For decades, cholesterol has been portrayed as a danger. As a number that must be lowered. As a substance that clogs arteries. As an enemy of the heart. Yet, cholesterol is one of the most important molecules of life. Without cholesterol, there would be no stable cell membranes, no bile acids for fat digestion, no steroid hormones, no vitamin D in its hormonal function, and no healthy communication between cells. Cholesterol is not just a blood value.
It is structure. Protection. Building material. Signaling molecule. Fuel.
This article is a tribute to Dr. Jorge García-Dihinx (MD, PhD), from whose work and lectures I have learned a great deal. He was a Spanish pediatrician with a specialization in pediatric gastroenterology, nutrition, and childhood obesity , as well as a valued health communicator who clearly and practically explained complex relationships regarding metabolism, nutrition, and lifestyle. His clear way of explaining complex physiological connections inspired me to write this article, where I present his thoughts through the BARAU lens on health, skin, energy, and conscious living.
IS CHOLESTEROL REALLY THE PROBLEM?
This is not about ignoring cholesterol levels or downplaying medical risks. It is about asking a question that is asked far too rarely:
Is cholesterol really the problem—or does the fixation on cholesterol distract us from the actual causes of modern metabolic diseases?
85% of cholesterol is produced by the body itself, primarily in the liver. Due to the body's own regulatory mechanisms, dietary intake has only a limited influence. Therefore, the fear of foods like eggs should also be viewed in a more nuanced way. Cholesterol levels should always be viewed within a broad clinical and metabolic context, not as an isolated number.
BUT WHAT IS CHOLESTEROL ANYWAY?
Cholesterol is a fat-like, vital molecule that the body mostly produces itself and requires for cell membranes, hormones, bile acids, vitamin D, and the nervous system. Since cholesterol is not water-soluble, it travels in the blood packed into lipoproteins—primarily LDL, HDL, and VLDL.
Simply put, LDL delivers cholesterol to the tissues, HDL supports the return transport to the liver, and VLDL primarily transports triglycerides from the liver into the body.
Triglycerides represent our most important form of energy storage, particularly relevant in fasting contexts. During fasting, the body obtains glucose from triglycerides and produces ketone bodies, which allows the brain's metabolism to be maintained for days without risk—something that is physiologically normal in humans. You can find more about this in our article Fasting.
The body does not produce cholesterol by accident. It produces it because it needs it.
The majority of our cholesterol is produced in the liver. The organism regulates uptake, production, recycling, and utilization very finely. This in itself shows: cholesterol is not a waste product that the body produces by mistake. It is a biologically necessary molecule.
Cholesterol is a component of cell membranes. It ensures that cells remain stable, flexible, and functional. It influences how permeable a cell membrane is, how well receptors work, and how cells communicate with each other. Furthermore, cholesterol is a precursor for bile acids, which we need to digest fats and absorb fat-soluble vitamins.
Cholesterol also plays a central role hormonally. From cholesterol, the body forms steroid hormones such as cortisol, aldosterone, estrogens, progesterone, and testosterone. An artificial reduction of cholesterol, for example through statins, can therefore also interfere with hormone production. This can affect libido, endocrine balance, and general well-being.
It is likewise closely linked to vitamin D synthesis. Anyone who views cholesterol only as a risk factor overlooks its role as the foundation of many regulatory systems.
Its significance in the nervous system is particularly impressive. The brain contains a significant proportion of the body's total cholesterol. It is essential for myelin, the protective sheath of our nerve fibers, for neuronal signal transmission, synapse formation, and brain plasticity.
Cholesterol also plays an important role in the immune system and in the context of cell protection. It is also of great importance during pregnancy, where the physiological increase in cholesterol is necessary for the creation of life and the healthy development of the fetus.
HOW CHOLESTEROL BECAME THE SCAPEGOAT
For many decades, the narrative surrounding cardiovascular disease was greatly oversimplified: Saturated fat increases cholesterol. Cholesterol clogs arteries. Therefore, animal fats must be reduced and cholesterol levels lowered.
