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Danbee Shin

👊🏼 A nutrition blog about making your own food decisions ⏲ On a timeout to make better things 👩🏻‍💻 Get in touch and I’ll let you know when we’re live

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My head’s been feeling very disorganised — I’m not writing regularly, or taking any new photos, or getting enough sleep. It doesn’t help that the World Cup is on. 💁🏻‍♀️ I know what I need to do to put things right but — I just keep spending what free time I have watching Netflix (I’ve just discovered the wonderfully trashy Revenge 🙈). But in the middle of this quiet chaos I did manage to clean up our new guest-room-slash-home-office so I actually feel like working at the desk. And I wrote this little post about something called apolipoprotein B-100, or apoB for short. ✏️ Some experts say LDL **apoB** levels are a better predictor of atherosclerosis than LDL **cholesterol** levels. This means decreasing the number of LDL particles in your blood could be more important than lowering the amount of LDL cholesterol in your blood when it comes to maintaining plaque-free arteries. Read the post here: (link in bio) . #foodblogfeed @foodblogfeed #foodblogeats #healthyish #feedyourglow #iamwellandgood #foodwinewomen #appetitejournal #eatprettythings #goodmoodfood #thenewhealthy #foodrevolution #foodinspo #kitchn #feedfeed #onmytable #flatlaybreakfast #avocado #homemade #nutritionfirst #foodfacts #wholefoods #foodscience #hearthealth #hearthealthy


I don’t even want to think about how long it’s been since I last published a post. The boyfriend and I just moved apartments (and he just moved countries and jobs!) so it’s been a hectic couple of weeks — we’re now almost fully unpacked and organised, and no longer eating breakfast on a blanket on the kitchen floor (though we still apparently need to wait six weeks for our sofa to arrive from China). I’ve been working on this post for a while and it’s time to share it in the form it’s in right now: . It’s all about how yes, our bodies *can* convert carbs to fat, but that really isn’t what we should be worrying about. Eating too many of our calories as carbs will make us fat — but not because those carbs are turning into fat. Yes, really. . #foodblogfeed @foodblogfeed #foodblogeats #healthyish #feedyourglow #iamwellandgood #foodwinewomen #appetitejournal #eatprettythings #goodmoodfood #foodrevolution #foodinspo #kitchn #feedfeed #onmytable #gloobyfood #breakfastinbed #pancakesunday #pancakestack #buttermilkpancakes #ahealthynut #inspirehealth #feelgoodfood


I dug deeper into what happens when we eat food that contain fats and cholesterol. How do we make low density lipoproteins — aka LDL, aka the bad cholesterol — from what we eat and what our bodies make? Today’s post breaks down the four main steps: . Why the hummus? Because it’s got a ton of olive oil in it and I want to eventually find out why people say olive oil is “good for your cholesterol”. . #hummus #foodblogfeed #foodblogeats #healthyish #eatprettythings #thenewhealthy #thekitchn #nutritionfirst #foodscience #hearthealth


Turns out, LDL cholesterol (the “bad” cholesterol) most probably *is* bad for you. It could also just be *oxidised* LDL — the version of LDL you get after reactive oxygen species (ROS) have had a go at them, which is what happens when your arteries suffer from chronic inflammation. Scientists don’t seem to know for sure just yet. I’ll try to find out what we do know. In the meantime, I’m going to keep gobbling up this awesome combination of coconut chia pudding and blueberries, and will the antioxidants to help keep my arteries clean. Find today's post at


I’m calling today’s post “Medical Terms I Thought I Knew”. This week’s “bomb” (à la “Happier in Hollywood” by @sfain and @lizcraft): failing to write the post I wanted this week because I skipped over the basics. Find it at


