Preventing post-natal nutrient depletion

Many women struggle with the after effects of childbirth and the overwhelm of having a little human who relies on them 24/7. The term ‘post-natal depletion’ (I first heard from my clinical psychologist friend Karen) accurately describes the nutrient state of a new mum, and whilst some women may experience depressive symptoms because of this, others feel general weariness and fatigue that is an expected part of being a mum. I recently listened to a podcast with the amazing Lily Nichols (well known for her work on gestational diabetes and diet) and her thoughts on the role of nutrients and if there is anything that can be done to mitigate these symptoms or help the recovery process, pre and post birth.

From a fitness perspective, if we consider the evolutionary picture, there is a definite mismatch between the activities of adults then compared to now. In activities of daily living there was a lot more squatting, lifting, lunging and pulling as part of gathering food and providing shelter. This made for a much stronger pelvic floor and core muscles than we have now. The strength and muscular fitness of the mother during pregnancy can really influence their recovery period post-birth. In addition, one of the main roles of the elders at the time of late pregnancy and childbirth is believed to have been to gather the additional calories required by the childbearing women, as it is difficult to obtain that amount of dietary energy. There was an enforced rest period post birth to help with recovery and bonding of child and mother, and this isn’t a focus in modern day life, where there seems to be real pressure to get back up on your feet after a few days and get going. From a food standpoint, the overwhelming and all-encompassing burden of being a mother to a new-born (first or third time around) makes it challenging to prioritise the nutritious meals required.

Childbirth is extremely energy demanding, whether you have a physiological (vaginal) birth or whether you have a caesarean section (c-section). For some, the double whammy of the intention to have a natural birth but, after 40 hours of labour, be whipped into surgery for a c-section likely even more so. The emotional and physical trauma relating to all of the above scenarios should not be understated, however while guidelines exist during pregnancy for nutrition, there are no real guidelines in place for postpartum recovery. The nutrient requirements of growing another human, plus the demands of labour leaves a woman in a very real depleted state, from a caloric perspective and from a nutrient perspective. It is therefore no wonder that women experience exhaustion and a depressive mood post childbirth. Furthermore, upregulation of protein turnover occurs post birth (both via c-section and vaginal) to help repair and heal tissue, and as a result of increased inflammation. This will certainly increase the requirements for protein and the amino acids responsible for musculoskeletal health.

And what about carbohydrate calories? It appears to be individual as to the requirement for most women. If someone develops gestational diabetes during pregnancy and has been limiting their carbohydrate intake, Lily suggests it is prudent to continue this lower carbohydrate approach post pregnancy for 6-12 weeks and ideally self-monitor their blood glucose responses to meals with a glucometer to assess if their levels has reduced to normal range.  There is no optimal intake amount for carbohydrate (as it isn’t an essential nutrient, the body can make it well enough), however a key indicator of individual requirement would be milk supply for the breastfeeding mother, and mood, energy and stress response may also be good indicators. Carbohydrate helps produce serotonin in the body and quality sources such as potato or kumara can be great for helping with mood and calming anxiety. There’s no right or wrong way here, but I wouldn’t recommend a ketogenic diet for most healthy women post-birth, instead aiming for a good intake of vegetable fibre and adding a couple of serves of fruit and/or kumara or potato into the day. This may take the carbohydrate content to around 80-120g per day which is still a low-moderate amount. Quality is key here.

It is well recognised that breastfeeding increases the caloric requirements of women by around 600 per day compared to pre-pregnancy,  however there are no guidelines for an increased caloric intake post-birth for women who don’t breastfeed, which may lead to some women feeling they should immediately return to pre-pregnancy food intake for fear of not being able to lose the ‘baby weight’. It is reasonable to consider that, breast feeding or not, the healing that needs to take place to recover from childbirth will require additional calories and expectations of dropping weight quickly would ideally be put on the backburner until the body is healthy enough.

From a micronutrient standpoint, there is an increased risk of anaemia with childbirth and more so with multiple c-sections. The estimated blood losses during a c-section is thought to be up to 1000ml, so it is no wonder that someone may come out depleted. And, worth mentioning, there is a clinical link between anaemia and postpartum depression, which highlights the important role of iron in the brain. In addition, the sudden drop of progesterone post-birth may create an imbalance until normal levels resume with the menstrual cycle. Coupled with fluctuating oestrogen levels, this is thought to be one of the major influences of mood and can have negative impacts. Finally, it can take time for the thyroid (which enlarges during pregnancy) to come back to normal size, and the problems this can create for thyroid function, triggering hypothyroidism or hyperthyroidism in the short term, leading to a low mood state. Therefore, along with iron, iodine, selenium, zinc and other cofactors in thyroid metabolism need to be considered.

Practically speaking, what steps should be taken to avoid post-natal depletion and adjust to the new additions to the family? Some tips from Lily Nichols:

Ideally, if possible, get strong and fit in a safe way, enlisting the help of a qualified fitness professional before and during pregnancy

While pregnant, once a week, for several weeks, purposely cook a meal to freeze for post-birth, and make sure it’s something you are going to want to eat. Casseroles, slow cooker, mince-meals, pre-cooked chicken breasts, frittatas are all things that can be frozen but if you don’t like the idea of thawing and eating these, then it’s not going to be worth making them. You may want to do this in the second trimester-beginning of third trimester, so you are sorted prior to the last few weeks when fatigue more rapidly sets in. This might require more freezer space, but this will help emulate the traditional ‘village’ feel of not having to do everything yourself post-birth. In addition, baking low sugar muffins, loaves and breads (if you’re a baker) and slicing and freezing will give something quick to consume when necessary, without you having to rely on processed refined foods. If budget allows, consider Plate Me Up, Jess’ Underground Kitchen or another company that creates prepared whole food meals to take the pressure off having to cook (and the temptation to buy take aways).

Post-birth: continue taking pre-natal supplements and look to get your nutrient blood markers taken perhaps 10-12 weeks post-birth, when inflammation and hormones that are disrupted during the pregnancy and birth have had time to settle down. This will give you a more accurate reflection of any nutrients that you may be running low in. Work with a health professional such as a nutritionist, naturopath or dietitian to provide you with good advice around quality supplements, as price of supplements don’t necessarily reflect quality.

Ensure adequate protein and fats at each meal, with a moderate amount of carbohydrate. If possible, avoid meals that are too skewed towards carbohydrate as these are going to cause blood sugar swings that will impact on energy levels and mood state. This is obviously problematic when also sleep deprived!

Don’t ignore your hunger signals. Remember you need more calories currently, breast feeding or not. Eat until satisfied and trust your body and the signals it is giving you. Now is not the time for Isagenix or fasting. That said, aim to eat your meals within a 12h window, avoiding snacking if you get up to feed during the night if possible. This is reasonable given what we know about circadian rhythm and the potential deleterious effect of food intake later in the evening.

