A study appearing in the journal Nutrition and Diabetes suggests that pasta may actually lower your BMI. Can that actually be right? A detailed look at the data, and how it relates to Simpson's paradox inside. For the video version of this post, click here.Read More
Tuna, shark, king mackerel, tilefish, swordfish. If you’ve ever been pregnant, or known someone who has been pregnant, this list of seemingly random aquatic vertebrates is all too familiar to you. It’s the “avoid while pregnant” list of seafoods, and it’s just one of the confusing set of messages surrounding pregnancy and fish consumption.
(For the video version of this post, click here).
Because aren’t we supposed to be eating more fish? Fish are the main dietary source for omega-3 fatty acids, which can cross the placenta, and may promote healthy brain development. Of course, some of these fish contain mercury which, as Jeremy Piven taught us all, may be detrimental to cognitive development.
These contradictory facts led the US FDA, in 2014, to recommend that pregnant women consume more fish, but not more than 3 times a week. You have to love the government sometimes.
A study appearing in JAMA pediatrics is making some waves with its claim that high levels of fish consumption, more than 3 times per week during pregnancy, is associated with more rapid neonatal growth as well as higher BMIs throughout a child’s young life. Now, contrary to what your mother-in-law has been telling you, more rapid infant growth is not necessarily a good thing, as rapid infant growth is associated with overweight and obesity in childhood and adulthood.
But fish as the culprit here? That strikes me as a bit odd. Indeed, prior studies of antenatal fish consumption have shown beneficial or null effects on childhood weight gain. What is going on here?
The authors combined data from 15 pregnancy cohort studies across Europe and the US, leading to a final dataset including over 25,000 individuals. This is the studies greatest strength, but also its Achilles heel, as we’ll see in a moment.
But first the basic results. Fish consumption was based on a food frequency questionnaire, a survey instrument that I, and others, have a lot of concerns about. Women who reported eating less than or equal to 3 servings of fish a week had no increased risk of rapid infant growth or overweight kids. But among those eating more than 3 servings, there was around a 22% increased risk of rapid growth from birth to 2 and overweight at age 6.
These effects were pretty small, and, more importantly, ephemeral. The authors looked not only at the percentage of obese and overweight children, but the raw differences in weight. At 6 years, though the percent of overweight and obese kids was statistically higher, there was no significant weight difference between children of mothers who ate a lot of fish and those who didn’t. When statistics are weird like this, it usually suggests that the effect isn’t very robust.
In fact, this line from the stats section caught my eye, take a look:
That means the authors used numbers predicted by a statistical model to get the weight of the children rather than the actual weight of the children. I asked the study’s lead author, Dr. Leda Chatzi, about this unusual approach and she wrote “Not all cohorts had available data on child measurement at the specific time points of interest… in an effort to increase sample size and…power in our analyses, we…estimated predicted values of weight and height”.
So we have a statistical model that contains as a covariate, another statistical model. This compounds error into the final estimate, and in a study like this, where the effect size is razor thin, that can easily bias you into the realm of significance.
And, at this point it probably goes without saying, but studies looking at diet are always confounded. Always. While the authors adjusted for some things like maternal age, education, smoking, BMI and birth weight, there was no adjustment for things like socio-economic status, sunlight exposure, diabetes, race, or other dietary intake.
What have we learned? Certainly not, as the authors suggest, that
That they wrote this in a study with no measurement of said pollutants is what we call a reach.
Look, you probably don’t want to be eating fish with high levels of mercury when you are pregnant. But if my patients were choosing between a nice bit of salmon and a cheeseburger, well, this study doesn’t exactly tip the scales.
For the video version of this post, click here.
Coffee. Its hard not to be biased when it comes to the ubiquitous drink. Many of us, myself included, depend on the stuff to start our day, continue our day, and give us something to do when we should otherwise be working. Studies linking coffee to better health get a lot of press. A few months ago, a big splash was made when a study linked coffee consumption to lower risk of melanoma (though they failed to account for sun exposure). Now, we have coffee staving off colon cancer.
The paper, appearing in the Journal of Clinical Oncology, examined roughly 1000 individuals with stage 3 colon cancer, who had been through at least the first round of surgery and chemotherapy. Each of them filled out a detailed food-frequency questionnaire within a couple months after the initial treatment, and they were followed prospectively for cancer recurrence or death.
The majority of the cohort reported drinking 1-3 cups of coffee per day. A small number, 6%, reported taking more than 4 cups per day. Heavy coffee drinkers were more likely to be male, white, and smokers, and had a higher level of physical activity.
After around 7 years of follow-up, 35% of the patients had experienced cancer recurrence or died. Among those who drank 4 or more cups of caffeinated coffee per day, the overall risk of recurrence or death was reduced by about 50% after adjustment for confounders.
Let that sink in a minute. 50%. Has one of the most potent anti-cancer agents been literally sitting under our nose all these years? Well, as much as Im a java fan, I might need to cool this off a bit.
First off, these patients were part of a clinical trial evaluating the role of adding irinotecan to standard adjuvant chemotherapy for colon cancer. Clinical trials recruit very specific patients - these results may not hold for your typical colon cancer survivor.
Another issue: Food frequency questionnaires generate a ton of data - you can't possibly control for everything people eat. The authors adjusted their results for total caloric consumption, but it is possible that foods that correlate with coffee intake are the actual drivers of the relationship here. Put simply, it's just as likely that this is a biscotti effect as a coffee effect.
Finally, the big issue: What do we mean when we say coffee? Is an espresso the same as a venti caramel macchiato? Does it matter where the beans come from? How they are roasted? How much sugar you add to it? This is the central problem of dietary research, and one that can only be overcome by randomized trials.
So lets do it. There seems to be enough data now to justify actually trying this under controlled settings. My prediction is that we wont see a 50% reduction in recurrence of colon cancer, but we may see something. After all, coffee is a drug. A wonderful, tasty, necessary drug that goes great with pie.
For the video version of this post, click here. What diet do you ascribe to? If you answered I have no idea what you mean, then you can join the rest of the 80% of Americans who dont follow a specified diet regime. Sure, lots of us try to avoid fat, or sugar, or meat, but when it comes to defining the health benefits of a particular dietary pattern, its hard to label people.
Before we get our pitchforks and charge over to Paula Deens house, lets take a minute to look how this study was done. The data comes from the REGARDS study, which was a large cohort study primarily designed to look at stroke risk factors. About half of the REGARDS cohort, 15,000 people, were eligible for this analysis and provided dietary data in the form of a food frequency questionnaire.
Whats cool about this study is that they derived the dietary patterns without any preconceived notions. Using a technique called factor analysis, they let the data speak for itself, and find which foods tend to hang together in the diets of individuals. Five major patterns emerged: the Southern diet (which is the focus of the study) was characterized by fried foods, eggs, organ meats, and sugar-sweetened beverages. Other dietary patterns included a plant-based pattern, a convenience food pattern, a sweets pattern and, my favorite, an alcohol and salad" pattern.
What I like about this study is that it doesnt force individuals into a specific category. The analysis allows your dietary pattern to be part Southern, part plant-based, for example. So were not in the situation of trying to label each person with one, and only one, diet.
After follow-up of around 6 years, greater adherence to the Southern diet increased the risk of incident coronary heart disease by around 35%. To stop one heart attack per year, youd need to convert roughly 1200 fried-organ meat gourmands to a healthier option, but that assumes there were no confounders at play. Clearly there were, as the southern dietary pattern was associated with male sex, black race, lower income, and diabetes. The authors adjusted for these factors, but its likely that other socio-economic factors including access to health care may play a significant role here.
In unfortunate news, the Alcohol and Salads dietary pattern, which describes my eating habits pretty darn well, had no relationship to heart disease in either direction. This may hurt sales of my upcoming diet book Alcohol and Salads: 20 blurry days to a better you.
The analysis doesnt allow for too much subtlety - describing anyones dietary habits using 5 criteria is limiting. In addition, the lack of signal in the sweets dietary pattern runs counter to a lot of prior research linking high processed carbohydrate consumption to heart disease. That said, I for one, am going to forgo that second helping of chicken-fried steak tonight.
For the video version of this article, click here.
Browsing through article titles this week, my eye caught one from the Journal of Clinical Oncology with the words melanoma and citrus fruit. Not worth looking at I thought, clearly a study linking citrus intake with melanoma is hopelessly confounded. People who eat citrus fruits are probably healthier in general, have better access to care, etc - clearly theyll have lower melanoma rates.
But then I read the abstract, and, go figure - people consuming more citrus fruits had higher rates of melanoma. This was worth a deeper dive.
The background here is that all citrus fruits contain compounds called psoralens. Psoralens are photo-reactive chemicals and, in pharmacologic doses, are used to sensitize the skin to UVA radiation in the treatment of psoriasis, for example. When exposed to UV light, these compounds can intercalate into DNA, causing mutations, so there might be some biologic plausibility here.
