Pumpkin Pineapple Strawberry Yogurt Oats

Irish Style Oats: These oats are essentially steel cut oats, only quicker cooking. Much less processed than say, quaker instant, but do no need to be cooked for 30 minutes on the stove! I got them at Trader Joes for about $3 for a bucket (32 servings-ish ?) So that is 1/4 cup of irish style oats, mixed with about 1/4 cup water and 1/4 cup organic pumpkin . Microwaved with cinnamon and a little brown sugar for about 4 minutes. It was so hot so I put a few frozen pineapple and a few frozen strawberries stuck into the oats to heat up

Then, I needed protein! I didn’t feel up to eggs So O% Chobani Plain it was! ( That is the big container I have had for a few weeks but its funny how it looks just like the single serving size. Either way, there was just under one serving left.. so…

The Final One bowl Product

I mixed pumpkin butter into the yogurt- SO DELICIOUS! I added a teaspoon of peanut butter but apparently it thought the bowl was a slide….” Weeeeeeee” all the way into the oats. I don’t mind so much with oats when things mix but I am totally the type that likes everything separate and not touching each other ( not in a weird way, just how i would prefer). In the middle is a little sprinkle of Uncle Sam’s cereal (mostly just flax seeds because thats all i wanted)

Body:
I am not tired or sore from yesterday! Which is great! I think I will stick to running 3+ miles every other day + biking and more cardio to equal about a 6-10 mile run would equal. I would be up for a workout, but since I had a great cardio session yesterday and have LOTS of writing to do for my paper due tomorrow- I decided on a pre-final/dinner workout this afternoon ( I use purple dumbells my mom got me for me about five years ago- they are 8lbs each)

strength- shoulders and chest: push ups, plank, bent over fly ‘s; abs: planks, figure 8′s, side to sides, my version of sit ups ( I have my arms above my head, knees bent, feet on the floor, keep my arms up and lift up then twist side to side and back down)

and… Yoga! 30 minutes felt fantastic, I wish I had more time!

Mind:
Paper #2. … (5 pages are written but I emailed it to the professor for revisions)

Minority health response paper. We have to read this week’s articles on concordance in healthcare, minority medical research views, and how these concpets tie into our own topics we researched (mine was native american children on reservations). Minority groups such as african americans, native americans, hispanics etc. have experienced racial discrimination for hundreds of years and this not only reflects in their culture and education and emotional well being, but it leaves most with negative views of healthcare practices also. The Tuskegee Syphillis Study is one very very bad example that has unfortunately not been made well-known for a variety of reasons.

Essentially, a group of about 400 men who HAD syphillis, were offered to take part in medical research to hopefully find cures for the disease. At the time there was no institutional review board that oversees the ethical practices of research. Well, as a graduate student and having been a student member of the Institutional Review Board in undergrad, there are ethical standards we must now abide by in research (both animal and human research) such as:
- informed consent ( which protects the participant in the research by securing their participation and fully disclosing what is happening in the research. If anything not explained on the consent form should occur, they would be protected by law because they signed what was on the consent form only so anything else would be illegal for the researchers to try).
There are many other aspects of IRB’s but essentially they were formed to protect the research participants- make sure they are not harmed etc.

Well, the Tuskegee study essentially gave some of their subjects the drug that helped the disease, while others got another drug that didn’t do any harm but did not cure it. Because there was no IRB or standards at the time, the study needed to maintain the groups as they progressed to make sure there were no other side effects, make sure they found the cure, etc. Well the people that did not get the right drug ( which the researchers did NOT know at first which drug would help ) eventually started passing away because of the disease. So the researchers then found out which drug was the “cure” and STILL did not offer the “other drug” group the “cure drug” because they wanted to continue research on the other “drug” .This was a HORRIBLE example of medical research and luckily in the 70′s when they found out about the “cure drug” , the researchers were slapped with a lawsuit and helped families of all the victims and tried to rectify their wrong-doings.

Unfortunately, this had major impacts of minority health research because now people that may be at a disadvantage are PURPOSELY not seeking health care because 1. they do not trust “white” doctors 2. they do not trust the government 3. Minority groups have been asked about the study and have complete misunderstandings of the TRUTH. (this was from a focus group that was one article I read this week). They believed researchers injected men with syphillis when that is not true. They believed that the government knew all along and was purposely trying to opress that group of men- all kinds of stuff.

So if you are interested in that study here is more info on it : http://www.cdc.gov/tuskegee/after.htm . I left out a lot of details but tried to give a basic understanding of what went on.

