High Fructose Corn Syrup!!!
First of all, what exactly is it? We all know that it makes an appearance in all of our food. According to the USDA, high fructose corn syrup is 3% water, 42% glucose, and 55% fructose. This particular mix is used in the soft drinks that most of us consume on a daily basis. High fructose corn syrup has replaced our table sugars as the sweetener in most of our meals. The main reason for this is because it is easier and cheaper to make. So, needless to say, since high fructose corn syrup is everywhere, do we have to worry about what it does inside our body?
Take a min to watch this SNL skit.
http://www.hulu.com/watch/223360/saturday-night-live-corn-syrup-commercial
Although humorous, the video does bring up valid points about the public being uninformed on the side effects of high fructose corn syrup, as well as the idea of moderation.
Related to the paper we just read, I found another paper that suggests that high fructose corn syrup reduces the amount of leptin and insulin in our blood stream. This is bad news for us, because leptin is what regulates our hunger, and our body’s ability to increase energy production. Without leptin, we will always be hungry. That will lead to caloric intake, and from there, to obesity!
Here is a neat graphic depicting the effects of leptin signaling from adipose tissue.
http://www.nature.com/nature/journal/v395/n6704/fig_tab/395763a0_F3.html
As you can see, increase in leptin, comes from weight gain, and this signals our body to stop eating. However, if our leptin is decreased, it will lead to hunger and caloric intake. The reason for this decrease in signaling, is that fructose doesn’t trigger the leptin signaling pathway. So, we just eat and eat and eat and nobody tells us to stop.
However, I’m still unsure on what exactly this means for our intake of high fructose corn syrup. Should I be eating it? Should I be eating only some of it? How much can really affect my body weight? These are a few questions I would like to explore further.
Which came first? Diabetes or obesity?
This week’s article talked about obesity and how some of the pathways that trigger in our bodies that we are full may not be working properly. These chemicals that signal we are full and can reduce or stop our food intake are called insulin and leptin. These chemicals work together so that when there are high levels of insulin and leptin we decrease our food intake and increase our energy spent, but when these levels are low we increase our food intake and decrease the amount of energy we spend. The article stated that there is a balance between the chemical levels, food intake and energy expenditure. When and if something gets off balance, something in the body goes awry one of these possibilities is obesity.
One theory out there is that obese individuals have a hard time lowering their food intake because of something called resistance. These leptin and insulin levels that used to be enough to tell us to stop eating are no longer at high enough concentrations so our brains and our bodies don’t know to stop eating. The increased glucose from the foods we eat can’t all be used in energy so it is stored in the body for later use as fat cells, thus causing a build up in fat stores and leading to obesity.
Some articles that I found focus more on insulin resistance as the key factor rather than leptin. According to one article, obesity is actually said to promote insulin resistance because the body no longer recognizes the smaller amounts of insulin to signal a cessation of eating. To find more about this article you can check out this link: http://diabetes.webmd.com/guide/insulin-resistance-syndrome
This diagram depicts other things that can also happen when the body is resistant to insulin.
http://table.ta.funpic.org/04/insulin-resistant-symptoms.html
There is also a link between type 2 diabetes, obesity and insulin resistance. Type 2 diabetes is characterized by the body producing insulin, but not enough for the body to use it correctly, thus resulting in insulin resistance. To learn more about Type 2 Diabetes, follow this link: http://diabetes.webmd.com/diabetes-men
So people that are overweight are more likely to develop insulin resistance and thus diabetes, but people that have diabetes are also more likely to become overweight. Therefore it is still unclear which comes first; it is kind of like the chicken or the egg debate. Scientists do propose that there is a genetic link however, so a word of caution to those that have either obesity or diabetes in their family; take care of your body, eat right and exercise so that you don’t have to find out which comes first for you, obesity or insulin resistance.
Step Away From the Ice Cream!