Liver, eggs, salmon, sardines and red meat that is close to the bone all contain essential amino acids and fatty acids that are important not only for baby’s growth and development, but for mum’s brain and blood sugar. Regular inclusion of these should be a priority for optimal nutrient intake.

Keep well hydrated and electrolytes up – a major source of fatigue is when plasma volume drops due to dehydration, therefore making the blood more viscous and increasing the work the heart has to do to pump it around the body.

PC: home-startcentralbeds.org.uk

Red meat doesn’t kill you (and a problem with nutrition science)

This week is world iron week. I’ve talked about iron deficiency on my blog and you will be aware of the risk factors and risks associated with iron deficiency. I know, though, there are those among us who are wary of consuming one of the best sources of iron in the diet: red meat. Because, well, you know – meat kills. The most recent of these news headlines came from this study published in June of this year.

It is challenging being an advocate for eating red meat, and (in a lot of cases) encouraging clients (particularly young and not-so-young women) to eat MORE red meat, in a climate of meat avoidance. It isn’t a popular message, particularly with the bad press that red meat consumption (and production) has received over the last few years. So I thought it timely to remind you of some of the pitfalls associated with nutritional research, and why it is problematic to rely on population based research for our nutrition wisdom. This has been well covered by people much smarter than I am (read here) and relates to the above study looking at red meat and all-cause mortality.

The Nurses’ Health Study is an observational-based study – in that, it wasn’t a study that went in to try and test the effects of a certain dietary condition, instead it merely reported on what the population was doing. The food data was collected using food frequency questionnaires (FFQ), a memory based method, to determine the intake of foods spanning a four-year period. Now, if you’re reading this, you likely think more about food and what you eat than the average population. How difficult, then, would you find it answering questions related to your food intake four weeks ago, let alone four years ago? Imagine then being someone who typically doesn’t give it a second thought. A separate analysis of the data collected in this study revealed that 67% of women and 59% of men participating reported a caloric intake so low that a 70-year-old frail woman wouldn’t be able to live on, much less people who are in the prime of their lives. It has been described as ‘physiologically implausible’. Further, the caloric intake of people categorised as obese or overweight was reported as being ‘incompatible with life’. As all nutrients we eat are attached to calories, this makes all nutrient information completely unreliable.

Secondly, any of the findings are, by virtue of being an observational study, correlational in nature and not cause and effect. Given a data set large enough, enough dietary variables and a number of statistical methods at your disposal, you are likely to see significant correlations if you go looking for them. An example I saw on a blog of Chris Kresser’s was s study reporting that eating 12 hazelnuts a day increased lifespan by 12 years. Or that two slices of bacon equated to a shortened lifespan by 10 years. Yet, all headlines reporting on the study we are talking about here, and indeed the language used by study authors, suggest causality – something that cannot be determined by observation alone. Quite possibly one of the only robust findings from correlational research is that on lung cancer and smoking, where a 2000 times increase in risk of diagnosis of lung cancer was found in those who smoked. The increased risk in the study regarding red meat consumption? 10%. In most fields of science, it takes an increase in risk of at least 200% to garner interest. In nutrition, most relative risk increases are to the tune of 10-50% in either a positive or negative direction. Almost not worth writing about. Remember, too, this is relative risk. Absolute risk (when these numbers are reported) looks quite a bit different (see infographic here, a great description).

Thirdly, the prevailing message in the last 30 years is that red meat is bad for us and we should be minimising our intake of it, something that health conscious people will make a concerted effort to do. Therefore (as the research shows) those people who tend to consume the most red meat aren’t generally those that follow public health messages. They are more likely to smoke more, drink more, do less physical activity and eat less fruit and vegetables – all things which place an individual at greater health risk. While the research statistician ‘adjusts’ for these factors by way of an algorithm, it is well acknowledged that no amount of statistics will account for these unhealthy lifestyle behaviours. This is the inverse (if you like) of a ‘healthy user bias’.

And what about clinical trials looking at the harmful effects of meat? We must put it into context. A hamburger patty served with cheese and aioli, in between two slabs of bread, along with a large side of fries and a soft drink is clearly quite different to a medium rare steak with garlic butter and a side of broccolini. The overall nutrient quality and context of the diet matters whenever we are determining the healthfulness or otherwise of a food choice. Dietary patterns matter. In line with that, there is no good evidence to suggest that meat causes inflammation, and one trial in particular (out of Australia) looked at the differing effects of one 100g serving of wild game meat (Kangaroo) and the standard feedlot beef on inflammatory markers, finding no increases in inflammation after eating the Kangaroo meat. The authors suggest that the fatty acid profile of the beef (higher in proinflammatory omega 6 fatty acids) compared to the wild game meat was the potential mechanism here, but more research was required to establish this. What would be great is to see if differences existed in a clinical trial of a whole food diet that incorporated red meat, rather than there being no differentiation between sources of red meat. Grass fed meat (the majority of our meat supply in New Zealand) is higher in omega 3 fatty acids and antioxidants as a result of the way they are raised – both of which reduce inflammation.

Finally, the tri methylamine N-oxide (TMAO) story. An increase in this enzyme (generated from choline, carnitine and betaine in the gut) is associated with cardiovascular disease and there is suggestion that red meat intake is responsible for higher levels of TMAO. However, it needs to be pointed out that fish (consistently found to be a feature of healthy diets, however you look at it) raises TMAO levels well above what is found with meat. In addition, TMAO is produced in the gut, and we know how much the health of your microbiome is important for overall health. Therefore, if someone has sub-optimal gut health due in part to a poor diet, they are likely to be at increased risk of health concerns.

There is a lot to unpack and this isn’t to try to convince anyone to eat meat if they don’t want to. It is more to remind you that nutrition science is a challenging field. Regardless of assertations made by headlines, health professionals (including me!) or your next-door neighbour, studying what people eat is rife with problems and we need to take everything with a grain of salt. Which, as you probably know,  also will not (in isolation) kill you.

PC: https://www.sciencefocus.com/nature/why-do-most-cows-in-a-field-face-the-same-direction/ (interesting link BTW!)

Iron deficiency and the athlete

A friend of mine alerted me to this super useful review on iron deficiency in athletes, however it is going to be one for anyone who has struggled with low iron status, athlete or not.  I’ve summarised the main points and recommendations below.

How prevalent is iron deficiency in the athletic population?

Although iron deficiency is most common in female athletes (~15–35% athlete cohorts deficient), approximately 5–11% of male athlete cohorts also present with this issue. For obvious reasons, potentially a result of increased iron demand to account for menses. However, low energy intake, vegetarian diets and endurance exercise have also been proposed as potential factors impacting both male and female athletes’ iron stores

How would you know? 