. 🤕 It’s an immune response . I promised to share here why it’s important that where blood flow in arteries is slower and disrupted, there are: . 1. More holes in the artery wall, and 2. More white blood cells. . 🧐 Let’s go back to LDL . LDL is called the bad cholesterol because it’s associated with plaque build up in our arteries. . This is why: . 1️⃣ LDL molecules are usually happily swimming through your bloodstream. But where blood flow is disrupted, they can enter your artery walls through leaky junctions. (More holes!) . 2️⃣ LDL molecules become oxidised by reactive oxygen species (ROS). ROS are highly reactive molecules. You might have heard of free radicals — they’re unstable and reactive because they contain unpaired electrons (electrons are stable in twos). Free radicals are a kind of ROS. . 3️⃣ Your body sees oxidised LDL as a threat, and activates your immune response: your white blood cells devour the oxidised LDL. (More white blood cells!) White blood cells + destroyed oxidised LDL = foam cells. . 4️⃣ When foam cells accumulate, they form that dreaded plaque. At first the plaque is made up mostly of soft, fatty cells.(fn) . 5️⃣ Muscle cells in the artery walls then multiply to form a hard shell around the soft, fatty core, adding to the plaque.(fn) . 😨 From plaque to blocked arteries . Plaque is worrying because it leads to heart attacks and strokes. Here’s how: . 1. Plaque can break through the inner layer of your artery walls, into the bloodstream. Scientists don’t yet fully understand why this happens. But one definite reason is because the dead cells in the plaque release substances that weaken the hard shell. . 2. After the plaque ruptures, a blood clot forms where the plaque leaves a hole in the arterial wall. This blood clot can get bigger and bigger, at first reducing the amount of blood that flows past it, then blocking the artery all together. . 3. This means your blood can’t deliver oxygen to different parts of your body. If your heart is affected, you’d get a heart attack. If your brain is affected, you’d suffer a stroke. . The good news: plaque **can** be reduced. More on this next time.


. 🍝 Imagine your blood vessels are hollow spaghetti . Atherosclerosis is when plaque builds up along your artery walls — actually, it builds up just under the inner layer of your artery walls, to be precise. . If you picture a piece of tube-shaped pasta, with the blood flowing through the tube, the plaque would accumulate inside the pasta dough, under the surface closer to the blood flow. . 🏎 Your blood flow changes speed and direction . Now forget the pasta. Pasta has the same shape throughout. . Your arteries don’t. They change shape — they branch and curve. This makes the bloodstream change in speed and flow pattern. . There are three important things that happen where blood flow is slower and disrupted. . 1️⃣ The artery wall makes less nitric oxide. This is important because nitric oxide protects against atherosclerosis by widening blood vessels, increasing blood flow. . 2️⃣ Artery wall cells are more likely to die. Where cells are dying (and dividing, to make up for those dying cells) small holes form in the artery wall. These holes are called leaky junctions (yes, really). Unsurprisingly, there are more leaky junctions where blood flow is slower and disrupted. . 3️⃣ More white blood cells come to hang out. White blood cells are your defence cells, and protect your body against foreign invaders. An increase in white blood cell count is a response to inflammation. Inflammation is your body’s response to injury. . Why are points 2 and 3 important? Find out in my next post.


. 🤔 What is cholesterol? . As soon as you start looking up different kinds of fats, articles pop up telling you how fats affect your cholesterol. . So I took a step back to ask: What is cholesterol, anyway? . But google virtually any phrase including the word “cholesterol”, and you’ll soon come across the phrases “high density lipoproteins” and “low density lipoproteins”. . 😦 What are lipoproteins? . What makes a protein a lipoprotein? Combining with lipids. . What are lipids? All sorts of substances in our bodies that do not dissolve in water. Think of them as fats for simplicity’s sake. Fatty acids and steroids are examples of lipids. . And where does cholesterol come in? It’s a type of steroid. Sex hormones are also steroids, and are made from cholesterol. . 😧 Why do we make lipoproteins? . So why do proteins and lipids combine to form these lipoproteins? . Lipids move around the body through the bloodstream. We need them for storing and producing energy, for getting our cells to work properly, for making hormones — we would die without lipids going where they need to go. . Blood plasma — the watery part of blood — can only transport substances that are dissolved in it. . And what do we know about lipids? They don’t dissolve in water. So they don’t dissolve in blood plasma, either. Instead of being carried by the blood, they would rise to the top, like oil on water. . Free fatty acids overcome this problem by binding to blood proteins and moving with them. But other lipids, like cholesterol, need to form a special structure that can be carried by the blood — and lipoproteins are the solution. . 🙄 Can we talk about cholesterol now? . There are many different kinds of lipoproteins, but in the context of cholesterol, we mostly talk about low density lipoproteins (LDL) and high density lipoproteins (HDL). This is because cholesterol is the major lipid in LDL and HDL. . LDL carries most of the cholesterol in our blood. HDL carries excess cholesterol from around the body back to the liver. The liver then removes the cholesterol by converting it into bile salts, which ultimately end up in our poop!


