Lessons from Leptin & Insulin
Hannah here with Team Squints to give you your weekly dose of the brain/body connection. This week it’s all about the hormones in your body that affect your well-being.
In the 1600’s Thomas Willis proposed that food affects mood and changes behavior, for better or worse. He was one of the first scientist that documented this proposal, but I presume that this notion had been in circulation far before Willis. Somehow our society has left this notion on the back burner and what we see today are people walking around with big bellies, low energy, depression, anxiety, and all that jazz. Is it really that novel that what we eat changes how our brain functions? The proof is in the pudding. The rise of diabetes and obesity strongly correlates with mental health issues and neurodegenerative diseases.
We know a health epidemic is happening. We can characterize the symptoms and say what’s wrong and temporarily relieve the pain. Antidepressants. Liposuction. Alcohol. They all lessen the discomfort for a little bit, but they aren’t sustainable. The problem is that we have focused too much on the symptoms and not on the root issue. The next leap forward lies in understanding the cause, getting to the bottom of the problem and mending the wounds from the inside out, not the outside in. Unfortunately this is the hard part because it comes with a lot of complications, like understanding and dissecting biology; what proteins and hormones are doing what in the body? How does our lifestyle and what we eat change our body chemistry? This is where the answer lies, but where no one likes to go there because it involves scary words like leptin, insulin, hypothalamus, cholecystokinin, tyrosine, iselts and a lot of non-words too like NPY, GLUT-2, alpha-MSH, PI3K, MAPK, Katp. Ah whaaaaa. Stop.
It seems like a foreign language, but it’s a foreign language that we can break down easily and once we do we’ll be able to better communicate with our bodies. Leptin and insulin are actually our friends, and just like anything else, they are best in moderation. So here we go, get excited to learn, understand, and take away some lesson to apply to your life. We’re gonna make it simple.
The insulin breakdown:
Insulin is a hormone secreted from the pancreas that captures the glucose (sugar) floating around in your blood stream after you have eaten and gives it to the cells of your body for immediate use or for storage. When the glucose is stored it is called glycogen.
Your cells need sugar to function, it’s their main energy source. However, cells in your body can’t directly take sugar in, they need a key to open up a gate that will allow the sugar in. That key is insulin. You can also think of it like this: a baby needs food and energy or else it will cry and cry and cry, but it can’t make the energy itself or directly obtain it. It needs the help of it’s parent. The parent, like insulin, grabs some food and feeds it to the baby. Viola! All is well.
How is this done? The pancreas has these little islands of cells called the Islets of Langherhans that have beta cells in them. When there’s glucose in the blood stream, the beta cells in the little islands secrete the appropriate amount of insulin.
That’s what happens when everything is normal. However, most of the time, nothing is normal. Sometimes the insulin is too high and sometime its too low. The ups and the downs of insulin are dependent on what you eat, how much you eat, and what you do with the energy you get from your food.
When you eat a lot of sugar or simple carbohydrates and starches, there will be a lot of glucose in the blood stream. This tells the beta cells in the pancreas to produce more insulin. If there is constantly excess sugar in the blood stream, the pancreas must constantly work. That’s really tiring. So as you can see, with chronically high glucose insulin is excreted at high quantities. This high quantity of insulin causes a down-regulation of insulin receptors; thus, the target cells respond less to the circulating insulin in the blood stream. AKA, knocking down the gates that insulin has the key to. The cells are already full of glucose and can’t take anymore, so it says no no, your key to this gate no longer works. Try again later. Vicious cycle begins here. Now you have excess insulin in the blood, which is saying ‘GIVE MA SUGAR!’ and you feel hungry, so you eat some more food. The glucose in that food is then stored as excess glycogen in the liver and/or converted into fat… which is totally fine if you’re hibernating for the winter, but not if you’re living a western lifestyle.
So what happens to the brain and your mood as a result of this…?
Connected to the pancreas is the vagus nerve which meanders up to the hypothalamus in the brain. The hypothalamus is responsible for hormone release in the brain, control of food intake, and certain behaviors. One of the hormones that the hypothalamus controls is dopamine. Lower levels of dopamine are linked to anxiety and depression, two behaviors that are also linked to diabetes. Surprising? I think not.
Ok, now what’s this leptin business? Leptin is a hormone that is secreted from adipose tissue, AKA fat. This is the hormone that tells you that you’re full or that you better eat. It directly communicates with the hypothalamus. The more fat you have, the more leptin you’ll have circulating around, so how is it that obese people keep wanting to eat if leptin is supposed to tell you to stop eating? Much like insulin, the brain can become desensitized to leptin, no longer being able to get the signal that the stomach is full enough.
Leptin acts directly on the hypothalamus, meaning that it can indirectly change the hormones being secreted and the behavior that you display. Leptin can either make you feel happy and satisfied or ‘hangry’ as hell.
Leptin acts in the central nervous system to not only control energy homeostasis (and indirectly to control mood), but it also seems to indirectly affect glucose production and therefore the circulation of insulin. Leptin deficiency and/or leptin resistance has been linked to insulin resistance. Think about that, if you’re resistant to leptin, the body doesn’t know when you’re full enough, that in turn may trigger overeating of foods that breakdown into glucose, which will trigger lots of insulin to be secreted, which may cause insulin resistance if this cycle of overeating persists.
The question is, which came first, the leptin or the insulin? It could also be that insulin resistance causes the increase of adipose tissue over time, which then increases the leptin to a point of leptin resistance, making the weight gain and behavioral problems even worse.
Either way it’s a bidirectional relationship with insulin and leptin. Both are needed: one for the proper use of energy in the body and the other to tell you when you can stop consuming energy. They are the yin and the yang of each other, they both need the other to stay in balance.
I hope that cleared up a little bit of the insulin/leptin haze. This is just the surface of the biology, but it’s a great place to start. The take home message: don’t each tooooo much sugar or carbs that breakdown into glucose and listen to your leptin when it tells you you’re full.