Diabetic! Lance bc why not
  • He was diagnosed @ age 9
    • His huge family helped support him
    • Lots of people to nag him to check his sugar all the time
    • Always someone there to take care of him if he was sick
    • Only one in his fam to have diabetes
  • When he was diagnosed he was afraid he wouldn’t be able to be a pilot anymore
  • Has a CGM ((with a blue sensor))
  • Pump??? ((idk if tslim, animas, or Medtronic)) or pens???
  • Makes good jokes about diabetes all the time
    • Will actively fight anyone who makes ignorant diabetes jokes
    • Likes to make people uncomfortable when they make jokes or misinforms or anything
    • “Im so alpha my beta cells stopped working”
  • looks up to shiro bc if he can be a badass fighter and pilot with his robo arm then damnit lance can be badass with a robo pancreas
  • SUPER STRESSED when he was launched into space
    • But I mean who wouldn’t be???
    • theres no insulin in space bro
    • and of course the //one time// he didn’t bring his meter he gets launched into fucking space
    • someone help this poor lost boy
    • his pump was probs running low on insulin too
  • he slowly started being high all the time bc he was trying to save his insulin in his pump for as long as he could
    • I totally didn’t do this when I went to the beach 3 years ago and forgot my insulin for 3 days and need to change my pump what
    • This got bad around the time sendak attacked the castle the first time
  • Lance was real high and had ketones and going into dka during the party
    • The reason he was feelin extra shitty and left early
    • When sendak attacked he couldn’t focus or shoot straight bc his sugars were all fucky
    • Adrenaline makes you high
    • Exercise w/ high blood sugar is a Bad Thing
  • When he went into the healing pods after getting hit it helps lower his sugars
    • Puts him back into honeymoon phase
    • He isn’t chronically high anymore
  • Pidge and hunk were the only ones who knew he was diabetic before the attack
  • He tells the rest of the team after he got out and realized how bad he got
  • Pidge hunk and coran work on making some new alien insulin type thing to help
  • During the mind meldy thing hes pretty low and the rest of the team can feel how he feels
    • Everyone super shocked at how he feels
    • “wait that’s how you feel?? Like all the time???” “well not all the time,,, only when im low??” “lance you say ur low like half the time”
    • hes also is hypoglycemic unaware sometimes so he didn’t even know he was low until keith pointed it out in the simulation
  • pidge and hunk hook up his pump and cgm to his lion
  • Blue can tell when hes high/low
    • Forces lance to take a break and correct when his sugars all wonky
  • When shiro found out for the first week or so he took up Dad Mode and was on his case nagging about if hes okay during training
    • Lowkey lance loves it bc it reminds him of his family at home being overly naggy
    • He comes in and checks his sugars in the middle of the night bc he cant sleep anyway and knew he was having a rough day sugar wise
  • Keith likes to watch him check his sugar and change his pump
    • Hes super lowkey about it tho and thinks hes being subtle
    • Like he’ll sit across the table and pretend to be playing with his knife or something else but is like watching out of the corner of his eye
    • Lance totally knows hes watching tho
    • At first he thinks its bc hes like weirded out by it since hes used to people from classes being weirded out when he checked
    • Eventually lance just shouts “Can I help you?????” at keith when hes changing his pump and is kinda annoyed
    • Keith just asks if he can help him bc hes actually really interested in it like the nerd he is
  • Everyone starts making good hearted good natured diabetes jokes
    • But lance is still the king of ‘em
    • And diabetic pickup lines
    • “her are you my needles bc ur super fine”
Diabetes: Type 1 vs Type 2


Total lack of insulin

  •  5 to 10% of people who have diabetes.
  • autoimmune disease - immune system attacks beta cells in pancreas that produce insulin
  • eventually eliminating insulin production from the body.
  • cells cannot absorb glucose to produce energy
  • symptoms usually start in childhood or young adulthood. 
  • episodes of low blood sugar level (hypoglycemia) are common
  • cannot be prevented  
  • treated with insulin injections or pump


 Too little insulin or cannot use insulin effectively 

  •  can develop at any age but most commonly becomes apparent during adulthood. 
  • vast majority of diabetics
  • body develops insulin resistance 
  • body compensates by producing much more, but can’t always produce enough and eventually beta cells may be destroyed from overwork - resulting in deficiency 
  • may not have symptoms before diagnosis
  • there are no episodes of low blood sugar level, unless the person is taking insulin or certain diabetes medicines.
  • can be prevented or delayed with a healthy lifestyle 

Both types increase a person’s risk for complications. Diabetes is the leading cause of blindness and kidney failure.