. 📺 We interrupt this programme . I’m supposed to be researching different kinds of fats right now, but I’m putting that aside — just for today — to share some news. I met with my endocrinologist today and received the results from the oral glucose tolerance test I took a couple of week ago. . 🔎 The numbers have spoken . It’s official. I do have insulin resistance. The situation is actually more serious than I’d ever anticipated — I’m prediabetic. . I have to admit I was more than a little surprised when my endocrinologist looked at my results a second time and said they show impaired glucose tolerance. . *He* looked surprised. He’d been saying things like, “you just look too healthy to be insulin resistant,” and “look at your BMI, it’s perfectly within the healthy range”. . We’d also looked at my fasting glucose, fasting C-peptide, and Hb1Ac numbers — all of which were normal. . I did pause before typing out my test results. But at the end of the day, I’d like to share helpful information more than I’d like to keep this data private. Head over to to see my numbers (and a more complete post). . The big takeaway: while my fasting numbers are normal, all three indicators — glucose, insulin, and C-peptide — are all far too high at two hours after “eating” glucose. This shows that although my insulin resistance is not *too* serious, my glucose and insulin levels are dangerously high. . I need to get better at using up glucose. . 📑 I have an action plan . I came home with 120 tablets of Metformin. Taking two a day is supposed to help improve my insulin resistance. You know I’ll be digging into the science behind this prescription before long. . The changes I made years ago to improve my insulin resistance — exercising more, eating fewer carbs, and sleeping for longer — now feel more important than ever before. . I’ve been planning on doing a February @whole30, and I’m super motivated to cut out the sugar and the alcohol I’ve been indulging in over the last couple of months to kickstart another year of healthful eating. (The holidays really are over, aren’t they?)


. 🥛 Remember fatty acids? . When we eat fats, they are broken down into fatty acids and glycerol. Three fatty acid molecules and one glycerol molecule make up one fat molecule. . It’s the structure of the fatty acids that determines the kind of fat. The first distinction: saturated or unsaturated? . 🥩 ‘Cause it’s all about the fatty acids . If a fat is saturated, it contains lots of saturated fatty acids. If a fat is unsaturated, it contains lots of unsaturated fatty acids. . What are these fatty acids saturated or unsaturated with? Hydrogen atoms. . A fatty acid molecule contains a chain of carbon atoms. Each carbon atom “holds hands” with two other carbon atoms to form the chain. Think: left hand left, right hand, right. . You might remember from middle school chemistry that each carbon atom forms four bonds. So there are two remaining bonds: two different possibilities. . 1. If the carbon atom uses them to join with two different hydrogen atoms, it forms two single bonds. . 2. If it uses them to join with just one hydrogen atom, the remaining bond doubles up with the existing bond with one of the next door carbon atoms. A double bond counts as two bonds. . In either case, you get four bonds in all. . If a fatty acid only has no double bonds between carbon atoms — i.e. scenario 1 for all carbon atoms — it’s *saturated*. . If a fatty acid has one double bond between carbon atoms — i.e. scenario 2 for two of the carbon atoms — it’s *unsaturated*. Specifically, it’s *monounsaturated*. . If a fatty acid has two or more double bonds between carbon atoms — it’s also *unsaturated*. You guessed it: it’s *polyunsaturated*. . 🍣 Why do we care about the fatty acids? . Different fats perform differently when they’re cooked, and when they’re digested. What determines these differences are the fatty acid structures. . The logical next step is to look at how each type of fat affects our food and our bodies, and that’s exactly what I’ll be doing over the next several days. . 👩🏻‍🔬 Annotated reference list:


. 🙃 Fats are full of emotions . There’s a lot of conflicting information out there about fats. Do you know what else there is a lot of out there about fats? Judgement. Guilt. Confusion. . Maybe your coworkers make exaggerated, snide comments when you pick up a freshly deep fried, breaded chicken katsu for lunch. How should you respond? Should you defend your (oh-so-delicious) choice? . Maybe you feel bad about enjoying the taste of pork belly melting in your mouth at your go-to Korean barbecue joint. Shouldn’t you be free to just savour the goodness? Aren’t you feeling bad just because you’ve been conditioned to feel that way when eating fattier meats? . Maybe you aren’t sure which kind of milk to add to your coffee so you play it “safe” by going half-and-half. That’s definitely supposed to be hip and healthy — right? No one likes that kind of uncertainty. Don’t you want to make that decision knowing full well what the consequences are, even if — no, especially if — it means you’re choosing what’s bad for your longer-term health? . 😉 I’ll tell you for free: stress is bad for you . Ideas about fats make for a very stressful life — so let’s separate the facts from the opinions, and call out the misinformation for the lies that they are.