The symptoms of compromised iron status include lethargy, fatigue and negative mood states with more severe cases (i.e. iron deficiency anaemia; IDA) also compromising work capacity. Such symptoms may impact the athlete’s ability to train appropriately and to produce competitive performances.

Getting blood tests – what to look for?

Stage 1—iron deficiency (ID): ferritin <15 g/L, transferrin saturation>16%

Stage 2—iron-deficient non-anaemia (IDNA): ferritin<15 g/L, transferrin saturation < 12μg/L

Stage 3—iron-deficient anaemia (IDA): Haemoglobin (Hb) production falls, resulting in anaemia (ferritin < 12μg/L, Hb. Additionally, serum-soluble transferrin receptor (sTfR) levels of 2.5 mg/L could be considered a reasonable threshold for identification of IDA.

How does training affect what you see in blood test results? 

Well it can, is that just using ferritin as a marker of iron status may not be a good idea as it is an acute phase protein, and the fact that ferritin levels are increased during periods of inflammation and after intensive exercise. Furthermore, measures of Hb are also affected by shifts in plasma volume, which, when unaccounted for, may present issues such as pseudo-anaemia or sports anaemia which does not appear to have any negative effects on performance. Considering training and/or heat adaptions can induce hypervolaemia these factors should be considered to avoid diagnosing deficiency that isn’t there.

What causes Iron deficiency?

• haemolysis exacerbated by ground impact forces (e.g. foot strike) and
• muscle contraction (e.g. eccentric muscle damaging exercise)
• haematuria,
• gastro-intestinal (GI) bleeding,
• sweating
• heavy menstrual losses and
• inflammatory/iron regulatory hormone (hepcidin) responses exercise has a transient impact on increasing levels of the master iron regulatory hormone, hepcidin (for 3–6 h post-exercise), likely a result of the well-documented exercise-induced inflammatory response and associated increases in the cytokine interleukin-6 (IL-6) Increases in hepcidin activity result in a decrease in iron absorption and recycling from the gut and scavenging macrophages, respectively. As such, it is likely that there exists a transient window of altered iron metabolism after exercise where nutrition strategies could be exploited to manipulate the outcome (i.e. strategic feeding times to avoid the window of decreased iron absorption). It’s tricky given how often athletes train, combined with the fact it’s lower in morning and rises during the day – however if you eat cereal in AM, this will impair absorption. Appears to be a window of an hour post-training where you can maximise iron absorption – before hepcidin rises too much. This increase happens in all athletes too, IDA or not. So best time for supplementation could be 60 min post exercise in AM after breakfast, using iron enhancers (vit C, acetic acid – apple cider vinegar) and not drinking coffee or tea or consuming too much calcium which will compete with iron for uptake into the cells.
• Both testosterone and oestrogen can influence iron metabolism via their suppressive effects on the hepcidin–ferroportin axis For athletes, it is possible that high training loads may alter an individual’s hormonal profile thereby suppressing gonadotropin-releasing hormone (GnRH), a precursor for sex hormones. In women, this can lead to suppressed luteinising hormone (LH), follicle stimulating hormone (FSH; to a lesser extent) and consequently oestrogen. Low oestrogen, less suppression of hepcidin, so higher levels impact on absorption.
• Consequently, chronic suppression of testosterone may be linked to higher hepcidin levels in male athletes, potentially impairing iron regulation, and thereby helping to explain the incidence of ID among this sex, especially as endurance athletes often have lower testosterone. In women, although lower levels of testosterone are present, its importance in iron metabolism should not be ignored. For example, higher testosterone levels have been associated with lower risk for anaemia in both healthy older women (n=509) and men (n=396)

How effective is supplementation?

It doesn’t give a performance boost if not deficient, however requirements may be greater, as studies have shown that 30-40% losses ferritin over a harder training block, so the typical 13-18mg / day recommended is probably not enough. Some researchers think that training adaptations typically associated with endurance training may only be maximised in the presence of adequate iron stores.

Does diet matter?

Outside of the obvious limitations that a vegetarian or vegan diet present with (low available iron that requires supplementation) a lower CHO availability (depleted glycogen stores) may increase inflammatory markers like IL6 and hepcidin which can impact on absorption – this has been found transiently but may not be a problem over the long term in presence of higher muscle glycogen and a higher protein intake. More research is needed in the area of CHO availability and iron status.

How to ensure adequate iron status? 

Strategy: check at risk athletes every three months, getting bloods in a fasted, rested state with no hard workout in the 48 hours prior (and ideally no injury present). Also, monitor diet via an app to check overall intake through diet (red meat, organ meat and mussels are the best dietary sources, we are able to absorb 20% of available iron from these compared to 5% from vegetarian diets).

Take supplements – ones which are easy on the gut – the commonly prescribed ferrograd is not. Thorne iron biglycinate, Spa tone and Carbonyl iron are three which are better tolerated. Generally, the overall response to oral iron supplementation in athlete cohorts appears positive (40–80% increases to ferritin) when consumed over an 8- to 12-week time frame. In addition, alternate day supplementation may increase the efficacy of effect via an improvement in the absorption of iron from a given dose, which, over time, results in a greater cumulative response (Stofel et al. 2017). Such regimens, in combination with iron absorption enhancers such as vitamin C.

With this in mind, IV infusion may be a better option when levels are super low and a situation requires rapid improvement in iron stores, or when gut issues appear to render supplementation  ineffective.

Also it is worth considering is the concept of maximising iron stores through supplementation during periods of lower activity (e.g. of-season). Inevitably, as training load and iron demands increase during the competitive season, higher iron reserves may limit the negative influence that exercise training has on the bioavailability of iron.

RBC… from yourfamily.co.za

Will that high protein diet kill you?

After last Tuesday’s television show ‘how not to get cancer’ I got a number of concerned emails and Facebook messages from people questioning their protein intake. Specifically,  information that a high protein diet increases health risk and mortality. As a nutritionist who advocates a higher protein load, here’s what I’ve read about the role of protein and disease, as written by people much smarter than I am:

Information regarding health risks associated with a high protein intake has been critically reviewed by experts in the field, specifically the way the population dietary data from the National Health and Nutrition Examination Studies (NHANES) was analysed to determine that higher levels of protein increase overall health risk. The major criticisms were:

• They eliminated half of the data points with no explanation;
• Their definition of low protein (below 10%) should in fact be labelled as ‘inadequate protein’ as defined by the Institute of Medicine (IOM) protein ranges (10-35% of dietary energy), and in New Zealand adequate protein is 15-25% of energy in diet. The arbitrary cut-off used by the authors meant less than 450 people fell into the ‘low protein’ group;
• The population data gathered dietary information via a single 24-hour diet recall once in an 18-year period; and
• Body weight or body mass index (BMI) was not reported – given the clear association between excess body fat and chronic disease such as cancer, cardiovascular disease etc, this was a massive oversight.

