Saturday, April 30, 2016

Self Assessment with the ORTO-15

In the previous post I mentioned how there are issues with the validity of the standard questionnaire (the ORTO-15) to diagnose orthorexia (or health fanaticism) in those orthorexia prevalence studies.  So I went through the ORTO-15 and surveyed myself, and this made me more strongly agree with those concerns of validity.  Before I go through the ORTO-15, just note that I would answer no to all of Dunn & Bratman’s proposed diagnostic criteria (see previous post)


 As a general note these questions are a bit ambiguous at times.  Besides wondering what ‘often’ and ‘sometimes’ should be operationalised to mean, questions along the line of ‘Do you think X’ (questions 9, 10, 11, 12, 14) could be interpreted in a few ways.  Just to use question 9 as an example, it could be interpreted to mean either: ‘how often do you do you think your mood affects your eating behaviour’; or ‘do you think your mood often affects your eating behaviour’.  In addition, the ‘your’ in questions like question 9 could be referring to yourself or to people generally, though I suspect the former.  I might be overthinking this, but I think it’s plausible that if you gave questions like question 9 to a bunch of people you would get 4 different interpretations of the question from the sample.  So I’ll answer that type of question two different ways and assume ‘your’ means yourself

Lower scores are more indicative of orthorexic tendencies

1.      When eating, do you pay attention to the calories of the food?
Sometimes (3).  It can sometimes be a good idea to know roughly how many calories are in something and that when considering a dessert for example, 100g of cake contains a lot more calories than 100g of fruit and is proportionally less satiating.  Most of what I eat doesn’t have a calorie label and that doesn’t concern me

2.      When you go in a food shop do you feel confused?
Never (1).  When I go into a food shop I know what I want to buy and don’t spend much time doing so (10-15 minutes for a weekly shop).  I think you could be confused if you had an introductory level of nutritional knowledge that was strongly influenced by the contradictory messages in the media, and then debating between various processed foods (should I buy the low fat muffin or the gluten free brownie, etc).

3.      In the last 3 months, did the thought of food worry you?
Never (4).  I don’t think it should unless you had something like IBS, IBD or coeliac disease, which would be quite understandable

4.      Are your eating choices conditioned by your worry about your health status?
Never (4).  I would describe myself as being invested in my health status, but not worried about it.  With questions like this and question 3 you can see how easy it could be for someone trying to do something about a health condition they have to be labelled as orthorexic

5.      Is the taste of food more important than the quality when you evaluate food?
Sometimes-often (2.5).  The food I eat is simple, but tastes nice.  But I don’t regularly eat junk food even though it tastes better

6.      Are you willing to spend more money to have healthier food?
Sometimes (3).  Healthy food doesn’t have to be that expensive and I limit expenses by generally only purchasing fruit and vegetables at ≤ $4/kg, and meat at ≤ $10/kg.  Berries might be the healthiest fruit, but at $20+/kg it’s hard to justify the need for them.  That being said, meat, fruit and vegetables are definitely more expensive per calorie than things like bread, pasta or rice.  Perhaps I would answer ‘often’ if I had a higher income

7.      Does the thought about food worry you for more than three hours a day?
Never (4).  That’s a very long time to worry about food and could be a sufficient diagnostic criterion in itself

8.      Do you allow yourself any eating transgressions?
Sometimes (2).  Unhealthy food doesn’t makes up a fairly small part of my diet, I eat a small amount of ice cream fairly regularly, some chocolate/etc when it’s gifted to me and eat out or buy lunch rarely (only without someone else and mainly because it’s much more expensive than making your own).  But ‘eating transgressions’?!  That’s pretty strong language and certainly not the kind of way I would describe eating unhealthy food.  Apparently only ‘sometimes’ is pretty orthorexic though

9.      Do you think your mood affects your eating behavior?
Interpretation 1: how often do you do you think your mood affects your eating behaviour.  Sometimes (2).  I rarely think about this probably because I don’t engage in very obvious emotional eating
Interpretation 2: do you think your mood often affects your eating behaviour.  Always (4).  Because mood always has some effect, just to varying degrees (note: I don’t think we have free will)