Anyway, that is what I need to write my paper about today.!

Final Exam at 5:00 pm at a diner! It is for my gastronomy class, we are eating at a local diner that serves only local, fresh, organic food . I am not sure what part of that is the exam but we will see!! I will be bringing my camera!

Soul:

I had a dinner at a local sustainable organic diner that serves fantastic wines, cocktails and is in this fantastic historical building for my first final exam of the semester!! How awesome is that!

Jeff and I talked about our christmas plans and who/when/where we will be seeing.

My brother is most likely going to visit since he didnt get to visit over thanksgiving!

Jeff’s cousin ( we went to their wedding in september in NY- Buffalo- Niagra Falls trip) is visiting the weekend after I am finished with exams.

My paper , although I am not satisfied completely with it, is pretty much done. I could hand it in as in, ( which feels great with all the other work I need to do) but I am a slight perfectionist.

Did I mention I had dinner as my final exam? I had a great conversation over dinner with classmates on top of that!

Insulin Resistance and Hyperglycemia : The Cellular Metabolism of What Leads to Type-2 Diabetes

This is the intro and conclusion to the paper I just handed in. I cut out all the middle /good stuff because if you aren’t into cell metabolism, it is probably not of interest.

Introduction

Hyperglycemia enhances the uptake of glucose into the liver, which thus increases the metabolic pathways of glycolysis, the citric acid cycle, and the generation of energy as ATP. An additional response to hyperglycemia involves the pancreatic release of the hormone, insulin. Beta-cells of the islets of Langerhans produce insulin in the pancreas and these cells are freely permeable to glucose via the glucose transporter, GLUT-2 .1 Glucose transporters (GLUT 1, 2, 3, 4, 5) are transmembrane proteins encoded by distinct genes and have distinct kinetic properties, substrate specificities, and tissue distributions that dictate their functional roles.

The liver, which should cease to produce glucose as the level of blood glucose rises, will increase its release of insulin to lower the blood glucose concentration and increase its utilization and storage in the liver and muscle as glycogen. 1 The utilization and storage of glucose as glycogen involves the glucose transporter, GLUT-4, which is located in heart, skeletal muscle, and adipose tissue. 1 Skeletal muscle is regarded as the principal site for insulin-stimulated glucose uptake, whereas adipose tissue does not take up as much glucose as skeletal muscle. 2, 3 The research indicates that while muscle is the primary uptake site, problems in adipose uptake affect whole-body insulin resistance as well. The goal of this paper was to examine the defects that occur in signal transduction contributing to insulin resistance, hyperglycemia, and thus the defects that lead to Type-2 diabetes. In researching for this goal, two specific areas seemed to be the most significant in these defects. These two contributing factors to insulin resistance involve the GLUT-4 glucose transporter and Beta-cell failure.

It is unclear whether the research indicates that GLUT-4 defects and beta-cell failure are both required to cause hyperglycemia, or eventually cause type-2 diabetes. However, each of these defects independently contribute to insulin resistance and hyperglycemia. The combination of impaired glucose transport, increased insulin resistance, and loss of Beta-cells are all characteristics in type-2 diabetes. At first when cells in the muscle, fat and other tissues become less responsive to insulin, Beta-cells try to keep up by producing more and more insulin.8 This excess insulin in the blood can cause a bout of hypoglycemia, which is a marker for type-2 diabetes. 8 However, the over-production of insulin itself by these Beta-cells could contribute to the apoptosis discussed earlier. Insulin resistance then continues to increase due to the impairments in GLUT-4 translocation potentially caused by increased Serum RBP4 levels, and/or the loss of Beta-cells due to increased apoptosis and/or decreased islet formation.

Conclusion
The mechanisms behind increased apoptosis and decreased islet formation are only being speculated at this point in research. Similarly, the mechanism behind impaired GLUT-4 translocation is also unclear, although other studies strongly indicate that elevation in free fatty acids decrease glucose transport and impair PI(3)K in skeletal muscle.4 The elevation in free fatty acids were associated with increased levels of serum RBP4, which were inversely correlated with GLUT-4 functioning. The research did suggest solutions for reversing insulin resistance, decreasing hyperglycemia, and thus decreasing risk of type-2 diabetes. These solutions include lowering serum RBP4 levels, lowering free fatty acid levels, ( hence why Type -2 Diabetes can literally stop the disease by losing weight aka excess fat) and preserving/restoring Beta-cell function.