While the paper outlined in the review also looked at laboratory trials, these were based on rodent studies and not clinical trials in humans. Differences in metabolic rate, the way we utilise nutrients and digestive tracts (the rodents more able to handle fibrous foods than ours) means that, despite interesting findings, we cannot conflate the findings here to humans, as they are not directly transferable.

Other points to note regarding research suggesting that a lower protein diet is good for longevity:

• Many of the studies are based on rodent studies (not humans) and, in addition to what I posted above, the type of protein studied is typically casein – a dairy protein that has more potential to be inflammatory and one rodents are not naturally adapted to consume;
• High amounts of dairy protein have been found to increase insulin, triglycerides and result in excess body fat compared to other sources of protein provided to the rodents;
• Much of the research also show that it could be an effect of a high methionine intake which – when not balanced with other amino acids such as gelatin) for some people, can build up the amount of homocysteine (another amino acid) that increases risk of cardiovascular disease;
• As we age, we are at greater risk of sarcopenia, dyopenia and poor health due to falls if we don’t have a decent amount of muscle mass, which requires protein to help lay down this muscle;
• The majority of studies point to a higher protein intake being protective for quality of life as we age, not detrimental; and
• We become more anabolic resistant as we age, meaning we are unable to lay down muscle the way we are when we are younger to the same extent. This could be as a result of both inactivity and lower levels of oestrogen and testosterone, meaning the a higher protein intake is required (in addition to resistance training).

And here is what I know regarding a low protein diet in the real-world setting:

1. People are hungry. Women, especially, struggle to eat an appropriate amount of food when they restrict protein. This restriction (intentional or otherwise) leads to poor blood sugar control, poor appetite control and mood problems (either low mood or increased anxiety).
2. People can only restrict for so long until it backfires. A lower protein intake might be totally fine on a Monday, things are okay on a Tuesday, but by Wednesday people are climbing the walls looking for something to eat. Or, for some, this process happens across the course of a day. This means that despite having a decent amount of food at dinner, the undereating of protein across the day leaves you standing in the kitchen at 8pm looking for something to eat and wondering why you are not hungry, but just ‘not satisfied’.
3. Practically speaking, when you restrict protein, what is there left to eat? Carbohydrate. We eat until our minimum requirement for protein is filled and, in the absence of quality protein sources we will overeat on calories (specifically carbohydrate calories) until this requirement is met. For many, this results in poor nutrient status, poor blood sugar control and excess body fat. It’s these three things which have consistently been found to result in increased risk of metabolic disease and cancer, not the protein load.
4. People (generally speaking) fare best when we base their meals around protein and then toggle the fat and carbohydrate around that, based on their body composition and their activity levels. For many, this is more than a palm sized serve at each meal, and across the course of the day, for most people, this is at least 100g of protein from foods that are quality protein foods. In New Zealand, we get most of our protein (according to the most recent nutrition survey – which is 10 years old, actually) from bread. Bread! Wheat derived protein is one of the lower quality sources we can eat, with the amino acids not being as easy to digest and assimilate as those from animal-based sources.

So, clinically I am not at all concerned about advocating a moderate-high protein load for most people, and the television show last Tuesday did nothing to change my view on it. A longevity diet approach which is low in protein looks promising for a week a few times a year to confer benefits of fasting related to lifespan, but in terms of a day-to-day diet it will likely leave you frail, hungry and irritable. There is not enough human data to show that this approach will lead to a longer life, but I gotta say, it doesn’t sound like an enjoyable way to live beyond 100 years. Most evidence points to muscle mass being extremely important as we age to maintain quality of life and health span. This requires adequate protein and resistance training. In the words of Robb Wolf (as said on a recent podcast), we need to “eat and move in a way that lays down as much muscle as we can now, and then fight like the devil to keep it”.

A good source of protein, and pretty delicious (PC: healthline.com)

Holiday weight gain? Read this.

Easter and Anzac has meant that, for many, it’s enough for more than just a mini-break. And who doesn’t love a holiday? A break away from early alarm clocks, work and household chores. When out of your own space you’re forced to leave behind the normal routines that are well established in everyday life, which is obviously why we come back feeling refreshed and ready to get back into it. The problem, though, is that many people panic about getting out of routine with their food and exercise – what if that 10 days in Fiji goes and undoes the last three months of hard work and they end up gaining weight?

Well, it won’t. Why?

1. You are a LOT more active on holiday compared to real life: driving to work and sitting in an office does not afford the same opportunity to be as active as sight-seeing does. I clocked up almost double the number of steps as I normally would when I was away. Even on days we didn’t run, relying on both public transport and my feet to see a city racked up enough steps so I was regularly doing 23,000 or more each day. However, if you’re a lounge-around-the-pool kind of vacationer, if you had a hit out in the hotel gym, you can avoid weight gain for a short term holiday in the face of a calorie excess.

2. You sleep more: lack of sleep will drive up insulin and cortisol levels and create a hormonal environment that is unfavourable for fat loss. Even if you have the perfect diet (if there is such a thing), no amount of calorie counting, carb watching, or protein eating will make up for the string of 5-6 hours a night you manage during the week when work, exercise and home duties take up so much time, you stay up later than you know you should just to enjoy a little time out.

3. You’re generally more relaxed. The everyday stress created by school pick-ups, work deadlines and weekend sport might be ‘normal’ life, but don’t underestimate the effect this can have on your ability to lose weight. While we may not know the underlying mechanisms, like the effects of sleep deprivation, a chronic overload of stress will increase hormones responsible for fat gain regardless of what you eat or how much exercise you do. In fact, for some, their normal stress relief of going for a run or doing an F45 class will only add to the stress bucket, further exacerbating a weight loss stall. And, when stressed, we often reach for food that is high in calories, low in nutrients.

What if it does?

If you were maintaining or losing weight prior to going away on holiday, then that tells me you’ve got the tools necessary to help you refocus on an eating style and exercise routine that will easily shed any fat gain that is the result of too many cocktails by the pool.

Actual fat gain will be quite minimal, and pretty easy to shift – potentially easier than what you were finding before your holiday. The additional calories eaten on holiday aren’t all stored as fat (at all!) We restock depleted glycogen, and for some, short term overfeeding  increases resting metabolic rate in response to increased food (as many of the overfeeding studies conducted under laboratory conditions have found). Even if you have a predisposition for weight gain, the amount of weight you can is usually far less than the excess calories eaten would predict.