That said, the dose you take as part of PUVA therapy is the equivalent to what youd find in about 10,000 liters of grapefruit juice
But lets push on. Here are the details:
Harvard researchers used two large, prospective databases: the Nurses Health Study and the Health Professionals follow-up study. Combined, these studies comprised about 170,000 people, but after applying various exclusion criteria (including excluding anyone who wasnt white), they had around 105,000 individuals to study. After a whopping 25 years of follow-up there were about 2000 cases of melanoma. They correlated answers from a food frequency questionnaire with subsequent melanoma incidence. Bottom line? A dose-response relationship, with the highest category of citrus eaters (>1.6 times per day) having a roughly 50% increase in the rate of melanoma.
Surprisingly, the annual UV exposure and number of sunburns werent different among the citrus consumption groups - so were not seeing a Florida effect here.
The authors strengthened their findings by looking at the association of other fruits and fruit juices to melanoma (none found), and looking at the association between citrus fruits and other types of cancer (none found), but there were still a couple of odd findings.
When they broke down the citrus fruits, they found that grapefruit, but not grapefruit juice, was associated with melanoma. Conversely, orange juice, but not oranges, were associated with melanoma. They argue that orange intake in its non-juice form was so rare that they didnt have power to detect a link, but we dont get numbers to support that, and frankly, Id be surprised if grapefruits are getting eaten more than oranges in this country.
Now, if you want to throw out a study, you can always argue (as many have) that food frequency questionnaires are terrible instruments. But even taking the study at its face-value, let me give you some data the authors dont include directly. The incidence of melanoma in this study was 7 cases per 10,000 individuals per year. To prevent one of those cases, youd need to convince around 2500 people who eat a lot of citrus to stop, whereas youd only need to convince 140 people to wear sunscreen. My advice? Keep your grapefruit juice, and wear a hat.
For the video version of this post, click here.
Weve talked a lot about diet studies here on 150 Seconds. I like to complain about them because most are observational. People who eat healthy diets are healthier. Randomized trials are better, but unless youre preparing every meal for the participant, you can never be 100% sure what they are getting.
Today were talking about a randomized diet trial that takes a somewhat unique approach to the issue. In fact, I think the methodology in this study is more interesting than the results. In an article appearing in JAMA internal medicine, a group of Spanish researchers report on the relationship between a Mediterranean style diet and cognition in a group of around 450 individuals at higher risk of cardiovascular disease.
Mediterranean diets are characterized by fresh fruits and vegetables, fish, nuts, and olive oil. Micronutrient-wise, were basically talking about higher amounts of mono- and polyunsaturated fats, which, in the lab at least, seem to have antioxidant and anti-inflammatory properties. In terms of cognitive decline, which may be partly a vascular process, tamping down these things could be beneficial.
There were 3 groups in the study. A control low-fat diet group, and two Mediterranean diet groups: 1 supplemented with nuts, one with olive oil. Heres where it got interesting. The participants cooked all their own food - basically, the intervention was just some education and a weekly food gift of either 1 liter of olive oil or 1 cup of nuts.
Despite the lack of rigorous dietary control, the intervention groups did change their eating habits. Caloric intake didnt change much, but carbohydrate intake went down and polyunsaturated fat intake went up in both mediterranean diet groups compared to the controls.
As for the primary results? I wouldn't call them sizzling. Cognitive function declined a bit more in the control group than either of the Mediterranean diet groups, but changes were mild overall.
The trial itself had a few blemishes. One is that, at first, the control group wasnt treated very similarly to the intervention groups. Controls had fewer visits, and didnt get weekly gifts from the study. This was remedied about halfway through the trial, but some damage had probably been done and its conceivable that controls who didnt feel as invested in the study wouldnt have performed as well on cognitive testing.
The second issue is a somewhat high dropout rate, around 25%, that was differential among the groups. Neither of these are killer, but when you combine a couple of flaws like this with relatively mild results overall, youre left wondering what to take home from this?
For me, its not the primary results. Im just impressed that the simple act of giving people healthy food, giving people olive oil, changed their eating habits. Thats pretty slick if you ask me.
An article appearing in JAMA internal medicine looked at around 100,000 Seventh-day adventists, and found that ht risk of colorectal cancer was significantly reduced among those who ate a vegetarian diet. But beware of large studies, folks - this statistically significant result isn't terribly clinically meaningful. You'd have to change 5300 people into vegetarians to prevent one case of colon cancer per year. Interestingly, you'd only need to convert 3000 people to Seventh-day Adventism to get the same benefit.
See my video on medpagetoday.com: