In class, we talked about obesity and the multiple mechanisms of causation and how both genotype and phenotype influence the development of metabolism and progression to obesity. Essentially, there’s a full gambit of biologically tested influences when it comes to obesity. In addition to the complex physiological components, obesity is so heavily saturated with social expectations, cultural meaning and structural impacts. When discussing the option of classifying obesity as a disease, we primarily focused on the ideological and medical consequences – How is a disease defined? What are the required components of a disease? How would such a decision affect the “treatment” of obesity? How would it affect health insurance and payment?
An aspect we didn’t really discuss was the effect of such a classification on the public. Other questions we could have asked include: How would someone react to obesity if it’s a disease? What does that mean for healthy lifestyle choices? What does that mean for preventive care initiatives? If it’s a disease, is there a cure? What is the cure? A NYT article and journal bulletin discuss the psychological impact of classifying obesity as a disease.
“Specifically, obese participants who read the ‘obesity is a disease’ article placed less importance on health-focused dieting and reported less concern for weight relative to obese participants who read the other two articles. They also chose higher-calorie options when asked to pick a sandwich from a provided menu. Interestingly, these participants reported greater body satisfaction, which, in turn, also predicted higher-calorie food choices. ‘Together, these findings suggest that the messages individuals hear about the nature of obesity have self-regulatory consequences,’ says Hoyt,” (APS, 2014).
Over the last couple of weeks, we’ve been discussing the importance of an evolutionary understanding of medicine, health and disease, and we often talk about the advantages of comprehending the ultimate explanations of fever, malaria and more. But at the same time, we also consistently ask what this information means to the average patient. Does an individual need to understand the complex relationship between melanin, sun exposure, and vitamin D when getting diagnosed with skin cancer? Does an individual need to know the thrifty phenotype hypothesis to better understand his or her obese state? Does providing an evolutionary reasoning for the condition make the suffering more bearable? Does it change the individual’s perception and though process when it comes to treatment and lifestyle choices? The above cited articles demonstrate a very possible disadvantage to the classification of obesity as a disease. We have to ask ourselves: how much does a person need to understand and what are the associated advantages and disadvantages to that understanding?
Link to TED Talk:
This TED Talk is particularly relevant to our Tuesday discussion regarding the accuracy and safety of using animal models to predict the effect(s) of a drug in humans. In this TED Talk, Dr. Geraldine Hamilton introduces a new model called Organs On A Chip. The chip recreates the basic functional units of an organ as well as the biochemical, functional, and mechanical environment normally experienced by the cells/organs in the body. For example, a recreated lung, in a nutshell, consist of a porous membrane, two fluidic channels (for blood and air flow), capillary cells, and lung cells. Additionally, the porous membrane of the lung is contracted and relaxed to mimic the mechanical strains that the lung cells experience during ventilation. To test various conditions – chemicals, bacteria, immune cells, viruses, etc can be added to the fluidic channels to monitor their interactions with the cells and one another. For example, to mimic a lung infection, bacterial cells were added to the air channel and immune cells were added to the blood channel; intriguingly, the immune cells crossed the porous membrane and phagocytosed the bacterial cells. Lastly, because Hamilton’s group has successfully recreated the liver, gut, heart, and bone marrow, these chips can be connected with fluid channels to further study the interaction of drugs/chemicals in the “Human on a Chip.”
I think Dr. Hamilton’s TED Talk is incredibly fascinating as it offers a novel, safe, and accurate model for testing drug interactions in the human body. Additionally, I believe this technology essentially carves the pathway for personalized medicine and pharmacogenomics as cells from specific individuals, populations, and age groups can be used to recreate organs. Furthermore, this model shows vast potential for studying the complex biochemical interactions between drugs and other chemicals/cells as a number of substances/cell types can be added to the fluid membranes to mimic an in vivo environment. Lastly, by simulating some of the complexities of a human body, the human on a chip shows potential for bypassing the unethical use of animal models.