Obesity has unarguably become one of the biggest issues facing our society. This week we discussed two molecules, insulin and leptin, specifically relating to obesity. Insulin and leptin are considered ‘adiposity signals’ meaning that the levels of these molecules is directly related to the amount of adipose tissue (fat) that we have circulating in our bodies. Research has shown an increase in insulin results in a decrease in food intake and therefore a decrease in body weight; conversely, those deficient in insulin experience hyperphagia (excessive eating) resulting in an increase in body weight. Leptin has been shown to be necessary for normal control of food intake and body weight. Individuals deficient in leptin or leptin receptors experience extreme hyperphagia and therefore obesity.
Neurologically, there are two sets of neurons located in the hypothalamus that can relay the signals of insulin and leptin. The two types of neurons have opposite effects on food intake and energy expenditure. First are neurons which express proopiomelanocortin (POMC); they are activated by an increase in insulin and leptin and result in a reduction in food intake and an increase in energy expenditure. Second are neurons which express neuropeptide Y (NPY) and agouti related protein (AgRP); they are activated by a decrease in insulin and leptin and result in an increase in food intake and a decrease in energy expenditure.
The issue with this system seems to be that we can become insulin or leptin resistant, meaning our brain can no longer control our eating habits. The exact mechanism of this is not entirely known however, high fat diets have been shown to lead to resistance. So, if we decrease the amount of high fat foods we consume, we could help ourselves prevent this control system from falling apart.
In order to do this we must look at reasons we have diets that are high in fat: one such reason is emotional eating. Emotional eating can be defined as eating for reasons other than physical ones. It occurs when we eat to satisfy or reach a certain feeling; we eat when we are sad, stressed, bored, happy – basically eating can be associated with any emotion. A representative from the University of Maryland indicated that, in fact, over 75% of over-eating is emotional eating – that is a shocking number considering the only reason we need to eat is for physical reasons (need for more energy).
Research has shown that ice cream is the number one go-to emotional food; for women, chocolate and cookies are next on the list and for men pizza and steak are most commonly eaten. Researchers have found that many ‘comfort foods’ consumed during emotional eating are very high in fat. This becomes an issue when emotional eating is the only coping mechanism one has to deal with emotions. We take in significantly more calories than our bodies need and the foods we eat tend not to be very healthy. So what can we do about it? Well many sources indicate that becoming aware of emotional eating is the start. Every time before you start eating, determine your emotion, how strong that emotion is, and what food you are reaching for. By keeping a food diary you may notice how often you are eating for reasons other than physical ones and how much of an unhealthy food you are taking in. So, put down the ice cream and rate your emotion!
*For more information on how to control your emotional eating check out: WebMD: Controlling your emotional eating
Obesity as a Disease
This week’s article was about insulin and leptin signalling in the human body. Signals from our fat tissues, or adipose, release insulin which tells our bodies to decrease food intake. Therefore, if we have less fat tissue, we will have less insulin signalling and increased food intake, and if we have more fat tissue, insulin will be released and food intake will decrease. Leptin is a similar adiposity signal. Mutations in the expression of leptin have been linked to morbid obesity.
For me, this was one of the first times that I have taken an in-depth look at the mechanisms surrounding food intake and weight gain. I have previously learned that obesity can have strong genetic links, and often it isn’t a person’s conscious decision to become obese. But learning of these intricate systems and how one little alteration can lead to increased food intake and obesity, has given me a better understanding. There are opinions out there that obesity isn’t a disease, that it is solely a person’s choice to not take care of their body that leads them to becoming obese. There is also the opinion that obesity is a disease. I have come to agree with the later of these opinions. If there is something that changes inside a person chemically that causes a chain reaction of events to occur, that is through little fault of the individual. Many of the foods that are being made today contain ingredients that can throw these insulin and leptin signals off. It is kind of like the issue of alcoholism as a disease. Yes, the first initial few drinks are conscious choices of the individual. But after that, it has been shown that physiological and chemical changes in the brain occur, making the taking of a drink beyond simple choice. I think the issue of obesity in some cases can be similar to this if changes in the leptin and insulin signalling are changed by the diets of those who are obese.
Obesity and Diabetes: Understanding the Link
Obesity is obviously a growing epidemic throughout many countries including America. There is rarely a day that goes by where I do not hear some mention to obesity on the television or radio. One of the complications which accompany this obesity is type 2 diabetes. Type 2 diabetes occurs when our bodies stop responding properly to insulin. Insulin allows our cells to take glucose in and glucose is important because it is the primary fuel for our body.
Obesity and Type 2
A key step involved in the development of type 2 diabetes is insulin resistance. Insulin resistance often precedes the clinical onset of type 2 diabetes by ten to twenty years. It is caused by abnormally high circulating fatty acid levels, these fatty acids signal to our muscle and liver cells stopping the normal response mechanisms to insulin. This is what causes the rise in blood sugar levels. An interesting fact about type 2 diabetes is that it can be reversed. Proper diet and exercise can lower blood sugar levels and in fact reverse the problems associated with insulin resistance. Not surprisingly, anti-diabetic drugs have been developed. These drugs redistribute fat from the muscle and liver cells to adipocytes, or fat cells.
Insulin Restistance
Although considered to be largely a preventable disease, diabetes 2 has shown to have a genetic linkage. It is interesting to consider the effect that our food industry has had on the development of type 2 diabetes. There is no doubt that it is a disease which is on the rise. So is cancer but what is interesting when comparing a disease like cancer and diabetes is the age component. The incidence of cancer is rising throughout the U.S., but then again so is our lifespan. We expect to see more cancer with advances in medicine which extend our lifespan and treat other disease more effectively. This “excuse” is not present for type 2 diabetes. It does not have the strong age dependent correlation that cancer, heart disease and neurological diseases have. So our food industry is producing food which raises our risk towards developing type 2 diabetes. There are healthy, organic options available throughout grocery stores. I completely agree that there are disorders which disposition certain people towards developing obesity, and certainly some more than others. In many of these cases however I believe that simply exercising, and eating healthy could prevent or solve many problems.
Bipolar Disorder
This weeks’ topic is Bipolar Disorder. Bipolar disorder (BD) has two types; one and two. BD 1 is characterized by manic and depressive episodes while BD 2 by hypomania and depression. Mania is an excited mental state characterized by physical hyperactivity. Hypomania is just a less severe form of mania. The fact that the exact mechanism underlying the pathology of BD is unknown is not unusual among mental illnesses. There are several hypotheses to why BP occurs. The particular pathway involving a signaling molecule, arachidonic acid, currently prevails as the most plausible. Arachidonic acid (AA) is a chemical signaling molecule. In the brain, AA acts as a signaling molecule that leads to various biological effects. Many of the metabolites, or breakdown products of AA, lead to inflammation.
Bipolar
There are three principal drugs involved in treating BD; Lithium, sodium valproate and carbamazepine. It is unknown how exactly these drugs act. It is known that they all lead to reduction of the Arachidonic acid pathway. This is why the AA cascade is believed to be involved in BD.
There are many questions surrounding bipolar disorder. The arachidonic acid pathway is just one mechanism that may explain the disorder. How much of the disease is caused by genetics, environmental factors or nutritional imbalances in undetermined. Due to the fact that so much is unknown, science and medicine should be hesitant to both rule out and accept hypothesis. It is entirely possible that hypothesis other than the AA pathway are involved in BD. The brain is a complicated, mysterious place but that is what makes it so interesting.