10.  Do you think that the conviction to eat only healthy food increases self-esteem?
Interpretation 1: how often do you think that the conviction to eat only healthy food increases self-esteem?  Sometimes (3).  I very rarely think about this
Interpretation 2: do you think that the conviction to eat only healthy food often increases self-esteem?  If someone resolves to eat healthfully and then successfully does so, that can increase self-esteem in a very healthy way, just like resolving to and then successfully completing any other activity (Often (2)).  It won’t increase self-esteem much for me though because my eating habits are quite routine.  But conviction on its own without action wouldn’t increase self-esteem for me though because I haven’t achieved/done anything (Never (4)), but may increase self-esteem in other people (Sometimes (3))

11.  Do you think that eating healthy food changes your life-style (frequency of eating out, friends, …)?
Interpretation 1: how often do you think that that eating healthy food changes your life-style (frequency of eating out, friends, …)?  Sometimes (3).  I very rarely think about this
Interpretation 2: do you think that eating healthy food often changes your life-style (frequency of eating out, friends, …)?  Sometimes (3).  I’m comfortable eating pretty much whatever in the odd social situation.  Paleo was a gateway for my interest in chronic disease research, the blog and the people I follow on twitter, but if I changed the way I ate, without changing what I think, then I don’t expect the other stuff would change

12.  Do you think that consuming healthy food may improve your appearance?
Interpretation 1: how often do you think that consuming healthy food may improve your appearance?  Sometimes (3).  I don’t think about this very often
Interpretation 2: do you think that consuming healthy food may often improve your appearance?  Sometimes (3).  For the most part the foods I eat have a unnoticeable effect on my appearance (as something that changes slowly anyway), but could easily have subtle long term effects on aging.  I find some foods (wheat, chocolate) can sometimes give me a little bit of acne

13.  Do you feel guilty when transgressing?
Never (2).  Again, such strong language with ‘guilty’ and ‘transgressing’.  I have never felt guilty when eating unhealthy food.  I have sometimes regretted those decisions, but eating unhealthy food isn’t something that’s morally wrong to feel guilty over.  But apparently my response is pretty orthorexic though

14.  Do you think that on the market there is also unhealthy food?
Often (2).  Of course there is unhealthy food in the market, most of it isn’t healthy and that shouldn’t be a controversial statement

15.  At present, are you alone when having meals?
Often (2).  Simply because I’m currently living by myself

I scored 40.5 with interpretation 1 and 42.5 with interpretation 2.  Most studies have used a score of less than 40 as the cut-off point that indicates orthorexic behaviours, so the ORTO-15 would suggest I have borderline orthorexia or are at risk of orthorexia, but you can judge for yourself on whether that is the case

I hope you can now see quite clearly how those prevalence studies were able to find such surprisingly high prevalence rates for orthorexia.  Another issue with the ORTO-15 is that the questions and responses (‘often’ and ‘sometimes’) can be interpreted in many ways and that some questions don’t necessarily do a good job of assessing orthorexia or lack thereof in some circumstances, and these other issues may explain how associations between orthorexia and other factors has been inconsistent or absent in the literature

Summary of the Research on Orthorexia

At the time of writing this post there are 49 papers on PubMed on orthorexia.  Needless to say, the research is in its infancy, but that doesn’t mean it isn’t a legitimate condition.  Most of the studies on orthorexia are looking at the prevalence of orthorexia in a specific population (mostly in university students, but also dieticians, people with other eating disorders, etc) and/or are looking at associations between various personality characteristics such as perfectionism with orthorexia.  There are also several pretty extreme case studies in the literature

The Othorexia Prevalence Studies

The prevalence studies used a questionnaire called the ORTO-15 (or a derivative of it) and have reported a very wide range in the prevalence of orthorexia (between 6 to 88.7%) that is generally very high (~30-80%) [1] [2].  The following table comes from [1]

Study
Prevalence rate (%)
Country
Donini et al. (2005)
6.9
Italy
Bosi et al. (2007)
45.5
Turkey
Aksoydan and Camci (2009)
56.4
Turkey
Fidan, Ertekin, Işikay, and Kirpinar (2010)
43.6
Turkey
Ramacciotti et al. (2011)
57.6
Italy
Alvarenga et al. (2012)
81.9
Brazil
Segura-García et al. (2012)
Men: 28 Women: 30
Italy
de Souza and Rodrigues (2014)
88.7
Brazil
Varga et al. (2014)
74.2
Hungry
Valera, Ruiz, Valdespino, and Visioli (2014)
86
Spain
Asil and Sürücüoğlu (2015)
41.9
Turkey
Brytek-Matera, Donini, Krupa, Poggiogalle, and Hay (2015)
Men: 43.2 Women: 68.6
Poland
Gubiec et al. (2015)
59
Poland
Jerez et al. (2015)
30.7
Chile
Missbach et al. (2015)
69.1
Austria
Stochel et al. (2015)
Study 1: 53.7 Study 2: 52.6
Poland
Segura-Garcia et al. (2015)
Clinical: 58 Control: 6
Italy

If the high and variable prevalence rates sounds weird, that’s probably because it is.  Several studies have brought up issues with the ORTO-15 including:

·         That “it is counterintuitive to believe that a phenomenon of restricted eating that is not well understood has point prevalence rates found to be as high as 88.7 %, with repeated findings of 30–80 %” [2]
·         That “in this study, it is remarkable that 80 % of the sample endorse that they do not restrict the type of food that they consume, yet the ORTO-15 identifies over 70 % of the sample suffering from ON” [2]
·         That the ORTO-15 doesn’t do well at distinguishing healthy eating from disordered eating very well [2] [3] [4]
·         Issues with the questions and scoring [3]
·         The inconsistent associations between ORTO-15 scores with age, education, BMI, smoking, alcohol, and sex [4]

Orthorexia and OCD

In contrast to the ORTO-15 (which I’ll show you in the next post), in a recent review Dunn & Bratman [1] proposed some diagnostic criteria for orthorexia

Criterion A: Obsessive focus on “healthy” eating, as defined by a dietary theory or set of beliefs whose specific details may vary; marked by exaggerated emotional distress in relationship to food choices perceived as unhealthy; weight loss may ensue as a result of dietary choices, but this is not the primary goal. As evidenced by the following:

1.       Compulsive behavior and/or mental preoccupation regarding affirmative and restrictive dietary practices believed by the individual to promote optimum health.
2.       Violation of self-imposed dietary rules causes exaggerated fear of disease, sense of personal impurity and/or negative physical sensations, accompanied by anxiety and shame.
3.       Dietary restrictions escalate over time, and may come to include elimination of entire food groups and involve progressively more frequent and/or severe “cleanses” (partial fasts) regarded as purifying or detoxifying. This escalation commonly leads to weight loss, but the desire to lose weight is absent, hidden or subordinated to ideation about healthy eating.

Criterion B: The compulsive behavior and mental preoccupation becomes clinically impairing by any of the following:

1.       Malnutrition, severe weight loss or other medical complications from restricted diet.
2.       Intrapersonal distress or impairment of social, academic or vocational functioning secondary to beliefs or behaviors about healthy diet.
3.       Positive body image, self-worth, identity and/or satisfaction excessively dependent on compliance with self-defined “healthy” eating behavior.

This is very similar to some other proposed diagnostic criteria by Moroze et al [5]:


Both sets of diagnostic criteria emphasise the two factors that for something to be disordered eating (as opposed to conscientious eating) it needs to cause suffering and impair function (the two key factors that really define whether something is a mental health issue or not).  They also emphasise that orthorexia is a very similar condition to obsessive compulsive disorder.  Something that is discussed well in the following review (and something I’m planning to write about later) [4]


* Orthorexia and anorexia are distinguished by orthorexia being about food quality for health and anorexia being about food quantity for weight loss.  It’s a simple story, but what about the two other combinations: an obsession on food quality for weight loss, and on food quantity for health.  The latter two could both fall into the category of orthorexia, and I can think of some examples for each of them

Monday, April 25, 2016

Ramsden et al Recovers Data from the Minnesota Coronary Survey

Ramsden et al have previously written a meta-analysis [1] and a review [2] critical of the mainstream view that replacing SFA with mainly n-6 PUFA would reduce the risk of coronary heart disease (as well as other research on n-6 PUFA).  They later recovered some missing data from the Sydney Diet Heart Study (SDHS) [3] and more recently did the same for the Minnesota Coronary Survey (MCS) (they call it the Minnesota Coronary Experiment (MCE)) [4].  SDHS and MCS are both unfavourable trials for the diet heart hypothesis [5].  This paper was widely publicised in the media because those guys love controversy

Ramsden et al described MCS as “perhaps the most rigorously executed dietary trial of cholesterol lowering by replacement of saturated fat with vegetable oil rich in linoleic acid. The MCE is the only such randomized controlled trial to complete postmortem assessment of coronary, aortic, and cerebrovascular atherosclerosis grade and infarct status and the only one to test the clinical effects of increasing linoleic acid in large prespecified subgroups of women and older adults.” [4]

It’s this autopsy and subgroup data that Ramsden et al’s paper has recovered and is largely publishing here (see table 1)

It’s previously been reported that compared to the control group, total mortality was equal in men (RR = 0.99) and slightly higher in women (RR = 1.16) (average RR = 1.08).  The newly recovered data show this slight increase in mortality to be due to people aged at least 65.  What’s interesting about the mortality figures is that the separation in the ≥ 65 age group starts to begin at around 600 days (figure 5)

This is similar to observation Chris Masterjohn made about the Los Angeles Veterans Administration Trial (LAVAT), that cancer mortality began to be higher in the experimental group at 2 years and non-CVD mortality at 4-7 years [6].  Forget about the defence against this paper that the trial was too short to demonstrate the benefits of n-6 PUFA – cholesterol levels change within a week or two and so if that’s the primary mechanism then the benefits should start right away.  On the other hand, if the harms of excess n-6 PUFA are somewhat mediated by changes in tissue lipid composition, then you would expect the harms of excess n-6 PUFA to take a while to develop

This is followed by looking at the relationship between changes in cholesterol during the trial with total mortality (figure 6 and table 4).  They found that a reduction in cholesterol during the trial was associated with higher mortality, in both groups.  This is really an observational study like result within an RCT and can’t be used to establish causality as you can’t determine whether diseases and their treatment lowers cholesterol or whether lowering cholesterol makes one more susceptible to other diseases.  It is consistent with reviews of observational studies that found the relationship between total-C and total mortality to be a U-shaped curve [7], and another that found among older people this U-shaped curve was shifted to the right (lowest mortality at higher total-C) or an inverse relationship [8]

The autopsies data found that: “41% (31/76) of participants in the intervention group had at least one myocardial infarct, whereas only 22% (16/73) of participants in the control group did (incidence rate ratio 1.90, 95% confidence interval 1.01 to 3.72; P=0.035). Also, participants in the intervention group did not have less coronary atherosclerosis or aortic atherosclerosis (table 5).”  However, as Ramsden, et al point out “These findings should be interpreted with caution because of partial recovery of autopsy files. There was no association between serum cholesterol and myocardial infarcts, coronary atherosclerosis, or aortic atherosclerosis in covariate adjusted models (table G in appendix)”.

Ramsden et al’s paper isn’t earthshattering but is certainly nice to have.  Reading this study brought to the front of mind a few things I’m aware of but haven’t emphasised much yet:

·         The diets used in MCS were based on diets in the National Diet Heart Study.  The experimental diet in MCS was based on diet BC and the control diet In MCS was based on diet D.  NDHS aimed for most of the fat to come from specially formulated food products (filled meats, dairy, etc).  The added fat in the filled foods came from vegetable oils for the experimental diets such as BC and “either animal fat or hydrogenated shortening” for diet D.  There’s more detail on the diets in [4].  When you consider this, even a neutral result in the trial would be unfavourable for the diet heart hypothesis

·         MCS finished in 1973 but the manuscript was published in 1989 – 16 years later.  There are three abstracts in a supplement of Circulation in 1975 as the trial was also discussed in an American Heart Association conference around that time*.  But still this could be argued to be borderline publication bias**.  I also doubt that the publication of MCS would have changed much in the first dietary guidelines.  Even after MCS and DART (a neutral trial) were published people who support the diet heart hypothesis still find ways to do so and to rationalise away unfavourable results (you only need to look at the rapid responses and the media for this)

·         On a somewhat related note, the favourable diet heart trials were the ones with the most publications (ODHS (4 + monograph), LAVAT (12 + monograph), FMHS (6), HDAT (4) and STARS (9)), while the unfavourable trials had the least (RCOT (1), SDHS (2) and MCS (1))

* The 3 abstracts are difficult/impossible to find online but I was able to find them at Melbourne University’s library.  They give very little additional information unless you’re totally obsessive, because they report a different number of participants (Abstracts 9449, Manuscript 9057, Ramsden et al 9570) and the number of participants who had a major CVD event (CVD M,P) whereas the manuscript reported the number of major CHD events (CHD M,E)

** Funnel plots are used in meta-analyses to look for the probability of publication bias, where an asymmetric funnel plot suggests publication bias (here are some really bad examples [9] [10]).  I noticed some asymmetry in my funnel plots of the diet heart trials for major CHD events (top left) and total CHD events (top right), but not CHD mortality (bottom left) or total mortality (bottom right).  This is limited by the small number of studies (N = 11) and may simply reflect methodological differences rather than publication bias.  But it makes you wonder


I would also recommend reading George Henderson's rapid responses and Chris Masterjohn's post

Tuesday, April 19, 2016

Palmitate In Vitro: Does Saturated Fat Impair the Circadian Rhythm?

A little while ago I wrote about a recent study that found a high fat diet induced weight gain and insulin resistance in mice – a thoroughly unsurprising result considering previous research and the mouse model used (blog).  Today I’m going to talk about another thoroughly unsurprising result, this time from a study that found palmitate (C16:0) is bad for cells – specifically shifting the circadian rhythm [1].  The study was reported in Science Daily, which reported that saturated fats 'jet lag' the body clocks, which triggers metabolic disorders [2]

The paper itself is quite lengthy, detailed and technical.  There’s a good chance the authors spent a fair bit of time on this.  In summary: palmitate alters the circadian rhythm, but DHA does not; and the effect of palmitate is probably due to inflammation [1].  The authors also cite similar results from other cell culture studies and results from mouse studies that found feeding them a high fat diet impairs their circadian rhythm

Palmitate (and LPS) are regularly used in cell culture studies to cause bad things to happen for your gene knockout/gene therapy/new drug/etc to protect against.  Below are a few studies I found following a brief search (just note that our study used 0.15-0.25 mM of palmitate or DHA [1]):

  • 0.5 mM palmitate (but not oleate) increases ceramide accumulation, the generation of reactive metabolites and apoptosis in CHO cells [3]
  • 0.1 mM palmitate impairs insulin signalling in hypothalamic cells [4]
  • 0.5-1.0 mM palmitate induces ER stress in adipocytes [5]
  • 0.3 mM palmitate leads to ceramide accumulation, inflammation and impairs insulin signalling in myotubes [6

But oleate protects against this:

  • 0.3 mM palmitate (but not oleate) causes mitochondrial dysfunction, insulin resistance, inflammation and substantially impairs viability of neuronal cells.  Pre-treatment with oleate completely protected against this and was more successful than linoleate (C18:2 n-6) or DHA [7]
  • 0.5 mM palmitate increases ceramide accumulation and apoptosis in CHO cells.  0.2 mM of oleate* was sufficient to protect against this because it promoted triglyceride storage rather than ceramide accumulation [8

* Information like this is really important.  How many meals have you had where the palmitate:oleate ratio is greater than 2.5?  Probably never!  Coconut oil and palm oil have a ratio of 1.38 and 1.19 respectively, and animal foods have a ratio of about 0.5 or lower

The article in Science Daily says “The reported findings predict the best time to eat a high-fat meal is early in the morning and probably the worst time is late at night” [2].  Cell culture studies are good for teasing out mechanisms, but I don’t think you should generalise the results from the petri dish to your dinner plate (and particularly in cell culture studies you shouldn’t generalise palmitate to all fat).  If inflammation, particularly postprandial inflammation is the issue, then I think the emphasis should be on consuming beneficial substances from whole foods (particularly fruit and vegetables) and reducing sedentariness (blog)

As for whether carbs of fat are better/worse at certain times of the day, that’s a question you’ll find many arguments or viewpoints for, and a topic for another day.  It’s also the kind of thing that people can experiment on for themselves quite easily and find what works for them

Thursday, March 31, 2016

New Paleo Study by Freese et al

A paper was recently published in the Journal of Evolution and Health (the journal of the Ancestral Health Society) that looked at the effects of simulating a few aspects of a hunter-gatherer lifestyle for 4 days and 3 nights

This study included 13 participants (7 male, 6 female), all Caucasian.  Average age was 39 (± 8.1).  9 of participants had a BMI between 19.3-25, 4 had a BMI between 25-27.4.  7 exercised for more than 3 hours per week and 1 was a smoker

  • Outdoors: the participants “lived and slept outdoors with no shelter”
  • Diet: the participants received fruits, nuts and tubers to eat for lunch and a Paleo dinner.  “The dietary composition of foods was aimed to reconstruct a paleolithic diet based on the recommendations of Cordain and others”.  The participants consumed 1567 calories per day on average during the study (the participants’ usual calorie intake isn’t reported) with a macronutrient ratio of 24:54:22 (P:F:C) (see table 2 for detailed information on the foods they ate).  (The participants got their water from a “nearby holiday apartment”)
  • Exercise: the participants hiked for 3.42 hours per day and did 2.5 hours of other forms of physical activity (“Other activities associated with nomadic hunting and gathering were: swimming, climbing, lifting and building a fire”)
  • Fasting: the participants had an intermittent fasting period of at least 12 hours per day, as they didn’t eat until noon and did the 4+ hour hike while fasted
  • Sleep: the participants slept an average of 7.9 hours.  That being said the participants probably had also benefited from less night-time light (depending on the moon).  (As this study was done in Germany it could be important to know what season is was and what the weather was like) 

The rationale of the study is that various aspects of our evolutionary mismatch leads to low grade inflammation, which promotes obesity and insulin resistance, and that exercise while fasted may be particularly protective against this.  I have written previously on how inflammation is an attractive mechanism of insulin resistance, but current evidence from RCTs in humans doesn’t support that hypothesis so far (blog).  I like the idea of researching tools to mitigate postprandial inflammation, but I doubt much would change in a fasted blood sample after 4 days

The researchers made many measurements related to the immune system/inflammation, the metabolic syndrome and body composition (see table 4 and 5 for more info).  Significant changes included:


Pre
Post
Change
Weight (kg)
69.7
67.0
-3.9%
RDW (%) (RBC distribution width)
12.9
12.5
-2.9%
Thrombocytes (nL)
212.5
235.5
10.9%
Lymphocytes (%)
31.1
26.7
-14.0%
Fasting Glucose (mg/dL)
87.2
71.3
-18.2%
CRP high sensitive (mg/L)
0.4
1.1
169.6%
Insulin (uU/mL)
4.2
2.1
-50.1%

With 1597 calories and all that exercise it’s not surprising that the participants, who appear already quite healthy, lost some weight and reduced their fasting glucose and insulin levels.  Surprisingly high sensitivity CRP increased quite a lot (despite the reduction in glucose and insulin levels) and the authors comment on this saying “We suppose, that living in the wild stimulates the innate immune system as shown by Qing [52] and Park [53] via activation of proinflammatory pathways in order to anticipate evolutionary old danger signals such as bacteria, viruses, insects or predators.”  That makes sense and the high level of exercise may have also contributed