05/09/the-scientific-7-minute-workout/)

Body weight exercises from the 7min workout – not a bad place to start. (http://well.blogs.nytimes.com/2013/05/09/the-scientific-7-minute-workout/)

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.

Not tonight, honey. I’m exhausted.

Have you heard the term ‘ironman widow’? Where someone’s husband (or wife) is basically invisible for the better part of 12 weeks as they prepare for an upcoming race. This not only relates to being physically present (which is diminished when the training time is upwards of 15-20h a week) but also ‘present’ when at home. Often exhaustion sets in, particularly nearer the end of the week or after a heavy training day, where the mere thought of moving from the couch is akin to another 6h ride. Sex? Don’t even go there. It’s a fairly common (yet usually unspoken) phenomenon that rolling around in the sack is off the agenda in the lead up to the event. And I’m not talking about the day before an event; it’s more like as a general rule because they are too damn tired. Does this sound familiar? Yes, being tired is a natural (and expected) part of the training cycle – however, much as we talk about adrenal fatigue and hormonal imbalance in women – this is not an uncommon occurrence in men. It’s just not often talked about.

When we talk hormones, I know that I’m guilty of just addressing women. You know – the stress hormones, thyroid hormones and sex hormones. However men are not exempt from the debilitating effects of overdoing it. Just as a ‘rushed’ lifestyle can affect the thyroid and sex hormones in women (including testosterone), men who undertake endurance sport are at risk of poor testosterone status.

Testosterone: a sex hormone (also present in women too) is a chemical messenger. It declines as we age, and some studies have found a that testosterone levels for a male in their late 30s are down by as much as 50 % on the levels that were present in their 20s. Just as oestrogen is controlled by the hypothalamus, it is the same for testosterone; when the hypothalamus detects a deficiency of testosterone in the blood, it secretes a hormone called gonadotrophin-releasing hormone (GRH). This is detected by the pituitary gland that in response starts producing follicle stimulating hormone (FSH) and luteinizing hormone (LH). These travel to the testes where testosterone is produced from cholesterol by the leydig cells with just a small amount produced by the adrenal glands. It’s then sent back into the blood stream and either attaches to sex hormone binding protein (SHBG) and becomes biologically inert, or remains free in the bloodstream.  Normal levels are between 300 ng/dl – 1200 ng/dl (10.41)-41.64 ng/dL. The three types of testosterone you might see reported are:

  • Total testosterone- As the name implies, it’s how much testosterone available and is the sum of free and bound testosterone.
  • Free testosterone is the most biologically active form of testosterone. Free but low biologically active test and therefore still have signs/symptoms of overall low testosterone.
  • Bound testosterone-This is the testosterone bound to the protein Sex Hormone Binding Protein (or Globulin) (SHBP/SHBG). A high amount of SHBG will usually indicate a low free testosterone.

Testosterone is not just important for reproduction and sex drive – it has a number of other roles including supporting bone mass, regulating fat distribution, muscle size and strength and red blood cell production. If you are a typical endurance athlete who tends to push themselves and have had stress fractures that can’t be put down to a lack of calcium, it could well be that low testosterone is a contributing factor. As we know, testosterone increases during training and contributes to overall energy levels; a low production of testosterone contributes to the fatigue that can be felt under a heavy training load, making someone feel worse than they should. It’s difficult though, to know what is a normal byproduct of a heavy training load (because, let’s face it, endurance sport requires longer and harder training than, say, golf). Below are some common signs and symptoms of low testosterone.

  • Decreased/absent early morning erection
  • Reduced sex drive
  • Erectile dysfunction
  • Loss of facial or pubic hair
  • Testicular atrophy
  • Low bone mineral density/fractures
  • Night sweats

Phew! That’s not you? Well, you may not be out of the woods just yet. Less specific (or earlier signs) include:

  • Decreased energy or motivation
  • Poor concentration and memory
  • Disrupted sleeping patterns
  • Moody
  • Reduce muscle/increased fat mass
  • Reduced performance

You can see that the early signs of a reduced testosterone level could be summed up by being a bit ‘tired’ and are fairly non-specific. The best way to know what is going on with your testosterone is to get it tested through your doctor (noting that the free testosterone is the important measure).

Thankfully there is plenty you can do with your diet to ensure you’re optimising your ability to produce testosterone without getting a prescription for the pharmaceutical type. Unsurprisingly, these come down to pretty much what I write about on a weekly basis:

  • Ensure adequate vitamin D – this is involved in the production of the corticosteroid hormones and it’s important we have enough available to support the production of our thyroid, stress and sex hormones. Food sources are full fat dairy products, a small amount in butter, liver, animal protein and fatty fish such as salmon, sardines and mackerel. Taking a supplement (that also contains vitamin K2) is warranted for a large part of the year in New Zealand, but particularly as we come out of winter and into spring, where the UVB rays are diminished and we’ve been spending the vast majority of time inside on the windtrainer to dodge the weather.
  • Ensure adequate zinc intake (through oysters and animal protein, and brazil nuts too) – a note here is that iron can reduce our overall ability to absorb zinc, and this may need to be looked at if you’re taking an iron supplement.
  • Ensure adequate selenium intake (seafood, Brazil nuts) and vitamin A (full fat dairy products, liver, eggs, animal protein)
  • Saturated and monounsaturated fat: Again, most of the foods mentioned above are good sources of saturated fat in the diet, and monounsaturated fat is found predominantly in olive oil, eggs, avocado and raw nuts. The reality is, all fats contain the range of fatty acids we need, and are labelled ‘saturated’ or ‘monounsaturated’ fats due largely to the amount they contain. Coconut oil (which has had some bad press of late, despite a lack of evidence of a relationship to heart disease) is particularly rich in saturated fat.
  • Cholesterol: another important co-factor in the creation of the sex hormones, and forms the backbone of these. Foods of animal origin help supply dietary cholesterol for this role. If you’re someone who has followed a low fat diet or vegetarian diet and has a low cholesterol level, then potentially your testosterone could be lower than ideal.
  • Ensure adequate B vitamins and magnesium also (present in the foods mentioned above and in abundance in vegetables).

Finally – on the life side of things: sleep more, ensure adequate recovery from training and have more sex. That will increase your testosterone.

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.