. 😍 I heart fats . Ah, fats. It makes everything taste better — I prefer chicken thighs to breasts, and think deep frying is food sorcery — and I hear we need the healthy kind. . 😦 Am I doing it wrong? . Yet so many people around me are still choosing zero fat yogurt and skimmed milk, and cutting out fatty bits from their steaks and pork belly slices. . I used to do this, too — but somewhere down the line I must have read something that convinced me it was all good to eat full fat dairy and every bit of the animal if it was raised in a happy place, free from hormones and antibiotics. . 🧐 I've got questions . I have a lot of questions about fats, but at the end of the day, I just want to know what I need to know to decide how much of which fats I want to eat, and how often. Is that so much to ask for? . After giving this topic some thought, I've broken it down to these five questions. . 1️⃣ What makes some fats better than others? (What makes some fats bad?) . 2️⃣ Eating fat doesn't make us fat — does it? . 3️⃣ What's so bad about deep fried food? . 4️⃣ How can we tell if our bodies are adapted to using fat for energy (instead of carbohydrates)? . 5️⃣ What happens if we don't eat fat? . Do you have any fat-related questions you'd like answered?


. 🙈 4,000 words and almost as many hours . This is hard to believe and a little embarrassing to admit — but this article has taken me a year to write and publish. No joke. . To those of you who have been following my previous posts: thank you! This is the culmination of everything I’ve been learning and sharing here over the past month. . ⏱ Here’s the TL;DR. . Insulin resistance disrupts the way our bodies use food for fuel. It’s also closely linked to obesity and diabetes. . With insulin resistance, our bodies become inefficient at using up the glucose in our blood. This leads to high blood glucose levels, which can result in life-threatening diseases that affect the heart, liver, and kidneys. . A more immediate effect of excess blood glucose: our bodies adapt by choosing glucose as the main source of energy. This means the we store new fats we eat, and don’t use up existing fat stores to make energy. . In everyday language: we get fat. . There’s a lot of ongoing research about how we can improve insulin sensitivity. In the meantime, I’ve made three simple (though not so easy!) changes to my lifestyle: exercising more regularly, eating fewer carbs, and sleeping for longer. . 📖 The full article is here, complete with a 39-item annotated reference list: (link in post!)


. 😎 Sleeping is “in” . Okay, this method for improving insulin sensitivity is more appealing than exercise — but I personally find it just as hard to practice. It’s sleep. . There’s a sleep revolution in the air and chances are, you’ve already heard that our bodies heal themselves while we sleep. . 😴 5 hours is not enough . It probably won’t come as a surprise then, to learn that sleep directly affects insulin resistance. Sleep actually has an almost immediate effect on how well your body responds to insulin. . Studies (though admittedly with small sample sizes, often looking at about 10 people at a time) show that it takes just one night of restricted sleep for your body to become less sensitive to insulin. Sleep restriction often means 4-5 hours of sleep a night in these studies. Scarily, this wasn’t unusual for me just a few years ago! . For this series on insulin resistance, I’m focusing just on answering the question, “What is insulin resistance?” — so I’ll save in-depth research about the effect of sleep on insulin resistance for another time. . 👩‍🔬 Annotated reference list here:


. 🏃🏻‍♀️ Not all organs are equal . Remember how having insulin resistance means your body is less sensitive to increases in your insulin levels? This in turn means your body is less efficient at producing energy from the food that you eat. . New fact: insulin resistance can affect specific parts of your body. For example, your skeletal muscles (the muscles we can move voluntarily, not the ones that make up our hearts or our stomaches) could be less sensitive to insulin than your liver, or your fat tissue. . The glucose that your body turns into energy using insulin? Skeletal muscles use up most of that. We obviously want *all* of your body to be insulin sensitive, but we especially want your skeletal muscles insulin sensitive. . 🏋🏻‍♀️ Good news: we have exercise . Exercise can overcome insulin resistance in skeletal muscles. (I know — this good news is also kinda bad.) . When put to work, your skeletal muscles become better at taking up glucose and using it for energy. The more you use them, the more efficient they get. . I mentioned lipotoxicity in my previous post. This is when fatty acids accumulate where they shouldn’t. This is anywhere outside your fat tissue, including kidneys, liver, heart, and — skeletal muscle. Fatty acids damage and kill the cells they occupy. . When you exercise, you also help break down fatty acids accumulated in your muscles more quickly, reducing lipotoxicity. This allows your muscles to work more efficiently. . This is certainly enough to get me in the pool 🏊🏼‍♀️ tomorrow morning! . 👩‍🔬 Annotated reference list here: