Good morning everyone,
Last week I sent you a news report about the prospect of "sugar taxes", extra monetary tax levied against sweetened drinks as a way to reduce their consumption and to (hopefully) induce some improved health in the persons who might normally consume too much sugar in their diets.
The article that I sent you last week considered some of the potential benefits, and potential difficulties, of implementing such taxes. It also described the limited amount of data available thus far, suggesting that it is still too early to know whether these kinds of taxes lead to health improvements.
In this news this week is report of a newly-released study on this very topic. Here, researchers followed the health of a focal group of 200+ people at the University of California-San Fransisco medical school, where a full ban on the sale of sweetened drinks has been in effect. Researchers report improvements in several subject health measures, including reduced waist size, less belly fat, and improved response to insulin. They suggest that these changes were directly a function of reduced sugary drink consumption in these subjects.
Note that this study described subjects under a workplace ban on the sale of sweetened drinks, not those under a "sugar tax". Here, subjects could purchases sweetened drinks elsewhere, or bring them from home, but could not purchase them at their workplace. This is likely to have a larger effect on consumption than a sugar tax itself, but it does suggest that the benefits of lowering the consumption of sweetened drinks is a very worthwhile goal. The available data suggests that most of us consume too much refined sugar (in some form), which suggests that most of us would benefit by reducing our sugar intake. As we have seen many times during the term, our health depends heavily on the choices we make.
Hope that you are enjoying the weekend - see you tomorrow.
Good evening all,
As I noted in lecture on Wednesday, we remain on-schedule with out lecture chapters, and do not have a chapter scheduled for tomorrow (Friday 25 Oct). So, I would like once again to propose that we do not meet in person for lecture tomorrow, and ask instead that you consider the reading that I am forwarding here.
In our last lecture on the endocrine system, we noted the central role of the pancreas and its hormones in the regulation of blood glucose ("blood sugar") levels. When levels of blood glucose rise (such as when we are absorbing digested sugars into our bloodstream after a meal), the hormone insulin is released by the pancreas. Insulin causes our cells (especially liver and muscle cells) to uptake glucose - that is, to take glucose out of the bloodstream and move it into cells by means of membrane transporters. This allows cells to have glucose available for fuel, and also allows cells to store the excess glucose for later use.
On the flip side, when our blood glucose levels decline (such as when we are several hours past a meal and done absorbing nutrients), other cells in the pancreas release the hormone glucagon, which causes our cells (especially liver and muscle cells) to release some of their stored glucose. Together, the use of the two hormones allows us to maintain a relatively even profile of blood glucose levels.
As we discussed yesterday, when blood sugar levels are not well-controlled, diabetes may result. The primary symptom of diabetes is high (and poorly controlled) blood glucose levels. This causes a number of immediate effects, such as excess urination, thirst, and excessive fat metabolism. Over the long term, high levels of blood glucose are very damaging to our tissues, particularly through scarring of the inner lining of our blood vessels. This can lead to the failure of organs with extensive capillary beds (such as the retina of the eye, and the kidney), and has negative effects on circulation in general, especially in the lower periphery. Persons with uncontrolled blood sugar often suffer poor wound healing (especially of the feet), which can lead to infections and, in some cases, require amputation.
In lecture, we distinguished the two general types of diabetes as well. "Type I" diabetes occurs when our own immune system causes the destruction of the insulin-producing cells of the pancreas. This is classified as an auto-immune disorder, as the disease stems from a problem with the immune system. Type I diabetes is often called "juvenile diabetes", because it is typically first diagnosed in one's youth. It can be treated (usually successfully) with injections of insulin - daily, often multiple times. Insulin pumps can also be used - these are small, battery powered pumps that infuse gradual, small amounts of insulin into a catheter. They are expensive and require maintenance, but are effective solutions for many.
"Type II", or "adult onset diabetes" is more challenging. It tends to appear in people with a combination of risk factors: obesity, poor diet, little exercise. Over time, the cells of their body gradually become resistant to insulin, and stop responding to it. Their pancreas produces normal amounts of insulin, but it is ineffective - blood glucose remains elevated, cells become starved for sugar fuels, and metabolize other fuels (mostly fats). Tissue damage accumulates because of the persistently elevated blood glucose levels. Additional insulin (injections) can help somewhat, but the most effective treatment is improvements in diet and exercise. Some people can almost completely reverse their condition through these lifestyle changes, and nearly everyone can benefit at least somewhat from them.
There is a lot of biology associated with diabetes: its causes, effects, and treatments. There also is a lot of sociology to it as well. Diabetes strikes populations very unevenly, and impacts populations of relatively poorer socioeconomic levels most severely. This is believed to be due to a number of factors, including reduced access to high-quality food, more-restrictive employment and familial responsibilities that limit time to exercise, and less access to good information about health. It has also been suggested that food corporations specifically target these populations with advertising and vendors for "fast food", including soft drinks ("soda", or "pop", depending upon where you were raised).