  • excessive build up of blood glucose causes an increase in osmotic pressure 
  • the kidneys no longer able to absorb most of the glucose - due to extreme concentration
  • the body pulls fluid from the tissues to try to dilute the blood and counteract the high glucose 
  • dehydrated tissues signal the need to drink more, subsequent increase in urination 

Type 2 diabetes is characterized by a combination of peripheral insulin resistance and inadequate insulin secretion by pancreatic beta cells. Insulin resistance, which has been attributed to elevated levels of free fatty acids and proinflammatory cytokines in plasma, leads to decreased glucose transport into muscle cells, elevated hepatic glucose production, and increased breakdown of fat.


Cardiac anatomy today… I had a quick formative and found it straight forward which was great - just need to review cardio, joints and neuroanatomy. Happy studying!

“There are two main endocrine cell lines of the pancreas. The most prolific - the beta cells - are responsible for the secretion of insulin. Alpha cells secrete glucagon and these cell types are collectively known as islet cells. Acinar cells are exocrine in nature and synthesise and secrete digestive enzymes.”

Science Morsel - Busting a Diabetes Myth

Traditionally, the two main types of diabetes have been known as the:

- Type 1 - the “genetic” diabetes which relates to the immune system killing the insulin-producing cells of the pancreas, otherwise known as the beta-cells. Without insulin, the glucose (sugar) has no way to move from the blood into the cell. It occurs more often in younger people.  

- Type 2 - the environmental/diet-related diabetes where the body becomes resistant to insulin. This means the cell does not open to let glucose in despite insulin being present. This type is more likely to occur in overweight people.

However the genetic influence is not as previously thought. Studies of identical twins have found a concordance rate of 90% for Type 2 and only 50% for Type 1. That means that if one twin develops Type 2 there is a 90% chance the other twin will also develop it whilst there is only a 50% chance for Type 1. This indicates a much higher genetic influence in Type 2 than previously thought. 

Source: Monash University PHY2032 - Endocrine Control Systems - 2015 Lecture Series

Genetically Engineered Mice Suggest New Model for How Alzheimer’s Disease Causes Dementia

Using a novel, newly developed mouse model that mimics the development of Alzheimer’s disease in humans, Johns Hopkins researchers say they have been able to determine that a one-two punch of major biological “insults” must occur in the brain to cause the dementia that is the hallmark of the disease. A description of their experiments is published online in the journal Nature Communications.

For decades, Alzheimer’s disease, the most common cause of dementia, has been known to be associated with the accumulation of so-called neurofibrillary tangles, consisting of abnormal clumps of a protein called tau inside brain nerve cells, and by neuritic plaques, or deposits of a protein called beta-amyloid outside these cells along with dying nerve cells, in brain tissue.

In Alzheimer’s disease, tau bunches up inside the nerve cells and beta-amyloid clumps up outside these cells, mucking up the nerve cells controlling memory, notes Philip C. Wong, Ph.D., professor of pathology at the Johns Hopkins University School of Medicine.

What hasn’t been clear is the relationship and timing between those two clumping processes, since one is inside cells and one is outside cells, says lead and corresponding study author Tong Li, Ph.D., an assistant professor of pathology at Johns Hopkins. Prior studies of early-onset Alzheimer’s disease have suggested that the abnormal accumulation of beta-amyloid in the brain somehow triggers the aggregation of tau leading directly to dementia and brain cell degeneration. But the new research from Li, Wong and colleagues suggests that the accumulation of beta-amyloid in and of itself is insufficient to trigger the conversion of tau from a normal to abnormal state. Instead, their studies show, it may set off a chain of chemical signaling events that lead to the “conversion” of tau to a clumping state and subsequent development of symptoms.

“For the first time, we think we understand that the accumulation of amyloid plaque alone can damage the brain, but that’s actually not sufficient to drive the loss of nerve cells or behavioral and cognitive changes,” Wong says. “What appears to be needed is a second insult — the conversion of tau — as well.”

In humans, the lag between development of the beta-amyloid plaques and the tau tangles inside brain nerve cells can be 10 to 15 years or more, Li says, but because the lifetime of a mouse is only two to three years, current animal models that successfully mimic the appearance of beta-amyloid plaques did not offer enough time to observe the changes in tau.

To address that problem, the Johns Hopkins researchers genetically engineered a mouse model that used a tau fragment to promote the clumping of normal tau protein. They then cross-bred these mice with mice engineered to accumulate beta-amyloid. The result was a mouse model that developed dementia in a manner more similar to what happens in humans, Li says.

The researchers found during brain dissections of the animals that the presence of beta-amyloid plaque alone was not sufficient to cause the biochemical conversion of tau, the repeat domain of tau — the part of tau protein that is responsible for the conversion of normal tau to an abnormal state — alone was insufficient for the conversion of tau, beta-amyloid plaques must be present in the brain for the conversion of tau and the tau fragments could “seed” the plaque-dependent pathological conversion of tau.

