bite my words

Dispelling nutrition myths, ranting, and occasionally, raving


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The dark green leafy truth about your kale smoothie

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I’ve been slacking again, sorry! No post on Monday and I had plans to write a post debunking this article about how kale is killing us all that a friend sent me over the weekend. My immediate reaction was that if kale is accumulating these toxins then it stands to reason that many other vegetables are, as if people need any discouragement from eating their veggies. My friend responded that it would be best if everyone stuck to corn dogs. Of course, that’s no solution as corn dogs are full of GMOs and carbs which we all know cause “grain brain”. Anyway… I was going to dig a little deeper but before I did, I saw this article by Julia Belluz that did that for me so, please, go read her article about how faulty the “science” is behind the headlines that kale is a killer. Sure, alliteration is a great literary device (possibly my favourite), it makes for great headlines, but it doesn’t make bad science good.

There are just a couple of things I really want to emphasis that Julia just touched on. First, despite what the articles indicate, this was not a strong scientific study. There was no true control group. There was no randomization of participants. This was a very small “sample” of 20 self-selected individuals who went to Ernie Hubbard for “detoxes” for myriad inexplicable medical complaints. Ernie started with the assumption that kale was causing their problems, he didn’t seek out other causes. His finding that they were all kale consumers was a self-fulfilling prophecy. Second, Please, please, please don’t stop eating vegetables because of these sensational headlines. The benefits from eating vegetables far outweigh any real risks. Variety is an essential part of any healthy diet so be sure to consume a wide variety of vegetables, including leafy greens and members of the Brassica family, such as kale.


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Eat for your microbes: lose weight fast, gain control of your blood sugar in only one week!

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Photo by Pacific Northwest Laboratory on flickr. Used under a Creative Commons Licence.

I know that I really shouldn’t comment on this research without reading the actual journal article but that hasn’t been published yet and I can’t resist jumping into the fray. Is there a fray? Not really. I just keep seeing people retweeting this and everyone seems all excited about the possibility of these individualized and I need to put a little rain on the parade.

The article starts off sounding great. Who doesn’t want a bespoke diet? Considering the number of people who have asked me as a dietitian to “just tell me what to eat” I think that most people want someone to hand them a nice little meal plan. Of course, most meal plans would be “bespoke” in a sense as any professional worth their credentials is going to tailor the menu to the client. But, I’m not here to quibble about what exactly makes a meal plan bespoke.

So, apparently the researchers looked at how different people react (in terms of blood sugar) to the consumption of different foods. They found a wide range of responses and linked those responses to the types of gut microbes residing in the participants digestive tracts. Then in another study (of only 20 participants) each participants was given a unique diet to control blood sugar and one that was designed to increase blood sugar. Unfortunately, the diets aren’t described in the article so it’s hard to say how much they differed for each participant. There’s also no explanation as to how this ties in to the earlier research looking at the microbiome. In a shocking turn of events, on the diets designed to control blood sugar some (again the article doesn’t indicate how many) participants blood sugar levels returned to normal. On the “bad” diets they had blood sugar spikes that “would be described as glucose intolerant” according to one of the researchers. Essentially, they exhibited diabetes or similar conditions.

The article then goes on to say that this research somehow shows that calories aren’t the only player when it comes to weight loss. What? I thought the research was looking at blood glucose levels. There was no mention of weight change in participants. While I certainly agree that there are many other factors at play, in addition to calorie consumption when it comes to weight management, I fail to see how this research examined this issue at all.

What makes me a little more leery about this study is that the researcher says it’s surprising that ice cream (for example) doesn’t cause huge blood sugar spikes, and that buttered bread has less impact on blood glucose than unbuttered bread. Have these people not heard of glycemic load before? Of course blood glucose responses are going to be mitigated when high carbohydrate foods are consumed with fat or protein. That’s why it’s important to look at how people are consuming foods rather than examining the effect of specific foods in isolation.

I’m trying to withhold full judgement until the research is published. I think that the human microbiome is a fascinating emerging area of research. However, on the basis of this article all I’m envisioning are more scam diet books urging people to eat for their microbes.


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Is 63 grams of liquid sugar the answer to high cholesterol?

A friend recently shared this tweet with me:

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She had asked the tweeter for more details but hadn’t received a response. My response: “Ugh. No wonder so many people don’t trust us as dietitians”.

Of course, it’s Florida orange juice that imparts these benefits. Because oranges from other locales couldn’t possibly impart the same benefits (<— please note this should be written in the yet to be developed sarcasm font). Even so, is the benefit even all that meaningful? I’d argue no.

While I can’t be certain that the study I found is the one the tweeter was referring to it was the top hit and was sponsored by Tropicana orange juice so it fits the bill. The study looked at a very small group of individuals with elevated cholesterol. There were only 25 participants, 16 healthy men, and 9 post-menopausal women. This means that the results cannot be extended to apply to pre-menopausal women or “unhealthy” individuals. There were additional strict criteria that participants had to meet: 1. have initial fasting plasma triacylglycerol (blood lipid) concentrations in the normal range, 2. be habitual or occasional orange juice drinkers, 3. be free of thyroid disorders, kidney disease, and diabetes, 4. have an alcohol intake of ≤2 drinks/d, 5. not be receiving hormone replacement therapy if female. With such a small sample size of people meeting such precise criteria, no concrete conclusions can be drawn from this study.

However, the researchers still drew conclusions. Namely that three cups of orange juice a day can lower LDL and increase HDL blood levels. They found that HDL levels were increased by 21% and the HDL-LDL ratio was decreased by 16%. That sounds fairly impressive but is it really? Well, no, not really. The average HDL level increased from 1.0 to 1.3. Anything over 1.0 is good anyway so they weren’t all that badly off to begin with. The HDL-LDL ratio really only changed because of the increase in HDL as LDL levels went from an average of 3.6 to 3.5. Not a significant change.

