All About Cholesterol: Busting the Myths About Fat and Heart Health
- Eleonora Patsenker
- Jun 19
- 12 min read
We’ve been told for decades: “Cholesterol clogs your arteries. Fat is dangerous. Statins are the answer.” But what if much of that advice is outdated, oversimplified — or just plain wrong? In this deep-dive guide, we’ll bust the biggest myths about cholesterol, fat, and heart health — and reveal what modern science actually says. You’ll learn the real roles of LDL and HDL, how sugar and insulin quietly drive cholesterol problems, and why fat isn't the enemy (in fact, it might be your ally).
Oh — and yes, we’ll even explore how cold exposure can help rebalance your lipid profile.
Let’s cut through the noise and get to the truth — with logic, clarity, and practical insights you can use right away.
🧬 Where And How Is Cholesterol Synthesized?
It's true — cholesterol is produced by the liver. In fact, 80% of the cholesterol in your body is synthesized by the liver, not directly absorbed from food. That means you don’t simply “eat” cholesterol — you give your body signals that influence how much it produces. For example, sugar, stress, and a sedentary lifestyle often have a worse impact than eating fatty fish or eggs.
1. Endogenous synthesis in the liver (main pathway)
Up to 80% of all cholesterol is produced by the liver
Starting material: Acetyl-CoA (a universal metabolite)
Acetyl-CoA comes from:
Sugar/glucose (via glycolysis → pyruvate → acetyl-CoA)
Fructose (especially fast → lipogenesis)
Fats (through their breakdown, but this contributes less)
Key enzyme: HMG-CoA reductase
→ This is the enzyme blocked by statins
2. Intake from food (~15–20%)
Cholesterol is found in animal-based foods (e.g., eggs, liver, meat)
However: the body regulates absorption!
If you eat a lot of cholesterol → the liver reduces its own production
If you eat less → the liver increases its synthesis
3. Synthesis in other tissues (additional source)
Intestines, adrenal glands, skin, brain
These tissues produce cholesterol for local needs (e.g., membranes, hormones)
Their contribution to overall blood cholesterol levels is small
4. Conversion from fats under energy excess
When overeating carbohydrates (especially sugar and fructose), the liver:
Converts the excess into fats (triglycerides)
Produces cholesterol as a byproduct
→ This is part of metabolic syndrome
🧬 LDL, HDL, And Cholesterol
Indicator | Role in the Body |
LDL (Low-Density Lipoprotein) | 🚚 Transports cholesterol from the liver to tissues: cells, adrenal glands, brain, reproductive organs — essential for building membranes and hormones |
HDL (High-Density Lipoprotein) | ♻️ Collects excess cholesterol from tissues and blood vessels and transports it back to the liver for reuse or disposal |
🔹 LDL (Low-Density Lipoprotein) is not fat or cholesterol itself, but a transport particle, like a packed delivery truck.
It consists of:
An outer shell made of proteins and phospholipids (Apolipoprotein B100)
Inside — fats (triglycerides) and a few cholesterol molecules
Its role is to deliver cholesterol and fats from the liver to the cells that need them
🔹 Cholesterol is a molecule that cannot float in the blood on its own because it’s not water-soluble→ That’s why it must be “packaged” into lipoproteins, like ships or containers
🚛 In other words:
LDL = a container carrying cholesterol to the cells via the bloodstream
HDL = a container collecting excess cholesterol and returning it to the liver
🤔 So why is LDL blamed for "clogging arteries"?
Here’s the key point:
LDL under normal conditions:
Delivers cholesterol where it’s needed (e.g., for membranes, hormones, vitamin D, etc.)
But if:
There is too much LDL
It circulates too long in the bloodstream
It gets oxidized
And there’s inflammation in the vessel wall at the same time
→ Then the oxidized LDL gets embedded in the vessel wall
→ It activates immune cells (macrophages)
→ Triggers an inflammatory response → plaque formation → atherosclerosis
❗️So it’s not cholesterol itself that’s the problem — it’s the damaged, oxidized form that ends up in the wrong place at the wrong time.
🔄 How Does HDL "Neutralize" LDL?