This narrative is catchy. But human metabolism is more complex.
One problem with this perspective is that observations were frequently treated as proof. If a link between fat consumption and cardiovascular disease was observed in certain populations, it was quickly turned into a cause-and-effect narrative. But correlation is not causation.
In this context, Ancel Keys and the 7-Countries Study from the 1960s are frequently referenced. Crucial to this is the criticism that only those countries that fit the hypothesis were selected, while other data that contradicted it were ignored. This created a narrative that strongly influenced official dietary recommendations for decades.
Furthermore, serious errors were made in this study in the classification of foods, where ultra-processed products combining sugar and fat were simply cataloged as "fat," which distorted the results.
And we all know that pure butter or an egg is not the same as an ultra-processed pastry made of white flour, sugar, and refined fats.
And a piece of meat from traditional livestock farming is not the same as a highly processed fast-food menu.
This is exactly where the distortion begins.
Another important point is older controlled studies, such as the Minnesota study. They showed that replacing animal fats with industrial vegetable oils could indeed lower cholesterol in the blood, but was associated with higher overall mortality. These results contradicted the then-dominant lipid hypothesis and were largely ignored for a long time.
Equally critical is the view of vegetable oils and margarines, which were promoted for decades as a "healthy" alternative to saturated fats—primarily because they can lower cholesterol levels. This effect occurs partly because vegetable oils contain sterols and stanols that compete with cholesterol in the gut and inhibit its absorption. But a lower number in a blood test does not automatically mean better health or a longer life.
Several older studies, which are being discussed again today, showed that lowering cholesterol through margarines and oils rich in linoleic acid could be associated with higher overall and cardiovascular mortality. The Sydney Heart Study is also frequently mentioned in this context.
Later large studies like the Women’s Health Initiative also could not show a clear benefit when saturated fats were reduced and grains and vegetable oils were increased at the same time. In certain subgroups with pre-existing cardiovascular disease, there was even an increased risk, even if these results were less visible in the official conclusions.
More recent meta-analyses and review articles of controlled studies up to 2023 also call into question the simple causal link between saturated fat and heart attack or cardiovascular death. The focus should therefore be more on factors that actually throw the metabolism out of balance: metabolic syndrome, chronic stress, elevated cortisol, poor sleep quality, lack of exercise, and a lack of alignment with our natural environment.
THE MORE IMPORTANT QUESTION: IN WHAT ENVIRONMENT DOES CHOLESTEROL CIRCULATE?
Cholesterol does not travel through the blood alone. Because fat and cholesterol are not water-soluble, they need transport systems. These are called lipoproteins. You can think of them as small transport boats that carry energy, triglycerides, and cholesterol to the tissues.
LDL is often referred to as "bad cholesterol." HDL as "good cholesterol." These terms are practical, but misleading. Because cholesterol itself is not good or bad. What is decisive is what happens in the overall metabolism.
It is important to note: Not all LDL is the same. The marker that is associated with a higher cardiovascular risk is primarily small and dense LDL—not an isolated elevated LDL value per se.
Small, dense LDL occurs particularly frequently when triglycerides are elevated, especially above about 100mg/dl, even if many laboratory ranges still classify this value as "normal." However, such normal ranges often reflect a metabolically burdened average population, not necessarily an optimally healthy state. Triglycerides below 80mg/dl, on the other hand, are often associated with good insulin sensitivity and a better ability to use fat as energy.
The relationship between triglycerides and HDL is also crucial. When triglycerides are high, HDL is often low. An HDL above 60mg/dl, by contrast, is often associated with a more favorable metabolic profile and larger, less dense LDL particles.
Therefore, lipid ratios like triglycerides/HDL or ApoB/ApoA1 are often more informative than total cholesterol or isolated LDL. A profile with elevated cholesterol, but low triglycerides, high HDL, and a favorable ApoA/ApoB ratio can point to a metabolically more stable state.