What the study doesn’t tell you is that cholesterol recommendations are only made in relation to risk of cardiovascular disease. If your risk level is low then an LDL of under 5.0 is fine. If your risk is high then an LDL of less than 2.0 is ideal. Risk level is determined by family and medical history. None of these factors were discussed in the current study despite the fact that the cholesterol levels measured are essentially meaningless without being placed in the context of CVD risk.

Can we just go back to that THREE cups of OJ a day again? The researchers found no significant change in cholesterol levels at one or two cups of OJ a day. Only at three cups a day. That’s a considerable amount of orange juice. Considering that a serving size of juice is 1/2 cup and most dietitians recommend no more than one serving per day I find it hard to fathom recommending 6 servings of juice every day for a slight increase in HDL levels. The researchers note that as OJ increased fibre intake decreased. They didn’t mention any other aspects of diet. There was no comparison to consumption of whole oranges, other fruit or vegetable juices, or any other dietary changes. Based on this study alone I would absolutely not advise anyone wishing to improve their blood cholesterol levels to drink 63 grams (more than 15 teaspoons) of liquid sugar daily.


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Skeptic or jerk? What’s the difference?

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Eternal Damnation by Stephen L. Cloud used under a Creative Commons Licence.

Last week I tweeted the question “When did skeptic become synonymous with a**hole?” (except without the asterisks because I’m much more brazen on twitter). Something I’ve been noticing a lot lately is that people seem to be using their self-proclaimed skeptic status as justification for being condescending and rude to other people. If you know me at all, you know that I don’t suffer fools gladly. It’s damn hard to bite your tongue in the face of ignorance and stupidity. However, I don’t understand why it’s become acceptable (especially on social media) to be patently rude to other people just because they have different opinions or beliefs than you do. And those are people that you’re attacking; not avatars, not bots. You’re not advancing your cause by insulting those who disagree with you.

The definition of skeptic (according to google) is: “a person inclined to question or doubt all accepted opinions.” I consider myself a skeptic. I question most things. I tend not to believe anything until I see evidence. That’s skepticism to me. It would appear that skepticism to many skeptics is belittling or insulting those who don’t hold the same values as themselves. Interestingly, most of those I’m seeing lately are not questioning accepted opinions, only tearing down those who dare to question the status quo. I’m pro science. That doesn’t mean that I unquestioningly accept every piece of scientific research and discredit every unproven theory. There is a plethora of terrible scientific research out there. Loads of poorly designed and biased studies are published in peer-reviewed scientific journals. We also haven’t done all of the science that there is to science so there’s always the possibility that unproven theories will one day be proved. Being a skeptic means questioning everything, not just the non-science, and not just the beliefs held by others. We need to hold ourselves and our beliefs up to the same level of scrutiny as all others.

Insulting other people doesn’t make you a skeptic. It just makes you a jerk.


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Can peanut consumption prevent allergies?

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Last week the headlines all boasted that feeding babies peanuts could prevent peanut allergies. A new study in the New England Journal of Medicine assigned children thought to be at high risk for peanut allergy development to either an exposure group or an avoidance group. It was found that 10.6% of the infants in the exposure group tested positive for peanut allergy at 60 months of age, versus 35.3% of infants in the avoidance group. I’m not quite as convinced as the headlines that this is a cure for peanut allergy. Certainly, there was a large difference between groups. However, we have seen in previous research that peanut exposure in allergic children may increase tolerance, although not to the extent that they would be able to safely munch on a peanut butter and jam sandwich for lunch.

This may be a matter of semantics, and it’s purely my own interpretation, but I think that the current study provides more support for the stance that peanut (and likely other allergens) avoidance in at risk children increases the likelihood of allergy development. More so than the consumption of peanuts decreases the risk of peanut allergy.

Peanut allergy does not occur upon the first exposure to peanuts. It usually occurs upon the second exposure. Although it may occur upon subsequent exposures, this is unlikely in the case of peanut allergy. I can’t help but wonder how this may have effected the results. The authors don’t mention whether or not the infants in the study had been exposed to peanuts prior to enrolment. I can’t help but wonder if this could have affected the results in some way. There is also the question as to whether the withdrawal of infants from the study was a result of the development of peanut allergy in the consumption group, or perhaps discovery of the absence of allergy in the avoidance group. Could this have significantly affected the results? Adherence was quite good, over 90% in both groups, however, reasons for withdrawal could still have an impact on the results.

While the infants included in the study were all identified as being at risk of developing peanut allergies due to either the presence of eczema and/or egg allergy, these are not necessarily the best ways to identify risk. The children at greatest risk of developing peanut allergy are those who have an immediate family member (i.e. a parent or sibling) who has a peanut allergy. The children in the study would be at greater risk than those without eczema or other allergies but they would not necessarily be those at greatest risk. Perhaps infants at greatest risk would benefit from early peanut exposure, perhaps not. Perhaps infants in the general population would benefit from early peanut exposure, perhaps not.

Okay, so, I’m sure that parents are wondering what all of this means. Firstly, what many of the news articles are failing to impart is that the current guidelines recommend waiting until 6 months of age before introducing solids. Introducing peanuts, or any solid foods, at younger ages is not recommended as infants do not have fully developed digestive systems. Peanuts and peanut butter may also be choking hazards for infants, please be sure to use age appropriate foods and supervise your infant during feeding. Finally, this research supports the current guidelines which indicate that there is no reason to avoid providing your infant potentially allergenic foods at the same time that you introduce other foods. Regardless as to whether or not early introduction reduces the risk of allergy development or later introduction increases risk, at this point we know that there is no benefit to waiting, and there may be disadvantages to doing so.