Not in the sense of “killing” it like a poison, but rather by balancing its function and preventing it from becoming harmful:
1. Reverse cholesterol transport
HDL collects excess or oxidized cholesterol from cells, macrophages, and blood vessel walls
It returns this cholesterol to the liver, where it’s either turned into bile acids or reused
2. Cleans the vessels of “debris”
When LDL gets oxidized and sticks to vessel walls, HDL arrives to “sweep it out”
This helps prevent inflammation and plaque buildup (atherosclerosis)
3. Antioxidant and anti-inflammatory roles
HDL carries enzymes and proteins that:
Reduce LDL oxidation
Calm down inflammatory processes in vessel walls
🧠 Why is this important?
If someone has high LDL, but also high HDL and low triglycerides, it means:
The system is functioning well
Cholesterol is “circulating properly”
Nothing is getting stuck in the vessels
There is no inflammation or accumulation of “gunk”
⚠️ But if LDL is high, HDL is low, triglycerides are high, and inflammation markers are elevated — that’s a high-risk situation: LDL starts building up in the arteries, and there’s no one to clean it up.
📊 Example:
Parameters | Interpretation |
LDL = 180, HDL = 60 | ⚖️ Balanced → the body is handling it well |
LDL = 180, HDL = 30 | 🚨 Imbalance → higher risk |
LDL = 180, HDL = 60, TG = 70 | 🟢 Ideal metabolic background |
🥑 What affects LDL levels?
You need to look at the full context:
Total cholesterol, LDL, HDL, triglycerides, atherogenic index
Insulin, fasting glucose, HbA1c
Inflammatory markers (CRP)
Your lifestyle, diet, weight, activity level
Genetic predisposition
🧬 PHYSIOLOGICAL BLOOD LIPID RANGES
(For a healthy person not on medication)
All values in mg/dL. To convert to mmol/L, divide by ~39 (cholesterol) or ~88 (triglycerides).
Marker | Reasonable Range | Comment |
Total Cholesterol (TC) | 160–240 mg/dL | Up to 240 is absolutely normal. Cholesterol is a builder, not an enemy. |
LDL (“bad”) | 90–150 mg/dL | Up to 150 is acceptable with a healthy background (low inflammation, normal TG & HDL) |
HDL (“good”) | >50 in women, >45 in men | The higher, the better. Vessel protector. |
Triglycerides (TG) | <100–120 mg/dL | Low TG = healthy metabolism. High = sign of sugar/fructose/alcohol/insulin excess |
Atherogenic Index | <3.0 | (TC – HDL) / HDL. Lower = safer |
non-HDL Cholesterol | <160 mg/dL | This includes all “bad” cholesterol: LDL + VLDL |
Lp(a) | <30 mg/dL (or <75 nmol/L) | Genetic marker, test it once in life |
VLDL | <25–30 mg/dL | Linked to triglycerides, reflects sugar and insulin levels |
🧠 Clarification & Logic:
LDL is essential for regeneration, immunity, and hormone production.
It only becomes “bad” in conditions of chronic inflammation, oxidation, or insulin resistance.
HDL cleans vessels and returns cholesterol to the liver.
It increases with movement, healthy fats, and good metabolism.
Triglycerides respond rapidly to diet. If they’re high — it’s usually due to excess sugar, fructose, alcohol, or insulin.
Atherogenic index is a valuable balance marker: low = low risk.
A total cholesterol of 240 mg/dL is not a problem — if everything else is fine.
🔄 When to worry?
Not by one number alone! Look at the context:
High LDL (>170–190) + low HDL + high triglycerides + elevated CRP or insulin = risky profile
But if LDL is high, TG are low, HDL is high, insulin is normal → you’re probably a healthy person, not a patient
🧘♀️ For a healthier lifestyle:
✅ Remove processed carbs and sugar
✅ Add physical activity (especially cardio and walking)
✅ Include omega-3 fats (fish, flaxseed oil)
✅ Sleep and rest — stress raises cholesterol
✅ Reduce alcohol, smoking, and excess weight
💡 If you’re overweight or have metabolic issues, insulin resistance is often the hidden root of high LDL.
ATHEROGENIC INDEX — One of the simplest and most useful ways to assess whether your cholesterol is actually “dangerous” for your blood vessels.
It shows the balance between the “bad” and “good” fats in your blood.
🔢 How To Calculate The Atherogenic Index:
Atherogenic Index = (Total Cholesterol – HDL) / HDL
In international practice, it’s often called the Castelli Index.
Example Calculation:
Total Cholesterol (TC): 220 mg/dL
HDL: 55 mg/dL
Then: (220 – 55) / 55 = 165 / 55 = 3.0
✅ Result = 3.0 → Upper limit of normal. Not alarming, but worth keeping an eye on.
📊 How to Interpret the Result:
Index Value | Risk Assessment |
< 2.0 | Excellent — very low risk |
2.0–3.0 | Normal/moderate risk |
> 3.0 | Elevated risk — consider lifestyle changes |
⚠️ Why It Matters:
This index is more informative than just saying “LDL is high”
Especially helpful for those with borderline numbers — e.g., when LDL is slightly elevated but HDL is also high
🧬 How Does Sugar Raise Cholesterol?
1. Excess sugar → turns into fat
When you eat sugar (glucose, fructose, pastries, juices, etc.) and your energy needs are already met:
👉 Your liver begins converting sugar into fats — including triglycerides and cholesterol.
📌 This is called de novo lipogenesis — creating new fats from carbohydrates.
2. Insulin — the “fat protector”
Sugar triggers insulin release, and insulin:
Tells the body: “Don’t burn fat — use sugar instead!”
Stimulates cholesterol synthesis in the liver
Raises LDL, lowers HDL
So every sweet snack adds not just to your belly — but also to blood fat levels.
3. Fructose is especially sneaky
Fructose (in juices, honey, corn syrup) doesn’t spike blood glucose, but:
Is only metabolized in the liver
Is almost always converted into fat
Raises triglycerides and small-particle LDL (the most dangerous type)
4. Sugar → inflammation → LDL oxidation
High sugar levels cause inflammation and oxidative stress. Oxidized LDL is the truly dangerous form — it damages blood vessels.
📊 Summary: Sugar = a hidden fat booster
You Eat… | You Get… |
🍩 Sugar & baked goods | ↑ Insulin, ↓ fat burning |
🧃 Fructose & juices | ↑ Triglycerides, ↑ LDL, ↓ HDL |
😬 Frequent snacking | ↑ Inflammation, ↑ LDL oxidation |
❄️ But cold exposure… | ↓ Insulin, ↑ fat burning, ↓ TG |
🧈 Dietary Fats: Harmful, Helpful, Or Neutral?
Sugar is the main hidden disruptor of fat metabolism. But that doesn’t mean dietary fats have no effect — their impact depends on quality, context, and combinations.
Fat Type | Effect on Lipids & Health | Comment |
✅ Monounsaturated (olive, avocado) | ↑ HDL, ↓ inflammation | Very beneficial — foundation of Mediterranean diet |
✅ Omega-3 (fish, flaxseed oil) | ↓ TG, ↓ inflammation, ↑ fat burning | Anti-inflammatory, protect blood vessels |
🧈 Saturated (butter, coconut, ghee) | May ↑ LDL, but also ↑ HDL | Context-dependent — can be neutral or beneficial |
⚠️ Trans fats (margarine, fast food) | ↑ LDL, ↓ HDL, ↑ inflammation | Universally harmful — drive atherosclerosis |
⚠️ Excess omega-6 (refined oils) | ↑ Inflammation, ↑ LDL oxidation | Harmful when overconsumed or heated |
🔬 What Science (and Common Sense) Show:
Saturated fats (like butter or meat) may slightly raise LDL, but:
They usually also raise HDL
LDL increase isn’t dangerous if inflammation is low
LDL particle size tends to increase → less atherogenic
Effects depend greatly on overall metabolic and insulin status
Monounsaturated fats (olive oil, nuts, avocado):
Improve lipid profiles
Reduce inflammation
Support vascular function
Trans fats and refined oils (sunflower, corn in excess):
Are genuinely harmful
Increase the risk of heart disease
💡 Important Principle:
Fats from food don’t end up in your bloodstream directly. It all depends on your hormonal and metabolic background at the time you eat them:
Eat butter with porridge and sugar → the effect may be harmful
Eat butter with eggs and greens → the effect may be neutral or even beneficial
Fat isn’t the enemy by itself. What’s harmful is fat in a chaotic environment — when insulin, blood sugar, or inflammation are high. Then, any fat can become dangerous. But if you're eating quality fats, not overloading on sugar, and staying active — your body will process them smoothly, without harm.