High Fructose Corn Syrup is Delicious
It really is. The ingredient that gives pop that sweet, mesmerizing taste. I could guzzle liters of it without blinking. If I could live off soda (and the occasional steak), I would in an instant. My pop consumption is off the charts due to its addicting, refreshing tastes. And I’m not the only one. According to a self-performed study, Americans drink the equivalent of roughly 24 cans of pop a week, translating to 288 ounces (over 8.5 liters!).(1)
What should we know about high fructose corn syrup and its effect on the body? HFCS is a popular industrially due to being cheaper and artificially sweeter than its natural sugar alternatives. I’m sure you are well acquainted with controversy surrounding this common ingredient in not only pops, but many other beverages and processed foods. You’ve probably seen the corn propoganda commercials where they claim “your body can’t tell the difference” and I’m sure you have a local dietitian (2) around the neighborhood that busts out a torch and pitchfork every time you pop a tab on your favorite soft drink. While both sides have some valid points (my heart/diet hopes desperately the former is unequivocally correct), research has shown a relationship between high fructose corn syrup intake and leptin and insulin levels in your body. Leptin and insulin play direct roles in obesity.
To understand the role of HFCS in this context, we must first understand the role of insulin and leptin in regulating our food intake. Our article this week essentially stated that low levels of leptin and insulin stimulate higher food intake, while normal or higher levels lead to decreased food intake. One crucial area in the brain responsible for this effect is the hypothalamic arcuate nucleus. In this case, we are interested in three types of neurons: POMC, NPY, and AgRP. POMC neurons decrease food intake and increase energy expenditure when activated, while NPY and AgRP increase food intake when activated. POMC neurons are stimulated by insulin and leptin, while NPY and AGRP neurons are more activated when leptin and insulin levels are low. In a normal functional body, these two systems work together to provide homeostasis in the body. If someone is losing too much weight, NPY and AgRP neurons will not stimulated by the lack of leptin/insulin and will “urge” the body to regain weight. If someone has an elevated level of insulin/leptin from increased food intake, POMC neurons will decrease food intake while NPY/AgRP’s effects will be essentially inhibited from their normal function. Insulin and leptin also can affect genetic expression of these neurons, inhibiting NPY while increasing the expression of POMC neurons. Consequently, insulin and leptin resistance can lead to increased food intake and obesity. Leptin and insulin are adiposity signals, meaning they rely on signals from fat stores for their function.
Ideally, we want to avoid low leptin/insulin levels or resistance. What role does HFCS play in the function/levels of leptin and insulin? A study in 2009 provided some not so exciting results for avid pop guzzlers.(3) Consumers of excess fructose (instead of typical glucose or sucrose) showed increased conversion of excess sugars into fats (in a process known as de novo lipogenesis (DNL)). HFCS also decreased insulin sensitivity. If the body can’t respond normally to insulin, it will act as if there is a deficiency which, as seen above, can lead to increased food intake and obesity. In another study, fructose consumption was linked to low ciruclation levels of insulin and leptin.(4) Fructose, unlike glucose, doesn’t stimulate insulin secretion. Insulin-regulated glucose metabolism is hypothesized to play a role in leptin secretion. Thus, both leptin and insulin are decreased, leading to increased caloric intake and further obesity. Besides influencing leptin and insulin levels, HFCS also alters metabolic hormones so we don’t feel full. These manufacturers know what they’re doing.
While it truly pains me to say this, high fructose corn syrup opponents may indeed have a point. It would be wise to reduce HFCS in order to prevent obesity and the diseases, such as type II diabetes, that often result. Sticking to natural sugars like sucrose and glucose in substitution for synthesized fructose can help reduce caloric intake (while it is probably unwise to overindulge in those sugars either). Even if we aware of these problems, can the possible consequences of high fructose diets deter us from indulging in soda and the plethora of other processed food containg HFCS? It’s up to the consumer.
(1) – Americans named Nathan Rodeberg.
(2) – Or dentist. The effect of pop on teeth will unfortunately not be addressed in this blog post.
(3) – Stanhope et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. Journal of Clinical Investigation 2009 119(5):1322-34.
