Healthy fats are one of the most confusing topics in nutrition because people argue like there’s one single answer for everyone. One side says saturated fat is the problem. Another side says saturated fat is misunderstood and sugar is the real enemy. Then you’re left with the question that actually matters: Can I eat butter, ghee, and animal-based fats and still protect my heart?
The honest answer is not a slogan. It depends on your overall diet quality, your metabolic health, your genetics, what you replace fats with, and what your personal labs do over time. Some people feel incredible on a higher-fat, animal-based diet and see triglycerides drop and HDL rise. Others see LDL and ApoB climb sharply. Both can be true, and that’s why this debate never ends online.
This post gives you a practical, research-aligned framework you can actually use. We’ll cover what mainstream heart organizations recommend, why “replacement foods” matter more than most people realize, how to think about LDL vs triglycerides vs ApoB, and how an athletic lifestyle changes the conversation. The goal is not to scare you or sell you a dogma. It’s to help you make decisions you can defend with both logic and measurement.
Executive Summary
1) Heart health is a risk profile, not one number: blood pressure, insulin sensitivity, triglycerides, HDL, LDL/ApoB, inflammation markers, and lifestyle all matter.
2) Many guidelines recommend limiting saturated fat for people trying to reduce cardiovascular risk because saturated fat often raises LDL cholesterol.
3) Replacement matters: swapping saturated fat for unsaturated fats generally shows better risk-marker outcomes than swapping saturated fat for refined carbs.
4) Individual response varies dramatically. If you increase animal-based fats, measure your response over 6–12 weeks and adjust.
5) For athletes, the best approach is rarely extreme. It’s high-quality food, adequate protein, stable fats, strategic carbs, solid sleep, and consistent training.
What “Heart Health” Really Means
Heart health is about long-term probability. It’s not a single lab value. A practical heart-health picture includes:
Blood pressure
Waist circumference and body composition
Resting heart rate and cardio fitness
Fasting glucose and insulin sensitivity
Triglycerides and HDL
LDL (and ideally ApoB if you can get it)
Family history and genetics
Smoking, alcohol, stress, and sleep
Nutrition influences all of these, but not equally. That’s why two people can eat similar diets and see different outcomes. One person’s triglycerides improve dramatically when they reduce processed carbs. Another person’s LDL spikes when saturated fat is high. A third person looks “fine” on standard labs but has high ApoB. Context matters.
Why Saturated Fat Became the Center of the Debate
Mainstream cardiovascular guidelines focus heavily on LDL cholesterol because elevated LDL is associated with increased cardiovascular risk. Saturated fat tends to raise LDL in many people. That’s the basic logic behind “limit saturated fat.”
But here’s where the internet gets sloppy: people treat this as a moral statement instead of a probability statement. The real question isn’t “Is saturated fat evil?” The real question is: How does saturated fat affect your specific risk profile, and what are you replacing it with?
If you remove saturated fat and replace it with refined carbs and processed food, you may not improve your risk profile at all. You might even worsen triglycerides, appetite control, and metabolic health. That leads people to say, “See, saturated fat isn’t the problem.” The truth is: the replacement was the problem.
“The benefits of a ketogenic, fat-based metabolism are many. There’s evidence that such diets can reverse insulin resistance and diabetes, lower blood pressure, increase mitochondrial biogenesis, turn on longevity genes, and reduce oxidative stress and DNA damage. There is further evidence that these diets can decrease appetite, lead to profound weight loss, improve mood, and be protective for our brain. From a cardiovascular risk standpoint, a ketogenic diet has also been shown to decrease triglycerides and metabolic dyslipidemia while increasing HDL. On the other hand, low-fat diets generally increase triglycerides, lower HDL, and raise levels of insulin. Many of us have been wrongly led to believe that eating lots of fat will cause weight gain, but this just isn’t true. It’s completely possible to lose weight, eating fat in a 1:1 ratio with protein. The secret to this is how satiating fat is as a macronutrient. Once we start incorporating more good fat sources in our diet, we may be surprised at how full we feel throughout the day. In this situation, it’s incredibly freeing to no longer be controlled by our appetite all of the time as so many are on carbohydrate-heavy diets. We are not used to thinking of animal fat as a nutrient source, but it’s a uniquely valuable food we have sought preferentially throughout our existence that should not be neglected or undervalued.” - Dr. Paul Saladino, Carnivore Code
The Replacement Rule: The Most Important Concept People Miss
In most practical nutrition decisions, what you remove matters less than what you replace it with. A clean way to think about it:
Replacing saturated fat with high-quality unsaturated fats tends to improve risk markers more consistently than replacing saturated fat with refined carbs.
Replacing saturated fat with ultra-processed “low-fat” foods often backfires because appetite, blood sugar, and total calorie intake become harder to control.
This is why a person can reduce saturated fat and feel worse: they replaced it with sugar and processed carbs, became hungry all the time, and ended up eating more overall.
LDL, Triglycerides, HDL, and ApoB: A Simple Working Model
You don’t need to be a cardiologist to understand the basics. Here’s a practical way to think about the common markers:
Triglycerides: often reflect carbohydrate load, alcohol, and metabolic health. Many people see triglycerides improve when they reduce refined carbs and improve training consistency.
HDL: often improves with training and better metabolic health. It’s not “magic armor,” but it’s usually directionally positive.
LDL: can rise with higher saturated fat intake in many people. It can also be influenced by genetics, weight loss, thyroid function, and overall diet pattern.
ApoB: often considered a stronger indicator of atherogenic particle number than LDL alone. Two people can have similar LDL but different ApoB.
The key point: you can’t make serious choices from one number in isolation. You need the overall pattern. Let's see how Dr. Paul Saladino, Carnivore Code, breaks it down:
“Most of the cells in our bodies can make a bit of cholesterol from scratch, but they also rely heavily on the delivered supply of this molecule to build membranes and hormones. In the ovaries and testicles, for instance, cholesterol delivered by LDL is necessary to make the lovely sex hormones estrogen, and testosterone, which are crucial for libido and reproductive function. Without LDL, these and many other steroid hormones wouldn’t be made effectively. Wait, haven’t we been told that LDL is “bad cholesterol” and that the lower it is, the better? I am sad to say that we’ve been led astray with regard to the true character of LDL, which is much more of a superhero than a supervillain. In addition to the vital role transporting building blocks and nutrients, LDL also serves important roles within the immune system. Yes, you read that correctly, LDL plays a valuable part in our response to assault by infectious invaders, as do many of the lipoproteins, including HDL. When gram-negative bacteria seek to invade our body, they release a cell wall component known as endotoxin, which is quite inflammatory and can strongly trigger the immune system. But don’t worry, friendly neighborhood LDL is around to bind up this toxin and prevent things from getting out of hand. LDL also binds to the alpha toxins produced by the gram-positive organism Staph aureus, which has antibiotic-resistance strains known as MRSA. Let’s take a moment to let all of that sink in. In both humans and animals, lipoproteins and LDL are known to serve invaluable roles in immune function. Increasing the amount of LDL in the bloodstream, something that 99% of physicians now fear in humans, resulted in profoundly increased survival when animals were challenged with virulent bacteria. Having a low LDL resulted in mice dropping like flies when exposed to bacteria, but the problem was immediately fixed by giving these poor critters some LDL back.
Clearly, LDL is a valuable particle on our blood and serves many indispensable roles. Doesn’t it seem a bit incongruous that nature would have designed something that is so valuable, but also damages our our arteries and causes atherosclerosis? How can LDL be both protective and harmful? This doesn’t seem to make any sense! The answers that LDL itself is not harmful, but in certain situations that can be involved in the process of responding to injury and inflammation, making it look like it’s a bad actor when it’s merely present at the scene of the crime. The currently accepted paradigm of plaque formation is known as the response-to-retention hypothesis. According to this theory, LDL in our bloodstream passes through the endothelium of the artery wall, and can become retained (“stuck”) in the intimal cell layer below. When LDL gets stuck in the artery wall, it may become oxidized, altering the structure of the APOB100 molecules in its membrane and triggering in immune response in which macrophages within the intima ingest LDL and become lipid-ladened “foam cells”. This is thought to be the beginning of an atherosclerotic plaque. In those with insulin resistance, HDL levels fall and triglyceride levels rise, a change in blood parameters known as dyslipidemia. [HDL levels correlate] directly with insulin sensitivity. Thus, those with the lowest levels of HDL are much more likely to have insulin resistance than those with higher levels of this lipidprotein. Atherosclerosis is about much more than just total cholesterol or LDL. In those who are insulin sensitive, rising LDL levels do not correlate with increased rates of heart disease. When it comes to total cholesterol and LDL, context is everything! If we are insulin resistant, higher levels of LDL may very well contribute to plaque formation and progression, but if we are insulin sensitive, higher levels of LDL are not associated with increased atherosclerosis and are likely protective.
There are more than a quintillion particles of LDL floating around in our bloodstream. That’s 1,000 times more LDL particles than there are cells in our whole body. If every LDL particle that entered the subendothelial space in our arteries led to teh formation of plaque, we’d be deader than a doornail long before our first birthday. Every second of every day, lipoproteins like LDL are moving in and out of the walls of both veins and arteries, delivering nutrients to the cells there for energy and the construction of membranes. Clearly, there must be another part of this equation that leads to retention of some of these LDL particles within the arterial wall. LDL is not enough to initiate atherosclerosis on its own, it has to get stuck in teh arterial wall to participate in this process. What determines how sticky the LDL particle and the intimal wall space are? There’s very good evidence that during the states of insulin resistance and inflammation, both the LDL particle and the intimal space get coated in “molecular velcro” and become more sticky. A whopping 88% of the American population has some degree of metabolic dysfunction [so] if the vast majority of people around us have insulin resistance, is it any wonder that some studies have shown a correlation between LDL levels and cardiovascular disease?”
Where Animal-Based Fats Fit in a Heart-Conscious Diet
Animal-based fats like butter and ghee can fit into a heart-conscious approach when the overall diet is high-quality and measured. “High-quality” looks like:
Protein-forward meals (meat, eggs, fish, dairy if tolerated)
Whole-food carbs when used (fruit, potatoes, rice, squash) instead of refined sugar and flour
Stable fats used intentionally
Adequate omega-3 intake
Minimal ultra-processed food
Consistent training and sleep
Ghee specifically is clarified butter—most milk solids are removed. Some people tolerate it better than butter if dairy causes issues. From a fat profile perspective, it’s still largely saturated fat, so it’s not “free” from a heart-health standpoint. It’s a tool.
Why Athletes Often Experience This Differently
Athletes and active people often have better insulin sensitivity, better triglycerides, and better blood pressure than sedentary people. Training can improve the metabolic environment in which fats and carbs are processed.
But training is not a cheat code that overrides everything. If your LDL/ApoB rises significantly on a very high saturated fat intake, you should take that seriously—especially if you have a family history of cardiovascular disease.
The goal is not to be afraid of animal-based fats. The goal is to use them as part of a broader plan that keeps you performing well and keeps your risk profile within a range you’re comfortable with.
How to Personalize Your Approach Without Guessing
If you want to increase animal-based fats, do it like a professional:
Step 1: get baseline labs (lipid panel; ApoB if possible).
Step 2: run a consistent 6–12 week phase: whole foods, consistent training, stable fats, carbs timed around training, minimal processed food.
Step 3: retest labs.
Step 4: adjust based on your response.
If LDL/ApoB climbs more than you want, you’re not “failing ancestral nutrition.” You’re simply learning your response. Options include:
Reduce total saturated fat dose while keeping animal-based nutrition intact.
Shift some fats toward monounsaturated sources (olive oil, avocado) while maintaining high protein.
Increase omega-3 intake (fatty fish, fish oil if appropriate).
Increase fiber-rich whole foods (vegetables, berries) to support overall health.
Tighten up alcohol and refined carbs, which can worsen triglycerides and appetite control.
Prioritize sleep and stress management, which influence metabolic markers more than most people admit.
Cooking Oils, Seed Oils, and the Real Risk Conversation
A lot of people get stuck in “seed oil wars.” Here’s the practical view: ultra-processed foods are a consistent problem for health. Whether your concern is refined carbs, industrial oils, or additives, the easiest win is still the same: eat mostly whole foods.
If you’re cooking at high heat, stable fats and oils matter. Many people choose ghee or other stable fats for cooking. If you use plant oils, choose ones that fit your tolerance and goals. The bigger risk is not the oil on your pan—it’s living on processed snacks and restaurant food every day while barely sleeping and barely moving.
Frequently Asked Questions
Is saturated fat always bad?
No. But it can raise LDL in many people, and guidelines aiming to reduce population risk generally advise limiting it, especially for those with elevated cholesterol.
What if my triglycerides improved but my LDL went up?
This is common. It’s why you need to evaluate the whole pattern and consider ApoB. Work with your clinician if you’re unsure.
Is ghee “heart healthy”?
Ghee can be part of a heart-conscious diet depending on total diet quality and your labs. It’s not magic, and it’s not automatically harmful. Dose and context matter.
What’s the simplest heart-conscious upgrade?
Reduce ultra-processed foods, prioritize protein, build fitness, improve sleep, and ensure omega-3 intake is solid.
Try Hunghee
If you’re fueling for performance and you want clean ingredients, keep it simple. Hunghee is built from organic grass-fed ghee, local raw honey, and ancient sea salt—portable fuel designed for adventure and training days, without seed oils or filler ingredients.
References & Resources
American Heart Association — Saturated fats guidance
American Heart Association — Dietary fats overview
Sacks et al. (2017) — AHA advisory: dietary fats and cardiovascular disease
Lichtenstein et al. (2021) — AHA dietary guidance statement
Hooper et al. (2020) — Cochrane review: reducing saturated fat
Siri-Tarino et al. (2010) — Meta-analysis: saturated fat and cardiovascular disease
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Disclaimer: This content is for informational purposes only and is not intended as medical advice. Please consult your healthcare provider for advice about a specific medical condition or before starting any new fitness or nutritional program.