✨ What to Do in Practice:
✅ Eat natural fats: fish, eggs, butter, olive oil
✅ Avoid refined oils and reused frying oils
✅ Don’t mix fats with fast carbs (e.g., bread + butter = 🚫)
✅ Don’t fear eggs and butter if your triglycerides and insulin are normal
🌻 The Problem With Vegetable Oils: Not All Are The Same
When people say “vegetable oils are harmful,” they don’t mean all plant oils — they’re referring specifically to refined industrial oils high in omega-6 fatty acids.
🧬 The Biochemical Problem:
Omega-6 fatty acids (e.g., linoleic acid) aren’t bad by themselves — but in excess, they promote inflammation, disrupt fat metabolism, and contribute to oxidative stress.
In modern diets (especially with processed foods), the omega-6 to omega-3 ratio can reach 20:1, while the ideal ratio is 1:1 to 4:1.
This imbalance fuels chronic inflammation — increasing the risk of metabolic diseases, atherosclerosis, obesity, and even depression.
🚫 Oils to Avoid — especially for frying:
Oil | Why It’s Harmful |
🌽 Corn Oil | Very high in omega-6, oxidizes easily when heated |
🌻 Sunflower Oil | Especially the refined type — extremely high in omega-6 |
🟡 Soybean Oil | Common in processed foods, disrupts balance |
🟠 Cottonseed Oil | Industrial, often contains solvent residues |
🌰 Peanut Oil (refined) | Low heat stability |
🌱 Margarine & Spreads | Contain hydrogenated fats → trans fats = dangerous for arteries |
✅ Safe and Healthy Fats:
Oil | Best Use | Why It’s Good |
🫒 Olive Oil (extra virgin) | Cold dishes & light sautéing | Monounsaturated fats, antioxidants, low omega-6 |
🥥 Coconut Oil | Baking and frying | Saturated fats = stable at high heat |
🧈 Ghee (clarified butter) | Excellent for frying | Heat-stable, minimal residues |
🧈 Butter (in moderation) | Cooking (not high heat) | Natural, contains vitamins A and K2 |
🐟 Fatty Fish (not oil, but crucial) | — | Omega-3 source, balances omega-6 excess |
🌰 Avocado Oil | Frying and salads | Rich in monounsaturated fats |
🌰 Macadamia / Walnut Oil | Cold dishes only | High in antioxidants, moderate omega-6 |
🧪 For the “Biochemistry Nerds”:
Linoleic acid (C18:2, omega-6) oxidizes easily → forms oxylipins (oxidized fat metabolites), which activate inflammatory pathways (e.g., via PPAR and NF-κB receptors)
The issue isn’t the fatty acid itself, but its excess and instability when heated
Especially harmful are repeated heating cycles (e.g., deep frying) → lead to the formation of aldehydes, trans fats, acrylamide
🧠 Practical Tips:
Avoid sunflower, corn, and soybean oils — especially for frying
Olive oil is OK, but don’t use it on high heat
Fry with coconut oil, ghee, avocado oil, or butter (in moderation)
Maintain your omega-3 levels: eat fatty fish, flaxseed oil, chia
Eliminate margarines, spreads, anything “low-fat,” and processed foods
🧬 Can HDL Be High But “Useless”??
Yes. HDL can be:
Numerically high, but
Functionally inactive: it doesn’t clean blood vessels, doesn’t suppress inflammation, and doesn’t carry cholesterol back to the liver
🧪 When Does That Happen?
Chronic inflammation (metabolic syndrome, obesity, type 2 diabetes)
→ HDL proteins get modified
→ HDL loses its antioxidant properties and may even become pro-inflammatory
Oxidative stress
→ Damages HDL’s structure
→ HDL can’t extract cholesterol from vessel walls
Hormonal imbalances
→ In hypothyroidism, high cortisol, etc., HDL function decreases
Genetic mutations (rare)
→ Some people have high HDL but still a high risk of heart disease
🔍 How Can You Know?
Unfortunately, standard lab tests don’t show whether HDL is working properly — they only show the amount, not the function.