This is a completely different perspective than: "Cholesterol high = danger."
The question is not just, how high is LDL?
The question is also:
-
- How high are the triglycerides?
- What is the ratio of triglycerides to HDL?
- How many atherogenic particles are circulating?
- How stable is blood sugar (HbA1c)?
- How high is the fasting insulin?
- What is the status of inflammatory markers?
- Is there oxidative stress?
- Is there obesity?
- Is there a lack of sleep?
- Is there chronic stress?
Because LDL in a stable, low-inflammation, insulin-sensitive metabolism is not the same as LDL in an environment of hyperinsulinemia, oxidative stress, high blood pressure, and chronic inflammation.
A typical pattern in metabolic dysfunction is: high triglycerides, low HDL, insulin resistance, high blood pressure, a tendency toward fatty liver, and often smaller, denser LDL particles. This pattern is described as atherogenic dyslipidemia and is closely linked to metabolic syndrome and type 2 diabetes.
SUGAR, INSULIN, AND THE BLOCKED FAT METABOLISM
One of the most important points in this context is insulin. Insulin is a vital hormone. It helps bring glucose from the blood into the cells and store energy. It becomes problematic not because insulin exists, but when it is permanently elevated.
Refined carbohydrates, sugar, fructose in an unfavorable context, sweet drinks, and constant meals can lead to the body repeatedly releasing insulin. If insulin remains permanently high, fat burning is blocked. Fat itself hardly stimulates insulin, while carbohydrates can do so much more strongly and for longer. This situation pushes the body into a storage mode and promotes obesity, fatty liver, and atherogenic dyslipidemia.
The combination of glucose and fructose, as found in sugar, sweet drinks, juices, and ultra-processed foods, is particularly problematic. Glucose increases insulin, while fructose is primarily processed in the liver and can be converted into fat there if it arrives in excess together with glucose. This mechanism can contribute to the development of non-alcoholic fatty liver—today even in adolescents.
However, insulin resistance affects more than just blood sugar and fat metabolism. It can also be associated with high blood pressure because elevated insulin can promote the retention of sodium and water via the kidneys. From this perspective, it is insufficient to hold only salt responsible. Modern high blood pressure is often in a broader context with chronically elevated insulin and metabolic dysfunction.
From this perspective, cholesterol is not the beginning of the problem. The beginning often lies deeper: in a metabolism that has lost its flexibility. A flexible metabolism can switch between glucose and fat burning. It can eat and fast. It can store and release. It can regenerate at night and provide energy during the day. You can find more about this in our article Metabolic.
A blocked metabolism, on the other hand, remains in storage mode.
ARTERIES NEED PROTECTION, NOT JUST LOW VALUES
Cardiovascular diseases do not simply arise because cholesterol is present in the blood. What is decisive is the condition of the vessels.
The endothelium, the fine inner lining of our blood vessels, is an active organ. It reacts to blood sugar, blood pressure, inflammation, oxidative stress, smoking, lack of sleep, lack of exercise, and stress hormones. If this sensitive system is permanently irritated, an environment can arise in which deposits, inflammation, and vascular damage become more likely.
Oxidized or glycated LDL also plays a role here. LDL that is altered under oxidative stress or by sugar behaves differently than normal LDL. In the context of metabolic syndrome, inflammation, and insulin resistance, this very altered state of LDL is discussed as a relevant risk factor.
The picture thus becomes more nuanced: the presence of cholesterol alone is not decisive, but rather whether it circulates in an inflammatory, oxidative, insulin-resistant environment.
This is why it is so important not only to think about "lowering," but about "understanding":
-
- What damages my vessels?
- What increases inflammation?
- What robs my body of sleep?
- What keeps my insulin permanently high?
- What takes away my metabolism's natural rhythm?
WHY RISK ASSESSMENT NEEDS MORE THAN LDL
In modern risk assessment, not only cholesterol levels are considered. Cardiovascular risk calculators like Framingham or QRISK take into account factors such as age, sex, blood pressure, smoking, diabetes, psychosocial factors, and cholesterol ratios, because these better reflect the overall metabolic context. ApoB, lipoprotein(a), and the coronary calcium score are also increasingly being discussed as additional markers to better classify risk.
ApoB stands for the number of potentially atherogenic lipoprotein particles, which include, among others, VLDL, IDL, and LDL. However, ApoB should not be viewed in isolation either. Its significance changes when combined with markers of insulin sensitivity, such as the ratio of total cholesterol to HDL. A favorable quotient may indicate a more stable metabolism, even if total cholesterol or ApoB levels are elevated.
Long-term observations show that people with high ApoB but a good quotient and good metabolic health can have a lower cardiovascular risk than people with lower ApoB but insulin resistance. This contradicts the simplistic notion that more LDL or more ApoB is always automatically worse.
This is important because people are different.
A young, slim, insulin-sensitive person with low triglycerides, high HDL, good muscle mass, good sleep, and no signs of inflammation is not automatically comparable to a person who also smokes, sleeps poorly, and has high blood pressure, belly fat, high triglycerides, low HDL, and prediabetes.
The same LDL level can have a completely different meaning in two completely different bodies.
This is precisely why the isolated fear of cholesterol is so problematic. It can lead people to fight a number while leaving the actual causes of their risk untouched.
STATINS: BENEFITS, MECHANISMS, AND OPEN QUESTIONS
Even with statins (also known as cholesterol-lowering drugs), a nuanced view is worthwhile.
Statins do not work by "eliminating" cholesterol. They block cholesterol synthesis in the liver. As a result, the liver forms more receptors and removes more lipoproteins from the blood. Cholesterol does not simply disappear; rather, it is shifted more strongly from circulation toward the liver. In blood tests, LDL levels drop—and this is frequently interpreted as therapeutic success.
However, from this perspective, the potential benefit of statins lies not exclusively in LDL reduction, but also in so-called pleiotropic effects: a mild anti-inflammatory effect, a certain anti-platelet effect, and the stabilization of existing plaques.
At the same time, this benefit should be viewed realistically. In secondary prevention, i.e., in people who have already had a cardiovascular event, studies show a certain benefit. In primary prevention, i.e., in people without existing disease, the effect on all-cause mortality is significantly lower and must be weighed individually.
Possible side effects should also not be ignored: an increased risk of diabetes, muscle pain, loss of strength, potential impairment of mitochondria, changes in libido, or cognitive complaints are mentioned repeatedly in discussions about statins. Particularly in older people, it is relevant that cholesterol also plays an important role in immune function and neuronal integrity.
Therefore, the same applies here: It is not about a blanket "for" or "against." It is about an individual risk assessment, about context, and about the question of whether the human being is truly being treated — or just a laboratory value.
MY PERSONAL PATH: WHY I SEE CHOLESTEROL DIFFERENTLY TODAY
For me, my change in diet was an important turning point.
I realized that healthy fats were not the problem, but rather my previous approach to carbohydrates — even in forms generally considered healthy, such as fructose, whole grains, or seeds.
At the same time, I began to prepare my body more consciously for food intake and to support it in a targeted manner afterward. For me, this included, among other things, fermented vegetables, diluted raw apple cider vinegar before meals, and baking soda with water in the evening.
Additionally, I focused on selected micronutrients and bitter substances, such as vitamin C, sulfur compounds, ginger tea, and other plant-based sources of bitters. Furthermore, I maintained strict light hygiene and used sunlight as a source of health. When I started integrating healthy fats and high-quality protein into my diet daily, not only did my energy levels change, but my blood values and sleep quality also improved.
This experience has fundamentally changed my view of cholesterol. Today, I no longer see it in isolation, but always in the context of metabolism, insulin, digestion, sleep, and the body's ability to truly utilize food well.
For the first time, this change did not feel like a short-term diet, but rather a path to metabolic health.
WHAT THIS HAS TO DO WITH SKIN AND WELL-AGING
At BARAU, we never view skin in isolation.
Skin is not just a surface. It is a mirror, a protective organ, an excretory organ, a sensory organ, and thus part of a larger system. When metabolism is under stress, when sleep is lacking, when blood sugar fluctuates constantly, or when inflammation becomes chronic, this rarely happens without effect on the skin. For me, well-aging does not mean fighting against ageing. It means not putting unnecessary strain on the body and supporting it in its natural regeneration. This applies from the outside and from the inside.
From the outside, it means:
no unnecessary irritants, no synthetic fragrances, no overloaded formulations, no aggressive routines. Instead, high-quality organic natural cosmetics, gentle care, plant-based active ingredients, moisture, protection and rituals that calm the nervous system.
From the inside, it means:
stable blood sugar, enough protein, healthy fats, real food, good sleep, sunlight, exercise, stress regulation and phases in which the body is not constantly busy with digestion.
Sleep is a central pillar here. Night-time screen time and artificial light can disrupt melatonin production, worsen insulin sensitivity and increase cardiovascular risk. Sleeping well is not a luxury but a direct lever for blood sugar, blood pressure, inflammation and regeneration. You can find more about this in our article Night's Rest.
The sun is also part of this picture. UVA light in particular is present all year round and can promote the release of nitric oxide. This supports vasodilation, i.e. the widening of the blood vessels, and is linked to important metabolic processes. From this perspective, systematically avoiding sunlight is a modern mistake with far-reaching consequences for metabolism, the cardiovascular system and wellbeing. You can find more about this in our article Sun-Kissed.
Chronic stress works in the opposite direction. Permanently elevated cortisol can raise blood sugar, promote insulin resistance and influence the tendency of the blood to clot. The body interprets persistent stress as a constant threat and adapts its physiology accordingly. In the long term, this has consequences for the blood vessels, metabolism and skin. You can find more about this in our article Resonance.
Exercise, daily activity and strength training complete this picture. It is just as important to reduce the number of meals and to respect the natural light times: eat during the day, sleep at night. Eating less often and avoiding night-time meals allows insulin to fall and the body to find its natural rhythm again. You can find more about this in our article Chronobiology.
Cholesterol fits exactly into this picture.
Because cholesterol is part of cell membranes, hormones, vitamin D metabolism and the nervous system. It is not separate from skin, energy or regeneration. It belongs to the inner environment from which healthy skin also emerges.
WHAT WE CAN TAKE AWAY FROM THIS
Perhaps the most important insight is not: cholesterol is always harmless.
That would be too simple again. The more important insight is: cholesterol is not automatically the enemy.
Cholesterol, like all other blood values, should never be viewed in isolation from the person – not in isolation from metabolism, insulin, inflammation, sleep, stress or lifestyle.
If we really want to understand heart health, we need to think bigger.
We need to ask whether the body is in balance. Whether it can switch between storing and burning. Whether the blood vessels are protected or constantly irritated. Whether the person sleeps, moves, gets real light, eats real food and finds enough rest.
Cholesterol is one part of the story. But not the whole story.
Note
This article does not replace medical advice. Cholesterol levels, statins, cardiovascular risks or changes in diet should always be assessed individually and together with medically qualified professionals – especially in the case of existing conditions, a family history or ongoing medication. It is based on the life's work of Dr. Jorge García Dihinx and our personal experience at BARAU.
Sources of the mentioned studies
-
Heart Disease and Stroke Statistics—2016 Update: A Report From the American Heart Association.
Mozaffarian, D., Benjamin, E. J., Go, A. S., et al. Circulation, 133(4), e38–e360 (2016). DOI: 10.1161/CIR.0000000000000350.
-
The Diet and 15-Year Death Rate in the Seven Countries Study.
Keys, A., Menotti, A., Karvonen, M. J., et al. American Journal of Epidemiology, 124(6), 903–915 (1986). DOI: 10.1093/oxfordjournals.aje.a114480.
- Lipoprotein Subfractions and Cardiovascular Disease Risk. Krauss, R. M. Current Opinion in Lipidology, 21(4), 305–311 (2010). DOI: 10.1097/MOL.0b013e32833b7756.
- Meta-analysis of Prospective Cohort Studies Evaluating the Association of Saturated Fat with Cardiovascular Disease. Siri-Tarino, P. W., Sun, Q., Hu, F. B., & Krauss, R. M. American Journal of Clinical Nutrition, 91(3), 535–546 (2010). DOI: 10.3945/ajcn.2009.27725.
- Statins and All-Cause Mortality in High-Risk Primary Prevention: A Meta-analysis of 11 Randomized Controlled Trials Involving 65,229 Participants.
Ray, K. K., Seshasai, S. R. K., Erqou, S., et al. Archives of Internal Medicine, 170(12), 1024–1031 (2010). DOI: 10.1001/archinternmed.2010.182.
- Use of Dietary Linoleic Acid for Secondary Prevention of Coronary Heart Disease and Death: Evaluation of Recovered Data From the Sydney Diet Heart Study and Updated Meta-analysis.
Ramsden, C. E., Zamora, D., Leelarthaepin, B., et al. BMJ, 346, e8707 (2013). DOI: 10.1136/bmj.e8707.
- Intake of Saturated and Trans Unsaturated Fatty Acids and Risk of All Cause Mortality, Cardiovascular Disease, and Type 2 Diabetes: Systematic Review and Meta-analysis of Observational Studies.
de Souza, R. J., Mente, A., Maroleanu, A., et al. BMJ, 351, h3978 (2015). DOI: 10.1136/bmj.h3978.
-
Lack of an Association or an Inverse Association Between Low-Density-Lipoprotein Cholesterol and Mortality in the Elderly: A Systematic Review.
Ravnskov, U., Diamond, D. M., Hama, R., et al. BMJ Open, 6(6), e010401 (2016). DOI: 10.1136/bmjopen-2015-010401.
-
Re-evaluation of the Traditional Diet-Heart Hypothesis: Analysis of Recovered Data From Minnesota Coronary Experiment (1968–73).
Ramsden, C. E., Zamora, D., Majchrzak-Hong, S., et al. BMJ, 353, i1246 (2016). DOI: 10.1136/bmj.i1246.
-
Effect of Statin Treatment vs Usual Care on Primary Cardiovascular Prevention Among Older Adults: The ALLHAT-LLT Randomized Clinical Trial.
Han, B. H., Sutin, D., Williamson, J. D., et al. JAMA Internal Medicine, 177(7), 955–965 (2017). DOI: 10.1001/jamainternmed.2017.1442.
- Malhotra, A., Redberg, R. F., & Meier, P. British Journal of Sports Medicine, 51(15), 1111–1112 (2017). DOI: 10.1136/bjsports-2016-097285.
- 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease.
Arnett, D. K., Blumenthal, R. S., Albert, M. A., et al. Circulation, 140(11), e596–e646 (2019). DOI: 10.1161/CIR.0000000000000678.
- Low-Fat Dietary Pattern and Risk of Cardiovascular Disease: The Women’s Health Initiative Randomized Controlled Dietary Modification Trial.
Howard, B. V., Van Horn, L., Hsia, J., et al. JAMA, 295(6), 655–666 (2006). DOI: 10.1001/jama.295.6.655.
- Is LDL Cholesterol Associated With Long-Term Mortality Among Primary Prevention Adults? A Retrospective Cohort Study From a Large Healthcare System.
Kip, K. E., Diamond, D. M., Mulukutla, S., & Marroquin, O. C. BMJ Open, 14(3), e077949 (2024). DOI: 10.1136/bmjopen-2023-077949.
- Effect of Reducing Saturated Fat Intake on Cardiovascular Disease in Adults: An Umbrella Review. Aramburu, A., et al. Frontiers in Public Health, 12, 1396576 (2024). DOI: 10.3389/fpubh.2024.1396576.
