Save Authors Time

This is a good suggestion, abstract:

Scientific journals ask authors to put their manuscripts, at the submission stage, sometimes in a complex style and a specific pagination format that are time consuming while it is unclear yet that the submitted manuscripts will be accepted. In the case of rejections, authors need to submit to another journal most likely with a different style and formatting that require additional work and time. To save authors' time, publishers should allow authors to submit their manuscripts in any format and to comply with the style required by the targeted journal only in revised versions, but not at the submission step when the manuscripts are not yet approved for publication.

What relevance does this have for the typical person who wants to improve their health?  Well, anything that facilitates the spread of biomedical knowledge is a good thin, anything that hampers that spread is bad.  Journal requirements, as discussed here, are one impediment.  Other times, reviewers nitpick on minor points or let personal biases get in the way of a fair review of important material, and so knowledge of potential use to public health remains unpublished - or the publication is delayed.

Synthetic Oxytocin And Postpartum Emotional Problems

Oxytocin is used to facilitate childbirth and is important for social bonding.  The latter role suggests that synthetic oxytocin would decrease postpartum depression or anxiety, but the opposite seems to be the case, conclusions from abstract:

CONCLUSIONS:Contrary to our hypothesis, results indicate that women with peripartum exposure to synthetic oxytocin had a higher relative risk of receiving a documented depressive or anxiety disorder diagnosis or antidepressant/anxiolytic prescription within the first year postpartum than women without synthetic oxytocin exposure.

There may be many variables involved here, but perhaps – and this is my hypothesis – excess oxytocin above and beyond natural levels causes a negative feedback with respect to its emotional effects?

In any case, this is how science is done, you make a hypothesis and test it.  The authors noted that their hypothesis was wrong, enabling the field to move forward. That’s how it is properly done.

A Potential Problem With The Popularization Of Science

Popularization of science is important, but like a double-edged sword, can have certain drawbacks. Here is an interesting paper, abstract:

Science popularization fulfills the important task of making scientific knowledge understandable and accessible for the lay public. However, the simplification of information required to achieve this accessibility may lead to the risk of audiences relying overly strongly on their own epistemic capabilities when making judgments about scientific claims. Moreover, they may underestimate how the division of cognitive labor makes them dependent on experts. This article reports an empirical study demonstrating that this "easiness effect of science popularization" occurs when laypeople read authentic popularized science depictions. After reading popularized articles addressed to a lay audience, laypeople agreed more with the knowledge claims they contained and were more confident in their claim judgments than after reading articles addressed to expert audiences. Implications for communicating scientific knowledge to the general public are discussed.

I believe that people who do not have a science background tend to underestimate the complexity of science, the high degree of “division of cognitive labor” in science (an expert on one field may know little to nothing about another field), and they also misunderstand the basic idea behind modern science.  On this latter point, science is not really about making final and definitive statements, but rather assigning probabilities to hypothesis based on the available evidence. Therefore, people take a single pronouncement as “the final word” and then get frustrated, or disillusioned with science, when that “final word” is later over-turned by a subsequent “final word.”  Popular writers of science also get facts wring, based in their overestimation of their own understanding of the topic, and pass on these misunderstandings to the public. One hope is that blogs like ApplyForLife will enable people with formal scientific training to directly communicate useful findings directly to the public, with the constant caveat that almost nothing in science is “final” – a point that often eludes the popular writers in scientific topics.

A Scientific Complaint

As an academic scientific researcher, I have to admit that it is highly annoying when other researchers publish on a topic as if they were the first to discover something and, do not cite your work that had discovered the exact same thing years before.  In fact, in some cases, not only have you published your findings, and then published follow-up extensions of it, but also have published review articles on that discovery and its implications in the field.  And despite all of that, easily accessible on PubMed or easily found in a Google search, others will, many years later, repeat the work and claim it as their own.  That is not only a form of plagiarism, but a waste of time and resources, and further shows the low quality of the editors and, especially the reviewers of that new article who haven’t bothered to look at whether the “new” work had already been done long ago.  

Certainly, there is a place for reproducibility and confirming results, but not presented as a novel discovery, nor published as such.

These things happen more often than you would think; it has happened to me several times already.

Fat Mice Get Bigger Tumors

It is well known that obesity increases the risk for various forms of cancer.  A National Cancer Institute fact sheet on the obesity-cancer link provides useful information on this topic, as does another information source from Cancer Research UK.

Mouse models of human cancer are often used to investigate the mechanisms of the human disease. A recent paper in the journal Oncotarget (free online) demonstrates that even in mice, obesity due to a high fat diet increases the development of cancer, in this case, colon cancer.  Thus, colon cancer cells injected into the mice resulted in larger tumors when the mice were fed a high fat diet.  The abstract of the paper is as follows:

There are an increasing number of reports on obesity being a key risk factor for the development of colon cancer. Our goal in this study was to explore the metabolic networks and molecular signaling pathways linking obesity, adipose tissue and colon cancer. Using in-vivo experiments, we found that mice fed a high-fat diet (HFD) and injected with MC38 colon cancer cells develop significantly larger tumors than their counterparts fed a control diet. In ex-vivo experiments, MC38 and CT26 colon cancer cells exposed to conditioned media (CM) from the adipose tissue of HFD-fed mice demonstrated significantly lower oxygen consumption rate as well as lower maximal oxygen consumption rate after carbonyl cyanide-4-trifluoromethoxy-phenylhydrazone treatment. In addition, in-vitro assays showed downregulated expression of mitochondrial genes in colon cancer cells exposed to CM prepared from the visceral fat of HFD-fed mice or to leptin. Interestingly, leptin levels detected in the media of adipose tissue explants co-cultured with MC38 cancer cells were higher than in adipose tissue explants cultures, indicating cross talk between the adipose tissue and the cancer cells. Salient findings of the present study demonstrate that this crosstalk is mediated at least partially by the JNK/STAT3-signaling pathway.

Mitochondria are the “powerhouse of the cell,” responsible for generating most of the ATP that provides the “chemical energy” the cells require, and mitochondria are involved in other important processes, such as programmed cell death. This paper shows that diet-derived obesity causes the mitochondria to malfunction and this contributes to increased tumor formation.  An important cell signaling pathway called JNK/STA3 is apparently involved in the association between obesity and cancer in these over-fed mice. The authors conclude:

We conclude from this study that (i) obesity induces mitochondrial dysfunction, promoting cancer in several organs adjacent to the visceral fat, such as the colon, and (ii) inhibition of the JNK/STAT3-signaling pathway in colon cancer cells seems to be critical for reestablishing mitochondrial function and overcoming the glycolytic phenotype. We assume that this signaling pathway may be partly responsible for the relation between obesity–leptin-induced mitochondrial dysfunction and colon cancer.

What does this mean for the typical person, who may not be familiar with all the scientific jargon used? This paper is yet more evidence of the serious damage done to the organism by diet-induced obesity, damaging the mitochondria and affecting signaling in many cells, and these negative effects contribute to cancer development. What is happening in these mice likely occurs in people as well. Losing weight to transition to a more normal BMI – and optimally, never becoming obese to begin with – must rank as one of the most important things you can do for your health. And of course, the benefits are not only restricted to cancer, but to cardiovascular diseases, metabolic diseases (e.g., diabetes), and much more.

The mice in this study didn’t have a choice about their obesity, they do not have the capacity to understand the diet they were given, and the effects that diet had on their bodies. We in contrast do understand and do have a choice, and we need to choose wisely.

More Excuses for Obesity?

There is an ongoing debate about the causes of the obesity epidemic. A recent academic study, described here, reported the following:

A given person, in 2006, eating the same amount of calories, taking in the same quantities of macronutrients like protein and fat, and exercising the same amount as a person of the same age did in 1988 would have a BMI about 2.3 points higher. In other words, people today are about 10 percent heavier than people were in the 1980s, even if they follow the exact same diet and exercise plans.

What may be cause of this observation (assuming it is valid)? We read:

In an interview, Kuk proffered three different factors that might be making harder for adults today to stay thin. 

First, people are exposed to more chemicals, some of which might be weight-gain inducing. Pesticides, flame retardants, and the substances in food packaging might all be altering our hormonal processes and tweaking the way our bodies put on and maintain weight.

Second, the use of prescription drugs has risen dramatically since the ‘70s and ‘80s. Prozac, the first blockbuster SSRI, came out in 1988. Antidepressants are now one of the most commonly prescribed drugs in the U.S., and many of them have been linked to weight gain. 

Finally, Kuk and the other study authors think that the microbiomes of Americans might have somehow changed between the 1980s and now. It’s well known that some types of gut bacteria make a person more prone to weight gain and obesity. Americans are eating more meat than they were a few decades ago, and many animal products are treated with hormones and antibiotics in order to promote growth. All that meat might be changing gut bacteria in ways that are subtle, at first, but add up over time. Dr. Kuk believes the proliferation of artificial sweeteners could also play a role.

Let’s consider these hypotheses (which may or may not eventually be supported by future data).

Diet affects the microbiome; in the article, meat is mentioned.  Other studies, including those in “humanized” mice, have shown that only one day on a “junk food diet” can alter the microbiome, the bacterial colonizing our gut.  Studies in human volunteers have shown the same.  These changes seem to be reversible. Diet is something that we have control over; we can eat less meat, and a healthier and higher-fiber diet enriched in while grains, fruits, and vegetables. Artificial sweeteners can be avoided. Other dietary factors linked to obesity, such as high fructose corn syrup or sugary sodas should be eliminated.

The researchers notes that the use of certain prescription drugs that have weight-gain as a side-effect has “risen dramatically.”  Although some people no doubt require such medications, the sharp increase in antidepressant use suggests the possibility that perhaps they are being over-prescribed and are not always necessary. This is another modifiable risk factor at both the individual and societal level.

Chemical exposure is a factor, one that can be avoided to the extent possible, although their ubiquity makes that difficult.  However, that same ubiquity suggests to us to look closely at the fact that while most Americans are sharing these same exposures, not all are obese/overweight.

What about other hypotheses and/or variables that can be controlled for? Was muscle-fat composition controlled for? If people today have, for original lifestyle reasons, more fat and less muscle than those in past generations, then this would account for less “burning” of calories, since muscle is more metabolically active than fat. So, it is possible people become overweight, with a higher body fat percentage, due to modifiable lifestyle changes, and then find that this change in body composition makes losing weight more difficult. There is the “cause vs. effect” issue here; one bottom line is prevention – it is better not to become overweight to start with, since losing weight will become much more difficult.

There’s an underlying problem with how this study is being presented, which mirrors how “fat gene” studies are also presented: the idea that things are beyond our control, no one is at fault, and we must be accepting of the obesity epidemic.  But, as stated, even if the abovementioned hypotheses are correct, many are modifiable, and it is imperative that these modifications be attempted.

After all, the problem can be looked at academically from another perspective: compare individuals from the same age group, contrasting those of normal weight to those overweight and obese. Let us compare their diet and activity level.  One hypothesis: those of normal weight will have healthier diets, and more activity, than those overweight and obese.

The problem exists and must be dealt with. Eat properly (including less [red] meat and artificial sweeteners. Do not take mind-altering medication unless it is truly necessary. Be more active. Avoid to the extent possible environmental stressors that promote obesity. We need to work together to eliminate as many of those stressors as possible. Do not accept an epidemic destroying the health of individuals and a society.