As a food, soda is of very low quality. It is mostly water, but the other primary ingredients are sugar, and often caffeine. It is also quite acidic, and has quite damaging effects on our teeth. So, why do we buy/drink it? We do so at least in part of because of very successful, and very prominent, advertising, which has allowed some soda companies to develop enough clout that they can contractually deliver soda to schools, hospitals, corporations, and even cities.
Think back to your middle- and high-school education: did soda vending machines exist in your school? Were fountain drinks available over the counter in the cafeteria? For most of us, the answer to these questions is "yes". Do you buy bulk quantities of soda? Do you see others around you who do? Again, for most of us, the answers here are "yes" as well.
In recent years, public health experts have recognized the dangers of over-consumption of soda, and more importantly, the danger of exposure to it in our youth. Too often, adolescents develop a "soda habit", and maintain it into adulthood. This, in combination with other lifestyle choices, has led to skyrocketing rates of juvenile obesity. Even more alarming, "adult onset" diabetes is now diagnosed in adolescents at alarming rates.
So what can be done? Well, the debate rages, because to eliminate soda from communities and diets is not really an option. Soda companies are large, and powerful, and they have an avid user base that wants their products. This is a situation similar to that faced years ago with the tobacco industry: large and powerful corporations, well-paid lobbies, a desirous user base, and mounting evidence of the dangerous health effects of the product. Here, too, numerous solutions were discussed and tried. One of the remedies that seemed to be most effective was to implement larger and larger taxes on tobacco, to the point at which fewer people were willing, or able, to financially support their tobacco habit.
Because of the success of this strategy to reduce tobacco usage, we now live in an era of the "soda tax". The idea here is the same: if a popular consumer product is legal, but unhealthy, tax it in order to reduce the number of people using it, and/or the amounts that they use. This remains a controversial idea. Why should companies producing a legal, desirable product be punished? Is this ethical? Does this not also punish the people that work for them, and their suppliers, accountants, and all of the other people who work in associated jobs? Does this also punish consumers of relatively lower income unfairly, because they would be the ones least likely to be able to afford a price increase?
With soda, too, the application of a tax is more complicated. Tobacco and alcohol are relatively uniform in how they are packaged and purchased, but sugary drinks exist across the spectrum (from soda, to sweetened milk, to orange juice and yogurt). Wait -- aren't milk, orange juice, and yogurt good for us? Well, yes, but less so if they have a lot of added sugar. Should they be taxed less than soda, because they are relatively more healthy? What about sugary cereals and granola bars? What about foods with artificial sweeteners? The lines are less clear in this current health debate.
The news report I am forwarding describes a recent assessment of the effectiveness of "sugar taxes". Dozens of other countries, and multiple large cities in this country, have imposed this tax. They have existed for a relatively short time, so there is much yet to be learned about them. They do appear to cause a drop in soda consumption, but whether that translates into improved health of the population is still to be determined. Not surprisingly, the soda companies have responded aggressively, with a variety of tactics. This battle is far from settled.
The next time you are at the grocery store, ask yourself if you are planning to put soda into your cart. And, look around: how many people do? It's common to see people pushing shopping carts with 6-packs of bottled soda (often multiple of them) draped over the edges of the cart. This behavior didn't exist 10 years ago! Have the bottles changed to make this more convenient? Or are we buying more? Our fast food restaurants and convenience stores offer *enormous* fountain drinks - 30, 40, even 50 ounces at a time! Does anyone rally need that much soda at once?
On this, and all of our topics, stay informed. Healthy habits require good information, and wise choices. There is plenty of information available on the health aspects of soda and its social implications. Be wise shoppers and consumers!
And, have a great weekend. See you on Monday for Chapter 17.
We've considered recently the concept of aposematism, the display of warning coloration to indicate to potential predators that one is unpalatable or otherwise unsuitable as a prey item. As we have seen, there are many implications to this type of signaling, including the costs involved, the degree to which it is effective, and its potential to be mimicked (and thus rendered potentially less effective) by palatable species.
The issue of aposematic costs is one that has been considered for some time, particularly the metabolic costs of producing warning coloration as well as the predation cost of being conspicuous. In addition to these are the metabolic costs of actually being unpalatable, and in no system has this been better explored than in monarch butterflies, conspicuous in both larval and adult forms, as well as highly unpalatable in each for the glycosidic compounds they acquire and sequester from milkweed plants (their near-exclusive forage). These compounds are highly toxic disruptors of Na+ channels, and being able to ingest and store them has required some evolutionary tinkering.
In the recent science news is consideration of this phenomenon, with some genetic work that explains the evolution of caterpillar resistance to these glycosides. The plant defenses have evolved to deter caterpillar feeding, but the caterpillars were able to evolve resistance with as few as three genetic mutations. These researchers were able to induce these same mutations in fruit flies, rendering them resistant to the glycosides as well - a very powerful experimental demonstration. The researchers also demonstrate some of the costs associated with the evolution of resistance to glycosides, including reduced ability to withstand physical shock. No evolutionary benefit is free, and beneficial changes to genes often are paired with deleterious side-effects. Here, the benefit (unpalatability) appears to outweigh the costs (reduced ability to withstand physical rotation).
Many of the plants and animals around us are conspicuous, while many others are cryptic. Those that are colorful and eye-catching may be silently playing potentially-deadly games of chemical warfare. Nature has been described as 'red in tooth and claw' (William Congreve); we might expand that to '... tooth, and claw, and toxin', for many toxins (including these glycosides) are quite deadly. What is remarkable to me is the role of simple sugars in glycosides, forming one side of the glycosidic bond. This is why some dangerous chemicals (such as automotive antifreeze, ethylene glycol) taste sweet and thus are dangerously attractive to the uninitiated. It makes me wonder whether glycosides have ever been used in nature as deadly bait, to lure, and then poison, potential prey. I'm willing to bet that it has...
Have a great weekend-
Good morning everyone,
Our lecture on Tuesday of this week described the essentials of digestion, and Thursday's topic followed with consideration of metabolism and energy balance as a whole. In the science news this week is a new study on these very topics, with description of a genetic mutation that influences both.
During our digestion lecture, I noted that much of its function is regulated autonomically, by local reflexes mediated in the ENS. That is to say, the digestive tract functions more or less on its own when food is presented to it. By inference then, regulation of food acquisition controls the overall amount of digestion we perform, and the number of calories we have available to use or store.
Regulation of hunger, food-seeking, and feelings of satiety (satisfaction of hunger, or "fullness") occur largely through the hypothalamus, where a variety of chemical signals are known to promote either orexigenic (food-seeking) or anorectic (satiety) states. These include a number of cryptically-named chemicals such as CART, alpha-MSH, agouti-related peptide (AgRP), and melanocortin (MC), each acting at hypothalamic cells bearing specific receptors for them. A great deal of experimental work over the last several decades (mostly in mouse models) has demonstrated that disruption of their signaling (via increased activation of their receptors, or blockade of them) can cause food consumption and body mass to either increase, or decrease.
Abnormally-elevated body mass to the point of obesity has reached critical levels in this country. Depending upon the guidelines one uses, it has been estimated that 30-40% of adults in this country are obese, with another substantial proportion of the population classified as overweight. Extra body mass is a significant health complication, raising one's risk of a number of diseases (including hypertension and diabetes) and complicating treatment and prevention of many others. As such, there is an enormous research effort underway to explore the roots of obesity. We know for certain that the issue is complex - socioeconomic status, willpower, behavior, access to high-quality foods, and sociality influence our food choices, eating habits, and body mass, in ways that are both many and complicated. Increasingly, there is growing appreciation of genetic components to obesity as well.
Modern genetic assessments of health have benefited by technological advances that allow sequencing of individual genomes, resulting in large databases of genetic information. When these are paired with health profiles and lifestyle data, they make possible genome-wide association studies (GWAS). GWAS represent a powerful way to take two very large sets of data (gene sequences and health/lifestyle data) and see how/where they intersect. In contrast to the twin study I described to you in my science news email last week, GWAS are useful only when based upon thousands (usually, hundreds of thousands) of individuals. These are not experimental methods, so they cannot provide definitive proof of anything, but they can reveal interesting "associations" - places where genetics and health vary in consistent ways.
This new study describes a GWAS that sought genetic bases for obesity. In a very large sample of human subjects (500,000 individuals), the researchers looked for consistent genetic mutations in people who were, or were not, obese. They found evidence for specific genetic variation in the MC4R gene (melanocortin receptor 4) that was associated with obesity: persons whose MCR4 gene was mutated (causing reduced function) were much more likely to be obese that those who carried the 'normal' version of the gene. To some extent, this finding was not new - this effect of MCR4 mutation had been described previously, in smaller studies. Here, though, the researchers also found evidence that if mutations in the gene(s) that regulate MCR4 cause it to be 'turned on' all of the time (instead of occasionally, such as after eating), it causes chronic satiety, or "fullness". Persons with this form of mutation are much less likely to be obese, so the researchers interpret this alteration of MCR4 function as protective, and preventive of obesity.
Thus, we may have a single gene, which if mutated in one fashion can contribute to obesity, and if dis-regulated in another way can protect against it. A second study described in this same article uses similar data to create a genetic risk assessment for obesity, with the hope of reducing its prevalence, potentially by intervening before it reaches criticality.
The genetic associations described in this study are not enormous, just a few percent (perhaps 6%). Still, they represent the largest known genetic association for obesity, and that in and of itself is a very worthwhile finding. Many persons who are obese suffer from anxiety, depression, and feelings of low self-worth, thinking (and too-often being told) that they are 'fat', or overweight, because of their behavior and lack of willpower. What if the problem lies in their genes, and not in their self-control? We all know how difficult it is to resist food when we are hungry - what if that feeling never goes away?
Like most science, these studies raise more questions than they answer. Obesity and weight control are such significant problems, though, that their investigation is crucial to improved public health. Here's to more studies and more information on these topics - they are likely to benefit us at a variety of levels: individually, via our loved ones, or as part of society as a whole.
Have a great weekend -