However, for those panicking about the additional fat gain (if any):

1. Up the protein intake. This will help reduce any carb-related cravings from too many pancakes/baked goods/fat chips. Aim for foods that will provide 30g of protein per meal (as an example, a 150g beef steak has about 37g of protein, 3 large eggs around 24g of protein). This will help fill you up and regulate blood sugar, preventing any dip in energy that might be exacerbated by lack of sleep or jetlag. Combined with strategies listed below, it’s a recipe for fat loss.

2. Lay off the alcohol. I tend to drink a bit more wine and beer when on holiday. Despite that I don’t drink any more than 1-2 glasses, it is more than what I’d normally drink in ‘real life’. If you’re like me, then take a break for a week or two  – not a long time, but enough to help get over my post-holiday blues (alcohol is a depressant after all) and to ‘break the habit’ as it were.

3. Drop back the fat intake – if you’ve gained excess body fat, then we want your body to tap into this (potentially) accessible fuel source – this obviously requires a calorie deficit. There is no need to seek out ‘low fat’ foods or avoid foods that naturally contain fat (i.e. egg yolks), however reducing down the amount of added fat to meals (via sauces, dressings, cooking oils, nut butters etc) will help reduce the calorie content of your diet with minimal effort.

4. Drop back the carbohydrate intake – some people benefit from doing a 21 day low (er than normal) carbohydrate diet. I know what you’re thinking – if I drop the fat AND the carbs, what do I eat? I’m talking short-term here – you base your meals around protein and titrate fat and carbohydrate according to that. If you know you feel better with a bit of carbohydrate in your diet, that’s no issue – just make it good quality (i.e. kumara, potato) and make it a moderate serving. However, ample amounts of even low sugar carbohydrate (like rice, pasta, bread etc) will make it more difficult to shift.

5. Include plenty of vegetables – base your meals around these. The prebiotic fibre can help improve the gut environment after a week or more of too much fried foods (though that cheese hoagie was delicious) and too much alcohol. Splashing raw apple cider vinegar (ACV) on steamed vegetables ups the taste factor and helps reduce post-prandial (post-meal) blood sugar, making you less likely to search for something sweet. In addition, you can go for gold on most non-starchy vegetables, so fill your plate to help fill you up.

6. Lift weights. Heavy ones. If you don’t have access to a gym then even body weight exercises (such as press-ups, squats, lunges) if not doing them, will create stress to help you build muscle. I’m not suggesting you avoid lacing up for your long run – I’m a long-distance runner after all! –  resistance training, though, is metabolically demanding in the short term, and in the long term will preserve your resting metabolic rate to allow you to burn fat in everyday life. Plus, you’ll improve strength. Bonus.

7. Consider fasting. Be it the 5:2 protocol that I utilise in my fat-loss plans, a 16:8 protocol that is popular (i.e. fast from 8pm to 12pm the next day, or Super-fasting as per the Schofield/Zinn protocol outlined in What the Fast, it’s consistently found to improve metabolic health markers and can reduce calorie intake to elicit a fat-loss response. Note: I’m not talking about some excessive ‘not going to eat till Friday’ type fast. But shorten that eating window.

8. Get plenty of sleep – try to get back into a 7-8h per night habit with this one and be disciplined about it, for reasons I outlined above.

And, finally (and most importantly), does it matter? I mean, does it truly matter that you come back from an awesome time away with a couple of additional kilograms? Part of the beauty of a holiday is leaving behind all of the routines of your day to day life, including exercise and your normal foods for breakfast, lunch and dinner. Many of us need a mental break almost as much as a physical one, and this includes a break from your usual diet and exercise regime. You will come back feeling refreshed and ready to embrace these with renewed energy (or being in a mindset of change for the better, if that is more appropriate).

LCHF and IF for the female endurance athlete (IMHO).

Following on from the couple of blogs I wrote about Dan’s LCHF athlete lifestyle, I got a lot of messages from women regarding my opinion of it for the female endurance athlete. Great question, especially as – if you look at social media – there are nutritionists who warn against the danger of LCHF (and intermittent fasting) for women, to the point that the blanket statement is that it is harmful and not to be undertaken. Whilst it is hard to be objective in the nutrition space – all of us influenced to some degree by our own experiences – the low carbohydrate and fasting space seems to bring with it its own special degree of hysteria. The prevailing message is that both low carbohydrate diets and fasting is too stressful on the endocrine system of females (which regulates hormones) and causes a reduction in metabolism and reproductive potential. Thus, it is to be avoided at all costs. This point of view may be drawn from clinical experience of the practitioner and be dependent on the type of client they see. If their target audience are women who have struggled with maintaining a healthy weight and have problems with eating enough, then the opinion of the practitioner could well be influenced by this (and is entirely sensible!) Likewise, I see many women who’s hormones benefit from periods of intermittent fasting while utilising a LCHF protocol. What we see in clinic will dictate our points of view, regardless of how objective we try to be.

I have in the past written about the negative impact of fasting and calorie restriction on the expression of genes that regulate kisspeptin in the body, a hormone involved in our reproductive cycle. However I will point out that the effects seen in studies conducted in rodents may be more dramatic than if they were carried out as clinical trials in humans. Rodents have a much faster metabolism, thus a 24h fast for a mouse is equivalent to a 3 day fast in humans. Likewise, chronic caloric restriction over a week, where the mice lose close to a quarter of their body weight (and which is thought to be responsible for the downregulation of the kisspeptin receptors that result in negative effects) may be equivalent to 12 or more weeks. Rodent models in science are great for illustrating potential mechanisms, but can never be viewed as hard data as it pertains to humans.

Alongside any scientific data that exists, I think it’s important to step back and consider perspective here. What we should all be aware of is that there is no one right dietary approach for everyone, and often there is no one dietary approach to suit someone for the rest of their lives. As things change, so do our nutritional requirements. Low carbohydrate diet and intermittent fasting is not exempt from this – therefore to say that it is not suitable for any woman is, quite frankly, erroneous and misrepresents what we see in the literature and what we see clinically. While certainly a vast majority of the studies investigating lower carbohydrate diets have been conducted in males, there are studies showing a positive impact for overweight women with infertility. Further, it is accepted best practice to include periods of low glycogen availability in the training schedules of athletes. Even in the researchers who err on the side of pro-carbohydrate diets recommend cycling carbohydrate intake to be sometimes low, and sometimes high, to upregulate fat oxidation pathways that allow the athlete to become more efficient at burning fat. To state that no female athlete should start an exercise session in a fasted state goes against current best practice for endurance performance.

Possibly the negative impacts of fasting and low carbohdyrate diets are not about the fasting period or the carbohydrate content – it’s much more likely to represent chronic underfuelling – i.e. a lack of calories over an extended period of time, with no thought given to cycling of both energy intake and/or macronutrients. It’s just low, full stop. That’s why it is important to work with an experienced sports nutrition practitioner (like me, Kaytee Boyd, Caryn Zinn as some top picks) to ensure these training tactics are used to the advantage of the athlete in a training cycle, not to the detriment of them.

Don’t misread this as a recommendation to do all sessions in a fasted state, to undergo an intermittent fasting protocol that involves skipping breakfast every day of the week, or that everyone should adhere to a very low carbohydrate approach. If you’ve read any of my information (or followed anything I’ve suggested) then you’ll know this isn’t the case. The point of this blog is to remember that there is no one right dietary approach for everyone, and that if you’re successfully adhering to a lower carbohydrate diet with periods of intermittent fasting and feel it’s working well for you (ie no sleep, hormone, training or recovery problems), don’t be concerned with the rhetoric that exists regarding the harmful nature of this. You are your own best investigator when it comes to your nutrition, and your experience is the most important data when it comes to you.

Post on IF, cue picture of empty plate with clock. #standard (PC http://www.stack.com)

The Plews on racing LCHF

Last week I detailed Kona Ironman age-group champion Dan Plews’ daily and training nutrition using a LCHF approach. How does this change in the lead up to an event, and what does he do on race day?

Like conventional sports nutrition principles, there is somewhat of a carbohydrate loading phase pre-race. This isn’t the 500-600g of carbohydrate that is recommended for most athletes in the three days before (which generally leaves an athlete feeling lethargic and bloated), however it is more than he would generally eat. Don’t forget that tapering for a race is, in effect, carbo loading, as the muscle glycogen stores are not depleted during training and it allows them the chance to be replenished and not in the deficit they normally are. Based on Rowlands paper which showed that a higher fat diet with a preload of carbohydrates, he’s dialled in his approach that Dan now feels works really well for him. He lifts his carbohydrate intake from the 80-100g he typically eats in the days prior. On the Wednesday (for a Saturday race), he will include additional potato or sweet potato in his evening meal, taking him to ~125g carbs per day. This increases to ~175g per day on Thursday and Friday (the two days before the race) – including fruit alongside the potato or sweet potato. In addition, he makes sure snacks etc on hand are low carbohydrate so  not to be caught out during the lead up period with having to rely on the petrol station or four square options. If you do have to rely on these, and are looking for lower carbohydrate, then biltong, cheese snacks, even lower carbohydrate protein bars can be good stop gaps. On race morning before Dan’s Kona race he opted for was porridge: oats with a bit of Super Starch added, which is a slow release carbohydrate to not inhibit fat burning, and is a higher molecular weight carbohydrate, so it is easier to digest.

During the race:

Despite research studies in this area using a ‘train low glycogen, race low glycogen’ model to determine the efficacy of a LCHF approach for sports performance, in practice Dan follows what practitioners advocate: a ‘train low, race high’ model. Ideally, the train low approach has enabled you to increase your efficiency to burn fat as a fuel source in addition to using carbohydrate that you have stored or take on board, thus maximising the amount of fuel you have available. Dan takes in around 50g carbohydrate per hour;  because he is very efficient at burning fat, he doesn’t need as much carbohydrate as he would otherwise. A real benefit of this is that it minimises the likelihood of gut issues many endurance athletes experience during a long event – the more carbohydrate fuel you have to take on board, the more opportunity there is to get the dose wrong. Importantly though, the more fatigued you become, the more your body will divert blood supply away from the gut to the muscles, and thus impacting on your ability to digest the fuel.  During Kona Dan used energy blocks with gels on the bike, and a couple of gels with some swigs of sports drink or coke during the run. His paper Different Horses on the Same Courses outlines how to take this individualistic approach to fuelling, as will his online course that you can sign up to by clicking here.

Finally, post-race, Dan gets back on board the LCHF approach fairly swiftly, as he has seen the impact that a higher carbohydrate fuelling day has on his blood glucose level across the course of the following week. It certainly doesn’t reduce down to normal levels the day after, and it’s likely that inflammation and muscle damage impacts on this too. Your best bet is to (as soon as possible) get back to your LCHF diet and help your recovery process.

LCHF for the top end:

Whilst LCHF is increasingly more accepted in the endurance space as part of the approach, what about at that top end – does it limit performance there? There is very little quality research on this, however Dan’s research group found that there was no detriment to perform high intensity intervals (as I blogged about here), but the jury is definitely out on this point and I wonder if, like many things, it is individual. A person’s ability to metabolise fat as a fuel source and use it at a higher intensity is trainable for sure (that’s what fat adaptation is all about), but there could be individuals who are less able to produce ketones to be used for energy – this is speculation though on my part. Yes, there is a down regulation in pyruvate dehydrogenase which helps turn stored carbohydrate into glucose for energy, however the importance of this is questionable given the increased availability of fat for fuel, and there may be other enzymes upregulated to counteract this change in the fuel use. A potential way around this issue (and to ensure glucose metabolism is continued on your LCHF approach) is to do higher intensity efforts in training that force liver to convert glycogen to glucose – thus keeping glucose oxidation pathways high. I’m also beginning to recommend that people take on a small amount of glucose pre-high intensity sessions if they are beginning the fat adaptation phase during a training cycle that incorporates higher intensity efforts. Ideally your fat adaptation phase will occur during base training when we can keep intensity low. But that isn’t always possible. Fifteen-20g glucose prior to training for these high intensity sessions can keep output high but is unlikely to be enough to “ruin” your adaptation process. Again, there is no research behind these numbers, but from a practice perspective I’ve seen this work well.

Finally, you know I’m an advocate of ketones to help support training whilst lower carbohydrate, and it certainly has helped me and many of my clients. We don’t at this point know enough about ketone utilisation in the body and whether taking exogenous ketones downregulates the body’s ability to produce them. This is an emerging field we are looking at with interest with regards to dosage, timing, type of ketone supplement etc. There has been decades of research into carbohydrate as a performance enhancer, and we can probably expect that it will take a few years of research for these questions to be answered in the science research space. Trying them yourself is likely the best approach to see how they impact your own performance (and I can help you with that).

Plews at Kona (PC http://www.trizone.com.au)

LCHF and the athlete: The Plews approach

Sfuels, a ketogenic fuel for endurance athletes recently had Dan Plews host a Facebook live event regarding his LCHF training and daily diet. Now those of you have listened to our Fitter Radio podcast will know Dan from the Plews and Prof segment. He’s an exercise physiologist who last year was the overall age group winner at Kona World Championships in a record time of 8:24. He’s been working in exercise physiology for the last 15 years and has a number of research papers both related to this, and in the ketogenic diet space (for athletes), one of which I posted about last year. Because I love Dan’s work (and this area in general) I wanted to outline for you what he spoke about in the Facebook live for those people, athlete or otherwise, that are interested. This week, due to length, I’ll cover the normal diet, and next week I’ll outline his pre-race and race-day strategy.

As a bit of background, Dan has been doing triathlon forever, however came into LCHF when he was at the Olympics as an exercise physiologist and came across work by Tim Noakes (who has heralded the latest Banting movement in South Africa). From 2012 he made a decision to give it a crack. Even now, though, six years after embarking on LCHF training and nutrition, Dan notes that adaptations are still occurring, and puts his incremental improvements in performance in the Ironman distance finishing times (in hours:minutes) being: 9:22, 9:11, 9:12, 8:54, 8:35 and 8.24 Kona 2018) down to not only the consistency of training , but the consistency of the dietary approach.

What is important in LCHF and endurance training? The end goal for performance is to conserve as much energy as possible – fuel availability is the limiting factor over such a long distance. We can’t store too much carbohydrate – around 2000 Calories compared to 40000 Calories of fat that is stored in even the leanest individuals. The problem, though, is that people can’t access their fat stores to exercise at a high intensity. Or even, for many endurance athletes, at a lower intensity (where we should be able to burn fat). The type of diet we eat influences our fuel preference when we exercise, and the modern diet (where carbohydrate is the predominant available nutrient) makes athletes much more reliant on carbohydrate which – like kindling on a fire – is likely to run out quickly.  We want to be metabolically flexible, that is, to burn more fat as a fuel source and only use carbohydrate when we really need it. Dan has tested his fuel utilisation in a laboratory and can burn fat at 1.3g/minute (the FASTER study reported around 1.6g/minute) – most people are around 0.6g/minute or thereabouts. However research such as that done by Volek and colleagues have shown it is possible to shift that if you go LCHF. From the testing that Dan has done, he knows that at his race intensity on the bike, an average 260 watts, his fuel utilisation is around 66% from fat stores. This allows him to preserve a lot of carbohydrate when working at this race pace intensity.

Ideally, that preservation of carbohydrate stores to use at the back end of a race when energy availability is limited should be the aim of the endurance athlete (and is extremely challenging if they are burning predominantly carbohydrate from the start). In addition, the lower LCHF diet means having lower blood glucose levels on a day-to-day basis,  important for overall health and body composition goals too. Higher sugars equals higher insulin, which is a nutrient delivery hormone – therefore there is more opportunity for fatty acids in the blood stream being stored in our fat tissue. Don’t go thinking we want rock bottom insulin levels all of the time, as insulin itself is critical for life! However ideally our levels would be low outside of the time period around meals, as elevated insulin is linked to a number of metabolic disease processes. In addition, when following a LCHF approach, we have lower stores of carbohydrate, which makes us more sensitive to the signalling for fat adaptation and upregulating of fat oxidation pathways.

So… the details?

Dan’s diet on a day-to-day basis:

• Coffee with cream, collagen and MCT (medium chain triglyceride, our body can’t store this and is an easily used energy source)
• SFuel bar (low carb snack)
• Training – doesn’t eat during training, but if he does it may be a SFuel drink (MCT/branched chain amino acid (BCAA) drink mixed with some other compounds, but it is a higher fat option)
• Breakfast is eggs, avocado, some vegetables
• Lunch is tuna salad or similar. During heavier training load, he may add a bit of paleo bread (around 20g carbohydrate, similar to normal bread but this is made of better quality ingredients)
• Dinner is salad with a steak
• Snacks may be macadamias, almonds and pickles.
• Fruit may come into it from time to time, particularly as the training load and intensity ramps up.

While not ketogenic in way that he eats, he will still likely be in ketosis during the day – by virtue of training and his normal diet is low carbohydrate – it’s around 80g – 100g carbs per day, thus naturally depleting his stored carbohydrate (glycogen). Ketogenesis is a is a physiological state, not a diet, thus it’s less important to stick rigidly to foods labelled as ketogenic and to think more globally about it. My athlete plan  is based around these dietary principles, and there are likely some nuances for the female athlete, but this general approach works well for most people I work with. It could be important for a carbohydrate refeed 1-2x per fortnight if following a very low carbohydrate diet, and that’s something I recommend to my athletes on the basis that hormonal responses will be favourable. This isn’t something I’ve seen a lot in the literature, but based more on clinical experience (and may be more important for the leaner athlete).

As I mentioned, I’ll cover off the race day side of things next week. However, if you’re keen to know more about what Dan recommends, then definitely check out his new site – he’s developing an online course that details specifics for coach and athlete alike, and is releasing it soon!

Kona 2018. (PC: oxygenaddict.com)

Another reason to love coffee…

Love your coffee? Here’s another reason to pour yourself a cup. A recently published study should the consumption of a dark roasted coffee brew (500ml) daily for one month resulted in a 23 percent reduction in DNA damage to white blood cells compared to baseline levels. The protective feature of coffee is thought to be the polyphenols that are found in coffee. These bioactive ingredients (such as caffeic acid, catechol, hydroxyhydroquinone, trigonelline and the alkylpyridinium compounds) have been studied for their antioxidant and anti-inflammatory properties. They are able to mop up reactive oxidative stress (ROS) molecules that are the byproduct of metabolism. Obviously a small amount of ROS is necessary, however too much can overwhelm our anti-inflammatory and antioxidant system, causing increased inflammation and the reduction in the ability for these pathways to function, causing DNA damage.

DNA damage accelerates ageing and is the underlying cause of the growth of carcinogenic cells in the body. It leads to telomere shortening – telomeres are like small caps on the end of your DNA chromosomes, protecting them from damage, and are used as a biomarker for ageing. The study was a randomised controlled trial; therefore, it is able to establish causation (unlike a lot of nutrition research, which is largely observational in nature).It is consistent with other studies that show a reduction in DNA damage after even short term exposure (such as this study, where healthy volunteers showed a reduction in damage after only 2h of drinking coffee). The current research was conducted in both healthy men and women, and the 500ml of coffee per day equated to around 372mg caffeine daily – equal to around four cups of espresso. That sounds like a lot of coffee (and it is!) however this is consistent with other observational and clinical trial research that has shown a reduction in cardiovascular disease risk, cancer incidence and all-cause mortality for people who habitually consume around 4-5 cups of coffee per day. This latest study adds to a body of knowledge regarding the health benefits of coffee. The polyphenols mentioned above help protect us from type 2 diabetes, stroke and cardiovascular disease, with improvements being seen in glucose and insulin metabolism (important for blood sugar control), blood pressure and markers of inflammation in the body.

I’ve talked before on the health benefits we see in coffee, and though this is great news for coffee drinkers, let’s not forget there is a fairly substantial proportion of people who are sensitive to the caffeine in the coffee and can’t tolerate its stimulant effects. Caffeine is metabolised in the liver, with the CYP1A2 enzyme responsible for detoxifying most of the caffeine. Our ability to produce this enzyme is coded by our genes, and there is variation as to how active this is for each individual. Those that have an active gene are able to metabolise caffeine efficiently, therefore the stimulating effects of caffeine are mild and short-acting. This may affect their enjoyment of caffeine and clearly their ability to tolerate it. The opposite is also true – someone with reduced activity of the gene will metabolise caffeine more slowly and its effects will be longer lasting and more noticeable. You can find out your genetic ability to tolerate caffeine through a Fitgenes DNA test(PM me for more information).  In addition to the genetic differences, environmental elements also influence our ability to tolerate caffeine. Even if you are a fast metaboliser, stress and lack of sleep can impact on caffeine’s effects – ramping up cortisol levels and with it anxiety and blood sugar dysregulation. Three coffees a day when on holiday and in a relaxed state may not be a problem, however when a work deadline is looming and you’ve been running on little more than petrol fumes rather than sleep, it is a different story.

With the present research, as the health benefits are from polyphenols present in the coffee, rather than the caffeine, the reduction in DNA damage may well be seen in decaffeinated coffee too, with previous research finding benefits with regards to type 2 diabetes and liver damage when consuming both decaffeinated and caffeinated coffee. has found health benefits from drinking this. However, without clinical trials to confirm this, at this stage it is unknown.

Obligatory cup of coffee (PC:stockphotos)

Should you take probiotics after a round of antibiotics? The answer may surprise you!

Two recent studies have recently been published that cast doubt on taking probiotics to help recover from a course of antibiotics. Crazy right? Ask anyone and they would tell you the opposite (as I would have). However sometimes research comes out that contradicts what we would previously have thought, and we have to be open to the idea that what we believed was in fact incorrect. The saturated-fat-heart-disease hypothesis is a clear example of dietary dogma that has been turned on its head* (and the difficulty that people have getting their heads around).

Gut health 101: The gastrointestinal (GI) tract is like a hollow tube, and the cells of the GI tract are covered by a thick protective gel, and that is the mucus layer (the inside cells of the gut are called the lumen). Each of these areas have a distinct microbial community, however these are rarely studied as they are difficult to get to (unless you have an invasive colonoscopy). The stool microbiome is also part of this gut picture and is the most often studied proxy marker as the gut microbiome and these are often used interchangeably (i.e. the bacteria you see in the stool is what we would expect to find in the gut). Interestingly, one study found that the stool microbiome is not representative of the gut mucosal or lumen microbiome, which really presents a challenge to any practitioner or patient who wants a better understanding of their gut health. It also doesn’t tell us about the gut endothelial microbiome which may be the closest to explaining our gut health as it is the closest bacteria to the gut tissue. They found that there was only a 20% correlation between the stool and the gut microbiome. While stool testing can be helpful for identifying pathogens or parasites, it’s not so useful for us to understanding the presence of ‘good’ or ‘bad’ bacteria. Stool testing is one piece of the puzzle, but it’s better alongside other tests (such as a SIBO test).

When you take probiotics, the presence of these in your gut is transient, and this is something that people are unaware of. Hundreds of trials have showed the safety and efficacy of probiotics in benefiting people, but it’s not typically through the colonisation of our gut. Like many things, we are different in the level of colonisation that occurs when bacteria is introduced into the gut – some people are more permissive than others, and some are really resistant to it. The researchers were not able to determine exactly what makes someone a ‘permissive’ coloniser and a ‘resistant’ coloniser, however suggested that the presence of certain bacteria in the gut may play a role in this. However, they are still beneficial despite this – with significant changes in the gene expression of people who took the probiotics (19 downregulated and 198 upregulated genes), confirming the idea that probiotics work at a cellular level and can enhance the activity of genes in the gut, aid in digestion, stimulate the immune system etc.

A surprising finding from a second study was that probiotics slowed the recovery of the gut microbiome after a round of fairly potent antibiotics. In fact, this is what I (and other practitioners) always recommend their clients do. Flooding the system with good bacteria has been thought to prevent the adverse effects of the antibiotics. The study wanted to see how the probiotics affect the long-term gut ecosystem after a single dose of the broad-spectrum antibiotic ciprofloxacin and metronidazole (to ensure all gut microbiome was wiped out). This particular study (conducted in both mice and humans) split the participants into three groups: one took no probiotic and were left to spontaneously recover; one group took an 11 strain bacteria probiotic for four weeks immediately upon finishing the antibiotics and the final group actually had what is called an autolagus fecal microbiome transplant (aFMT) – this is when a person takes capsules of their own fecal matter that had previously been collected when their gut is in a good space. Remember, the gut doesn’t like change, so what better than to replace the bacteria with some of your own? The results found that treating the gut with a course of probiotics delayed the return of the normal gut microbiota by as long as five months after stopping the probiotic treatment, and microbiota diversity stayed low too – well lower than the group who took nothing. In fact, the researchers found the group left to their own spontaneous recovery had no major differences in their stool microbiota within 21 days post-antibiotics. This is so different to what we understood about the ability of the gut to recover post-antibiotics. Again, there will be differences in what practitioners recommend, but to the best of our knowledge we thought that it took a good 18-24 months for the gut to fully recover from a round of potent antibiotics. This is actually incorrect too: previous research (when you delve further) shows that this may be the case for one or two strains of bacteria, but the majority actually recover fairly quickly and the composition of the gut microbiota resembles pre-treatment composition.

The gut microbiome is resilient, perhaps more so than what I (and others) had believed. This is only good news!

The researchers found the lactobacillus in the probiotic was what prevented the colonisation of the native bacteria in those that took the probiotic. This is the most commonly used bacteria in most probiotic strains. Again, this doesn’t mean that probiotics are NOT helpful in general (from the immune regulating benefits and what I’ve mentioned above) and we also don’t know how other probiotics which don’t contain the lactobacillus bacteria affect the gut (such as the yeast saccharomyces boulardis). There are so many different combinations of antibiotics and probiotics out there – and this is specific to this particular strain of probiotics and the type of antibiotic used. So it’s by no means the nail in the coffin for probiotics post-antibiotics, however it does call into question the broad recommendation and is something worth talking to your health practitioner about.

*I’ve linked to one academic’s thoughts, and could have also linked to many many more (and studies) such as this one or this one. But this isn’t a post about saturated fat so I didn’t.

LIttle microbiota in your body are more resilient than you think… so we may need to leave them to do their thing. PC: oregonsportsnews.com