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.

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”.

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

What’s the best exercise for longevity?

Well, that’s a bit of a loaded question, really. As any is better than none, and there will be different points of views by different experts (of which I am not one of them). However, the older I get, the more I am interested in the effects of ageing on our overall health span. Ageing is unavoidable; it happens to the best of us. Listed below are some of the physiological and biological changes that can occur the older we become:

  1. Insulin resistance – this is in healthy weight older adults also, with research showingthere is more peripheral insulin resistance compared to a younger population (an inability to dispose of glucose into the tissue).
  2. Decreased availability of anabolic hormones, and increased frailty with lower levels of hormones
  3. Increased anabolic resistance, so not only is there a decrease in the hormones that signal tissue growth, the muscle tissue is less responsive to the stimulus of amino acids (protein) and exercise, and there is less muscle protein synthesis in comparison to breakdown.
  4. Greater protein requirementsfor the same relative gains in muscle, strength and function compared to a younger population
  5. Decreased motor neuron function, therefore less neural signalling to muscle tissues and reduced motor function.
  6. Increased intracellular oxidative stress, causing inflammation and reduced cell functioning
  7. Reduction in satellite (stem) cellsnumbers and regenerative capacity – these cells are essential for the maintenance and repair tissues in normal physiological processes or in response to muscle damage/trauma.
  8. Elevated myostatin signalling, a protein that blocks our ability to build muscle
  9. Increased chronic inflammation (also known as inflamm-aging)
  10. Changes in autophagy, where ageing reduces our ability to clear out damaged DNA
  11. Mitochondrial functioning abnormalities, where we can’t utilise energy metabolites as effectively to fuel mitochondria
  12. Reduced ability to be physically active (due to many of the reasons listed above)

This is a long, daunting and rather depressing list of what can occur as we age – and we are an ageing population. There is no doubt that if we don’t look after the body we have got, then we really are staring down the barrel of a loaded gun. The list above describes many of the mechanisms to explain the loss of muscle mass and function. It’s not about being ripped or having gainz, it’s about having proper functioning of the muscle so it can work effectively in our older years. This is what is shown to have the most positive impact on our cardiovascular, neurological and musculoskeletal systems.

Inactivity is the broader environmental issue that we need to address any (and all) of the physiological issues I have mentioned above. We need to be active – in everyday life, and with some structured activity too. Hanging out washing and housework isn’t going to cut it, I’m afraid. I see a lot of people who have this idea that you don’t need to exercise in order to lose weight, and you can do it solely on diet alone. This is true, of course, but when you embark on any weight loss plan that restricts calories (i.e. any weight loss plan that is out there), then you will lose both fat weight and muscle mass – lowering your overall metabolic rate along with it. This is one of the reasons why weight regain is so prevalent, however the powerful combination of diet plus exercise helps sustainable weight loss. As I alluded to above, exercise isn’t just moving around the house, doing chores – this should just be part of everyday living. Data looking at the effects of exercise show that resistance training confers benefits over and above what we would see if we were just doing 30 minutes exercise per day.

The right type and duration of exercise:

The challenge is to get people exercising. And this is especially so for those who read what I have said above, and think that – on top of 30 minutes of aerobic training they don’t have time to do, they then need to put some resistance (or weight) training in.

I’m not writing this to encourage you to find an additional 3 hours in your week, though.

In fact, a study that is yet to be published (I heard about it on STEM talk) suggests that just 72 minutes a week in total is enough to help many of the conditions associated with ageing and poor health that I’ve mentioned above. Egan and colleagues found a combination of both resistance and cardiovascular exercise in a circuit-type setting for adults over 65 years just three times a week for 24 minutes increased walking speed, leg strength and reduced trunk fat. These measures speak to better muscular function, obviously increased strength, and will help reduce metabolic health risk. The improvements were more potent in this combined group than either resistance training or aerobic training for the same duration.

So this was a very long preamble to the main message: if you are currently NOT exercising, then please start. While there are modalities that are better than others, seriously, anything will be better than nothing. The study I talked about is in older adults, you likely don’t need me to tell you that any age you start is obviously better than not starting at all. AND the earlier you start, the better the overall health outcomes.

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Seriously. Those pink dumbbells. Because obviously an older female couldn’t possibly lift anything heavier, right?! (PC:www.fabafterfifty.co.uk).