One implication of the new research, Wong says, is to possibly explain why some drugs designed to attack the disease after the conversion of tau haven’t worked. “The timing may be off,” he says. “If you were to intervene in the time period before the conversion of tau, you might have a good chance of ameliorating the deficits, brain cell loss and ensuing consequence of the disease.”

The work also suggests that combination therapy designed to prevent both the beta-amyloid plaque formation as well as pathological conversion of tau may provide optimal benefit for Alzheimer’s disease, the researchers say. Their mouse model could be used to test new therapies.

An estimated 5.4 million Americans are living with Alzheimer’s disease, according to 2016 statistics from the Alzheimer’s Association. There is no cure, but there are some medications that may help stabilize cognition for a limited time or help with related depression, anxiety or hallucinations.

Shoutout to my pancreas and immune system

My pancreas is the innocent victim of a tragic accident.

My immune system isn’t murdering my beta cells. If anything it’s accidental manslaughter. It thinks it’s doing its job, it just misunderstood the directions. Somewhere in the network there’s a communication error.

I don’t blame my pancreas, and I try not to hold a grudge against my immune system either. They’re doing their best.

I hate T1D but I don’t hate my body.

Designer protein gives new hope to scientists studying Alzheimer’s disease

A new protein which will help scientists to understand why nerve cells die in people with Alzheimer’s disease has been designed in a University of Sussex laboratory.

In people with Alzheimer’s, Amyloid-beta (Abeta) proteins stick together to make amyloid fibrils which form clumps between neurons in the brain. It’s believed the build-up of these clumps causes brain cells to die, leading to the cognitive decline in patients suffering from the disease.

It is not known why this particular protein’s “stickiness" causes cells to die and scientists have been unable to properly test whether the sticky clumps of Abeta proteins have different effects, compared with individual proteins that are not stuck together.

Now University of Sussex scientists have created a new protein which closely resembles the Abeta protein in size and shape, but contains two different amino acids (the building blocks that proteins are made up of). These changes mean that the new protein does not form amyloid fibres or sticky clumps, and, unlike Abeta, is not toxic to nerve cells, according to a study in the open access Nature Publishing Group journal Scientific Reports.

The new protein will be an essential laboratory tool for researchers working to understand the causes and role Abeta plays in Alzheimer’s disease. The scientists who designed it are now working closely with the Sussex Innovation Centre, the University’s business-incubation hub, to research commercial opportunities for the protein.

Dr Karen Marshall, who led on the study, said: “Understanding how the brain protein Abeta causes nerve cell death in Alzheimer’s patients is key if we are to find a cure for this disease.

“Our study clearly shows that the aggregation of Abeta into bigger species is critical in its ability to kill cells. Stopping the protein aggregating in people with Alzheimer’s could slow down the progression symptoms of the disease. We hope to work towards finding a strategy to do this in the lab and reverse the damaging effects of toxic Abeta.“

Professor Louise Serpell, a senior author on the study and co-director of the University of Sussex’s Dementia Research Group, said: “This is a really exciting new tool that will contribute to research to uncover the causes for Alzheimer’s disease and enable tangible progress to be made towards finding targets for therapy.”

Peter Lane, Innovation Support Manager at the Sussex Innovation Centre, said: “This is a really exciting development. The Centre is thrilled to be working alongside Professor Serpell to make sure the benefits offered by this new laboratory tool are made widely available to the Alzheimer’s research community in the very near future.”

A Simple Breakdown of Type One Diabetes

What is Type One Diabetes?

Type 1 diabetes (T1D) is an autoimmune disease in which a person’s pancreas stops producing insulin, a hormone that enables people to get energy from food.

What are symptoms of Type One Diabetes?

 Extreme thirst

 Frequent urination

Drowsiness or lethargy

 Increased appetite

 Sudden weight loss

 Sudden vision changes

 Sugar in the urine

 Fruity odor on the breath

 Heavy or labored breathing

Stupor or unconsciousness

How/Why does it happen?

It occurs when the body’s immune system attacks and destroys the insulin-producing cells in the pancreas, called beta cells. While its causes are not yet entirely understood, scientists believe that both genetic factors and environmental triggers are involved. It has nothing to do with diet or lifestyle. There is nothing you can do to prevent T1D, and right now there is nothing you can do to get rid of it.

Who does it effect?

Type 1 diabetes strikes both children and adults at any age. It comes on suddenly, causes dependence on injected or pumped insulin for life, and carries the constant threat of devastating complications.

How is Type One Diabetes managed?

Living with T1D is a constant challenge. People with the disease must carefully balance insulin doses (either by injections multiple times a day or continuous infusion through a pump) with eating and other activities throughout the day and night. They must also measure their blood-glucose level by pricking their fingers for blood six or more times a day. Despite this constant attention, people with T1D still run the risk of dangerous high or low blood-glucose levels, both of which can be life threatening. People with T1D overcome these challenges on a daily basis.