Some research labs can test for:
Cholesterol efflux capacity (CEC) — HDL’s ability to extract cholesterol from cells
Enzymatic activity of HDL (e.g., paraoxonase)
But these tests are not available in regular clinics.
🧠 So What Should You Do?
👉 Look at the whole picture, not just HDL:
If... | Then... |
HDL is high | 🔍 That’s good — but not a guarantee |
Triglycerides are low | ✅ Excellent — sign of good metabolism |
Insulin and CRP are normal | ✅ Low inflammation |
Weight, blood pressure, and activity are fine | ✅ HDL is likely functional |
But if TG are high, insulin is elevated, there’s excess weight | ⚠️ HDL might be “pseudo-beneficial” (looks good, doesn’t work) |
🎯 What Affects HDL Level And Quality?
Factor | Effect on HDL |
Physical activity | ↑ Increases HDL |
Low insulin / low sugar | ↑ Increases HDL |
Saturated fats (in moderation) | ↑ Raises HDL |
Omega-3 intake | ↑ Improves HDL function |
Smoking | ↓ Lowers HDL |
Chronic inflammation | ↓ Reduces HDL quality and function |
Insulin resistance / obesity | ↓ Lowers HDL |
Moderate alcohol (e.g., red wine) | ↑ May raise HDL (in some cases) |
❄️ How Does Cold Affect Fat Metabolism And Blood Lipids?
Cold is a metabolic stressor that triggers:
Activation of brown adipose tissue (BAT)
→ Enhances thermogenesis
→ Increases energy expenditure from fats (including triglycerides and lipoproteins)
Improved insulin sensitivity
→ Less insulin = less fat storage
→ Normalization of lipid metabolism
Reduction of chronic inflammation (if cold exposure is regular and not excessive)
→ Less oxidation of omega-6 fats
→ Fewer pro-inflammatory oxylipins
→ Reduced need for “anti-inflammatory” omega-3s
🧬 Connection to Fatty Acids:
Mechanism | Effect of Cold Adaptation |
📉 Reduced triglycerides | Due to increased lipolysis and energy use |
⚖️ Stabilized omega-3/6 balance | Less inflammation → less omega-3 “consumed” to calm it |
🧯 Lower omega-3 demand | Body initiates fewer inflammatory responses |
💪 Increased mitochondrial activity | More fat oxidation → better lipid profile |
🧊 Improved lipoprotein composition | Studies show reduced LDL, increased HDL |
🔬 What Studies and Observations Show:
In one small study, men who regularly practiced cold exposure (e.g., winter swimming) had lower triglycerides than the control group.
Another study showed higher HDL and lower inflammation markers.
BAT activation requires a lot of fatty acids — and it preferentially uses unsaturated fats, including omega-3s.
During cold adaptation, fatty acid composition of cell membranes may shift — especially in mitochondria and BAT.
💡 What Does This Mean?
👉 Cold adaptation helps rebalance fat metabolism:
Fewer harmful omega-6 metabolites
Reduced need for anti-inflammatory omega-3s
Improved LDL/HDL ratio
Lower triglycerides
Less insulin resistance → less internal “spark” for inflammation
✨ Final Thoughts
Cholesterol isn’t the villain — it’s a vital molecule your body depends on for hormones, cell repair, and brain health. The real issue isn’t cholesterol itself, but how your body is handling it.
For too long, we’ve been told to chase numbers and fear fat, while ignoring the bigger picture:
👉 What’s the metabolic state?
👉 Is there chronic inflammation, insulin resistance, or stress overload?
👉 Is your lifestyle working with your biology — or against it?
Mainstream guidelines often push medication as a first solution, especially statins — but that approach doesn’t always address the root cause. In many cases, it may even distract us from what truly matters: the system’s balance, not just lab values.
Instead of fearing "high cholesterol," start asking better questions:
Is my body inflamed?
Am I moving, sleeping, and eating in a way that supports my health?
Is this fat harmful — or healing?
Through conscious choices — reducing sugar, managing stress, moving regularly, and even embracing cold exposure — you help your body do what it was designed to do: self-regulate. Not with fear. Not with guesswork. And not always with pills. Just with clarity, consistency, and care.
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