(4) Teff et al. Dietary Fructose Reduces Circulating Insulin and Leptin, Attenuates Postprandial Suppression of Ghrelin, and Increases Triglycerides in Women. Journal of Endocrinology and Metabolism 2004 89 (6): 2963-2972.
(5) Google Images.
A Knitting Prescription
Bipolar Disorder
Bipolar disorder affects almost six million American adults and is characterized by episodes of depression and mania. The onset of bipolar disorder is often in late adolescents, but it can develop at any stage in life. Mood stabilizers such as lithium, divalproex, carbamazepine, and lamotrigine seek to suppress the swings between mania and depression to treat Bipolar Disorder. Of the mood stabilizers only lithium and lamotrigine, to a lesser degree, are effective at treating both mania and depression. The other stabilizers try to reduce mania, which is thought to indirectly improve depression by “breaking the cycle” and keeping patients out of bipolar episodes altogether. There is also a horde of other drug types, such as antipsychotics and anti-anxiety drugs, which can be indicated for treatment of bipolar disorder under certain circumstances. Every drug has a list of possible side effects that range from mild to (in my opinion) worse than the issue they are treating. This brings me to the topic I wish to talk about this week.
Overmedicated and Unsatisfactory
One of the points made clear by this weeks review was that the underlying cause of bipolar disorder and the reason treatments like mood stabilizers work is still quite unclear. The mood stabilizers are labeled as such not because of a known mechanism of action, but simply from an observed effect. When this is compounded by the possible side effects and the lack of a clear empirical way of diagnosis, I see a lot of room for error. I do not want to sound too critical because I know that psychological disorders seldom have a clearly understood etiology, but trial and error doesn’t seem like a good way perform medicine. That said, I don’t have a better way to go about treating bipolar disorder so take complaints with a grain of salt. However, I do have an idea about what might be done.
Brain Health
I think there might be ways to improve mental health without completely relying on pills. This is a controversial idea, especially in America, because Americans love pills. Our busy lives demand that we continually find the most time-effective way to go about our day. Unfortunately, this applies to our health. Many Americans would much rather take a blood pressure medication than exercise or eat healthier, both of which take time and effort to do. The healthiest approach would be to take the medication along with exercise and diet changes. Brain health should be treated similarly. I think therapy, support groups, and hobbies should supplement medications. Stimulating the brain through contact with other people and enjoyable diversions has the potential to improve mental health significantly. The best part about my suggestion is that it is risk free; taking up knitting may not prevent a bipolar episode, but it sure won’t cause one, which is more than taking up a new medication can say.
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001924/
http://www.dbsalliance.org/site/PageServer?pagename=about_bipolar_overview
Defensive Bipolar
While I was wondering around the internet searching for information on bipolar disorder, I stumbled across an interesting blog by a person (Bp) who was diagnosed with bipolar. This person’s story was interesting to me because Bp displayed the normal symptoms of bipolar, but that was not all. Later on he developed other symptoms. Bp was diagnosed with bipolar at age 14, and was promptly placed on medication (Risperdal). Bp complained that the medication induced a vegetative state, and went off the medicine wanting to try therapy. Then Bp started to hear a voice in his head, named Maverick. Maverick would take over Bp’s body. When Bp asked his therapist about this new development, he was told that it was just a defense mechanism for dealing with people. He was then put on Lithium, and it only got worse. So then Bp went off medication.
This got me thinking about what bipolar really is, and I thought, what if bipolar is just a defense mechanism as well? Maybe mania is a faulty coping mechanism for major depression? Almost like a rebound. Then once your body is exhausted from the manic state, it slumps back down into depression? This is similar to Multiple Dissociative Disorder (multiple personalities). Multiple personalities are just coping mechanisms for dealing with stressors. For example, a woman who was raped by her father every night, created different personalities, one to deal with the rape, and one to live normal school life. Eventually, she created other alters as well.
Bp’s story also got me wondering, how effective treatment by pharmaceuticals is. As of right now, the DSM-IV just tries to objectively diagnose the disorder, and then pump the patient full of drugs. It needs to reform to give us objective suggestions for treatment based on the individual, not just generalized. I think in Bp’s case, actual cognitive therapy would have been way more helpful than a prescription. I think psychologists need to seriously consider the patient when proscribing treatment because every disorder is really unique. Everything is very subjective, and it’s hard to diagnose a subjective disorder. What are your thoughts?
Beethoven Without Bipolar: The Cost of Creativity
This week’s discussion topic was on bipolar disorder. So far we have only focused on the negative effects of bipolar disorder and finding ways to treat it. I am going to take a different perspective on the disease and hopefully shed an alternative light on mental illness.
Can you imagine a world without Beethoven’s Ode to Joy (from his ninth symphony) ringing through churches? And we can’t forget his Moonlight Sonata and the seasonal Fur Elise. Or the daunting Funeral March of his seventh symphony. This music of the late 18th century has captured the hearts every listener for centuries and possibly centuries to come. People have mixed, rearranged and borrowed from Beethoven’s work into present day. Beethoven has been featured in countless modern films such as Fantasia, Mr. Holland’s Opus, Misery, Along Came Polly, The King’s Speech and even Die Hard and Austin Powers in Goldmember. Many others are also included on this list. Even advertisement agencies also use snippets of Beethoven’s work in present day televised commercials. This demonstrates the impact of Beethoven’s musical talent as well as his legacy as his music continues to entertain us for over more than 2 centuries.
Image from: http://omahype.com/event/beethovens-ninth-2/
But, what if it never happened? What if the music inside of Beethoven was never released from his mind? What if something in Beethoven’s genetic make-up allowed him to excel in music and create the enticing melodies that have captivated the world? What if the deeply emotional and soul-filling music could not have been made because some of his inspiration was taken away? What if much of his inspiration came from something that modern people would call a “disease”? Would we have tried to cure him of the disease and have missed out on his timeless piece of music that we have used and reused since the late 18th century? Perhaps we will never know the answers to these questions. But I guess the question I’m trying to pose is: Does mental illness, and more specifically bipolar disorder, carry all negative baggage or can some good come from it? Now for those of you who do not know supposedly Beethoven had a form of bipolar disorder though it was not officially diagnosed. Beethoven went through bouts of depression and then into manic phases, in which he would compose his deepest most emotionally saturated works.
I know that many people may argue against me, but what if Beethoven’s bipolar disorder, with the creativity provided by these drastic mood swings, allowed him to compose the timeless pieces we have today? If that is the case maybe we should take note of the good that may come from some types of mental illness like bipolar disorder. There are many musicians, actors, and artists that have been “diagnosed” with bipolar such as Amy Winehouse, Sinead O’Conner, Vincent van Gogh, and Virginia Wolfe. Perhaps some their success can be attributed to bipolar. Now I’m not trying to say that bipolar makes you successful. I am just trying to play the devil’s advocate. Maybe we should shy away from the negative reputation that bipolar has and look at some of the good aspects. Bipolar disorder is not something that you should wish upon anyone, however it’srtant to keep in mind that not all parts of mental illness are completely negative.
Read more about the connection between bipolar and creativity/inspiration at:
http://serendip.brynmawr.edu/exchange/node/1726
http://www.springerlink.com/content/w68x7qp16374380x/
http://www.manic-depression.net/symptoms/creativity_symptom_of_bipolar_disorder.htm
Get more information about bipolar disorder and its timeline and discovery at:
http://www.thebalancedmind.org/learn/library/about-pediatric-bipolar-disorder-timeline-english
Learn about other famous individuals with bipolar at:
http://www.famousbipolarpeople.com/
And read more about Beethoven in modern culture at:
http://classicalmusic.about.com/od/classicalmusic101/a/aa021906_2.htm
http://classicalmusic.about.com/od/onestopbeethoven/qt/beethoven_movie.htm