I remember in one of our class discussions, lactose intolerance came up and I thought that a change in the lactase (the enzyme that breaks down lactose or milk sugar) gene made it possible for expression after weaning. This meant that individuals could digest milk and other dairy products and supplement their diet with other sources of calcium and vitamin D. To me, that seemed a completely sufficient explanation for why the new allele for lactase was selected as advantageous. After all, we’re all told to drink milk to build strong bones, so why wouldn’t the same apply to early shepherds. This explanation is known as the “Calcium Assimilation Hypothesis.”
We need vitamin D to absorb calcium. That vitamin D can come from one’s diet or come from sunlight. So in geographic regions of less sunlight, there is a greater need for a diet containing vitamin D than say in equatorial regions. In other words, the Calcium Assimilation Hypothesis really only holds for northern European populations.
From here on out, I think it’s important to consider lactose intolerance as more than the digestion of milk, or more specifically lactose, but as an evolutionary culmination of culture, geography, and sunlight.
This article in the New York Times talks about how dust mites are proof that evolution does not always move forward but can actually regress. A study in the University of Michigan found that the phylogenetic tree of dust mites shows that dust mites themselves are free-living organisms, and they evolved from parasites, and parasites evolved from free-living organisms. This article stood out to me because it reminded me of our discussion in class that covered how no one organism is the “most advanced,” but rather all organisms have evolved to be best fit to their particular environments. Understanding that concept, I would suppose that a long time ago free living organisms were no longer a good fit for a certain environment and so after a long period, parasitic organisms evolved by natural selection. Then, in another environment, being a parasitic organism was no longer favorable and being free-living was a better fit, and so natural selection created the free-living dust mite. Natural selection selects for organisms to fit their environments, there is no goal of creating the ultimate, perfect organism. If becoming a better fit for the environment means the return of a trait of an ancestral organism, the fact that the trait was previously discarded is irrelevant; that trait is now a good fit again.
To tie this in with medicine, the article concludes by saying that discovering the free-living nature of dust mites gives a new genetic insight into these organisms that will help scientists to understand how people with dust allergies react to dust mites, possibly leading to the production of a better allergy medication. If only there could also be some medical advancement in spring allergies too; it’s almost that time of year. Makes you wonder why evolution has not eliminated allergies in general: dust or pollen based.
The article’s link is below:
Many found it interesting that the prevalence of H. pylori infections did not correlate with cancer incidence. In a study of two Colombian populations, a coastal population of African ancestry had a low incidence of gastric cancer compared to a population of largely Amerindian descent in the Andes Mountains. By studying the tissue samples of patients from these populations, molecular biologists and researchers found out that the H. pylori strain affecting those in the coastal region were of African descent, while the H. pylori strain affecting the Amerindian human population were of south European descent. The results demonstrated that a “shared evolutionary history of humans and bacteria resulted in a less virulent host-pathogen relationship.”
“[It’s] fascinating,” said El-Omar. “If you have African strains affecting African-ancestry hosts, it doesn’t cause too much damage, whereas if you’ve got African-origins strains infecting Amerindians up in the mountains, that’s when you get most precancerous changes. So it looks like if you’ve coevolved with your strains, you get less and less virulence.”
This article didn’t go into too much detail about the evolutionary mechanisms so I did some more research on this host-pathogen coevolution. I found out that one explanation for why one population is more affected by diseases is tolerance evolution. The evolution of tolerance results in a changed selection on parasite populations, which can lead to parasite evolution despite the fact that tolerance is not directly antagonistic to parasite fitness. The evolution of tolerance is like our attempts of vaccination in order to decrease the prevalence of disease, without reducing parasite densities or eradicating the infection. These vaccinations can select for more pathogenic viruses, creating a greater risk for those unvaccinated who come into contact with these pathogens. Tolerant individuals also select for parasites with greater virulence, causing a more devastating effect on those intolerant who become exposed to the disease.
Link to article: http://www.the-scientist.com/?articles.view/articleNo/38845/title/Human-Pathogen-Coevolution/
Cancer is more common in older people than the young, and there is by no means agreement on why this is true. Antagonistic pleiotropy has been proposed as the genetic mechanism underlying life-history trade-offs. Dr. Sharpless studies the process of aging and its relationship to cancer and degenerative diseases. This is a video of an interview in which I think he does a good job to explaining his research – both in mice and in humans. It’s long, but gives a good example of both scientific hypothesis testing and a bit of the history of this field.