Why LDL Cholesterol Goes Up with a Low Carb Diet

Is it Bad for Your Health if LDL Cholesterol Goes Up With a Low Carbohydrate Diet?

Dr. Nadir Ali

Discover why a low-carb, high-fat diet can raise LDL cholesterol on your lab report, what that means for your heart and brain, and whether higher LDL in this context may actually reflect better metabolic health rather than harm.

Dr. Nadir Ali, an interventional cardiologist, explains why LDL cholesterol often rises when people adopt a low-carb or ketogenic diet and challenges the automatic assumption that this is dangerous. He walks through the essential roles of cholesterol in cell membranes, brain function, hormones, bile acids, and vitamin D production, then connects how increased fat burning and ketosis naturally drive higher cholesterol synthesis and LDL levels. Using fasting studies, mechanistic biochemistry, and observational data, he argues that in lean, fat-adapted individuals with high HDL, low triglycerides, and low insulin, elevated LDL may coexist with lower infection risk, better cognition, and potentially lower mortality. He closes by advocating for an animal-based, low-carb dietary pattern that typically raises LDL while improving other cardiometabolic markers, and he invites viewers to reconsider whether higher LDL in this specific metabolic context should be celebrated rather than feared.

Summary

• LDL often rises on low-carb or ketogenic diets because the liver ramps up fat metabolism and cholesterol production when carbohydrates are scarce, especially in lean, highly fat-adapted individuals.
• Cholesterol is fundamental for cell membrane integrity, brain structure and neurotransmission, adrenal stress hormones, sex hormones, bile acids, and vitamin D, so LDL particles play a central role in delivering this cholesterol.
• Fasting and low-carb states shift the body from glucose to fat and ketones, and at the biochemical level, shared pathways (acetyl-CoA → HMG-CoA) can produce both ketones and cholesterol, increasing LDL output by design.
• On low-carb diets, studies suggest more cholesterol is eliminated in bile and feces, LDL receptors in the liver downregulate, and LDL particles become more cholesterol-rich while triglyceride-rich VLDL production falls.
• Experimental data indicate LDL can bind and neutralize bacterial signaling proteins and inflammatory endotoxins, potentially reducing infection virulence.
• Observational cohorts cited here found that higher total cholesterol was associated with lower overall mortality, lower cancer and infection deaths, and, in one aging cohort, better cognitive function and lower rates of stroke and heart disease.
• Dr. Ali contrasts a standard American, high-carb, processed diet with a low-carb, animal-based diet, arguing that the latter better matches human physiology, supports brain energy demands, and improves HDL, triglycerides, and insulin despite higher LDL.
• He concludes that for people with high LDL but simultaneously high HDL, low triglycerides, and low insulin on a low-carb pattern, elevated LDL may signal robust fat metabolism and resilience rather than elevated risk.

Description

Dr. Nadir Ali – Why LDL cholesterol goes up with low carb diet and is it bad for health? 💥 In this talk from Low Carb Down Under, Dr. Nadir Ali, an interventional cardiologist with over 25 years of experience and chairman of the Department of Cardiology at Clear Lake Regional Medical Center, explores why LDL cholesterol can rise on a low carb or ketogenic diet and whether that is necessarily harmful. He previously served as an assistant professor of medicine at Baylor College of Medicine in Houston, where he also completed his medical training. Since 2013, Dr. Ali has championed low-carb nutrition in the Clear Lake area, organizing monthly nutritional seminars at Clear Lake Hospital that attract more than 100 local attendees. His clinical focus includes heart disease, obesity, metabolic syndrome, and diabetes, and in this presentation he shares insights from both research and practice on LDL, cholesterol metabolism, and metabolic health. (Note: The original description primarily contains this biographical and contextual information and does not include additional external links in the fetched content.)

Transcript Summary

Why LDL rises on low carb

Dr. Nadir Ali opens by explaining that his goal is to unpack why LDL cholesterol often increases on a low-carb diet and to evaluate whether this increase is inherently harmful. He notes that he has no financial disclosures and emphasizes that modern medical knowledge is no longer the monopoly of professionals, crediting his own transformation to “citizen scientists” and patients who challenged his assumptions and pushed him to rethink the role of diet in cardiometabolic health. For about five years, he has told his patients to eat animal fat, fatty meat, and fatty fish, and in practice he consistently sees HDL go up, triglycerides go down, and insulin drop, which most clinicians agree is beneficial. However, he also sees that LDL, the “darn” cholesterol everyone worries about, tends to rise most in those who adhere most rigorously to this way of eating, which motivates the central question of the talk.

Cholesterol’s essential functions

Before “demonizing” LDL, Dr. Ali stresses that cholesterol is an evolutionarily important molecule necessary for life, crucial for maintaining cell membrane fluidity and integrity in every cell. He discusses the brain membrane specifically, explaining that cholesterol-rich rafts in neuronal membranes enable proper neurotransmission and that the brain values cholesterol so highly that it synthesizes its own rather than relying on other organs. He adds that he would not be able to stand and present without LDL cholesterol supplying the adrenal cortex with cholesterol to make cortisol, a key stress hormone that helps him handle speaking stress. He also notes that LDL delivers cholesterol to the ovaries and testes for the production of sex hormones, contributing to physical characteristics in men and women, and that cholesterol-derived bile acids are essential for absorbing fats and fat-soluble vitamins. Vitamin D is another cholesterol derivative, and because cholesterol and triglycerides are fats that do not dissolve in blood, the body relies on lipoprotein particles with phospholipid shells and identifying proteins to transport them effectively.

Fasting, fat metabolism, and rising LDL

To understand why LDL goes up, Dr. Ali turns to research on fasting, citing a small study of seven people who fasted for seven days in which LDL cholesterol rose substantially, even though fasting is generally considered beneficial. He explains that carbohydrate stores are limited; when we stop eating or restrict carbs on a low-carb diet, glycogen is quickly depleted within four to eight hours. For tissues that still need glucose, gluconeogenesis initially ramps up but then tapers as the body adapts to burning fat as ketones, with prolonged fasting driving ketone levels to around five millimoles, roughly comparable to blood glucose. He contrasts a person on a standard high-carb diet, whose brain runs mostly on glucose, with someone fasting or on low carb, whose brain shifts to using ketones for about two-thirds of its fuel, indicating a “fat-adapted” state. He even cites neonatal metabolism, describing how newborns rapidly enter a ketotic state with high beta-hydroxybutyrate levels and consume triglyceride-rich colostrum with little lactose, framing ketosis as a fundamental human capacity from birth.

Biochemistry of ketones and cholesterol

Dr. Ali then introduces a liver cell model to show how fat is converted into ketones when carbohydrates are reserved for the brain, focusing on the enzyme HMG-CoA as a key branch point. He explains that as fatty acids enter the liver and are converted to acetyl-CoA, they then form HMG-CoA, which can be directed either toward ketone production or cholesterol synthesis. This shared pathway means that in someone who is very good at fat burning, such as the “lean mass hyper-responder” described by Dave Feldman, increased fat flux to the liver will by design increase cholesterol and LDL levels. Dr. Ali illustrates how a fat-burning liver synthesizes a lot of cholesterol and, in response, also produces more bile for cholesterol elimination through the gut, where less bile is reabsorbed in the terminal ileum and more cholesterol leaves via feces. He references human and animal studies suggesting that in these states, LDL receptor activity in the liver is downregulated, since the liver already has enough cholesterol and does not need to reclaim as much LDL from circulation, resulting in higher circulating LDL.

Changes in lipoprotein patterns with fasting

To add detail, Dr. Ali shows data from fasting studies in humans who were not necessarily on low-carb diets or prolonged fasts, but nonetheless demonstrated distinct lipoprotein changes in the fasted state. These data indicate that during fasting, the liver produces much less VLDL, which is rich in triglycerides, while producing more LDL, which is relatively rich in cholesterol, reflecting a shift from triglyceride transport toward cholesterol-rich particles. He connects this to his clinical observations that patients who eat “fatty food” and are in ketosis show a characteristic pattern: high LDL, high HDL, and low triglycerides. Studies also suggest that people on low-carb diets eliminate more cholesterol in feces and have lower LDL receptor expression, which collectively explains why LDL levels rise even as other cardiometabolic markers improve.

LDL as part of immune defense

Dr. Ali then explores the idea that LDL has been unfairly maligned, asking what benefits LDL might confer in host defense against infection. He describes rat experiments where bacteria in the lungs release a signaling protein (agr protein) that helps them sense when enough bacteria are present to become virulent and cause pneumonia. According to the studies he cites, LDL can bind and soak up this agr protein, preventing the quorum-sensing needed for full virulence and thereby reducing infections. Additionally, bacteria release inflammatory mediators such as LPS and LTA that can cause cell death, and LDL appears to neutralize these endotoxins as well, decreasing bacterial virulence and tissue damage.

Observational data on cholesterol, mortality, and cognition

Moving to human data, Dr. Ali presents findings from the “Leiden 85-plus” or similar cohort of about 700 older patients followed for around ten years to examine how cholesterol predicted mortality, cancer deaths, and infections. In this analysis, “high” cholesterol was defined as 300 or greater, “middle” as around 250, and “low” as around 200, and the group with the highest cholesterol had the lowest overall mortality. The high-cholesterol group also had the lowest cancer mortality and the lowest risk of death from infections such as pneumonia, which he ties back to LDL’s potential role in neutralizing bacterial factors.

He then cites the Lothian birth cohort of individuals born in 1936 and followed into their 70s to see how cholesterol levels related to cognitive function and vascular disease. Again using 300, 250, and 200 as high, middle, and low thresholds, he reports that those with the highest cholesterol had the lowest risk of hypertension, stroke, and heart disease. In terms of brain health, higher cholesterol was associated with better general cognitive ability, faster processing speed, better memory, and higher IQ scores. Among roughly 1,000 participants, about 300 were on statins, and Dr. Ali notes that those on statins had lower cognitive performance compared to their non-statin peers, which he suggests may reflect the importance of cholesterol for brain function.

Critique of the standard diet and plant-heavy patterns

Dr. Ali contrasts these findings with what he calls the standard American diet, characterized by grains, added sugar, and industrial plant oils, which he argues drive insulin resistance and a host of metabolic disorders. He then discusses what he believes constitutes an optimal human diet, noting that humans have energy-hungry brains, a digestive system centered on the small intestine for absorbing nutrient-dense food, relatively limited fermentation capacity, and a single-compartment acid stomach designed for protein digestion. Because the pancreas struggles with high glycemic loads, he suggests that modern high-carb diets overtax it and contribute to early dysfunction.

He briefly outlines his arguments for why an animal-based, low-carb diet is superior to a whole-food plant-based diet, asserting that a high-fiber, plant-based pattern designed to reduce glycemic index requires large volumes of food and long eating times to provide adequate brain calories. He suggests this could interfere with productivity and social life and may increase bathroom time, as one of his colleagues previously joked. This critique sets up his preference for nutrient-dense animal foods combined with carbohydrate restriction.

Dietary recommendation and closing message

In closing, Dr. Ali urges the audience to “start eating like this,” referring to a diet rich in animal fat, animal protein, and fatty fish, combined with carbohydrate restriction sufficient to induce ketosis. He reiterates that people who do this typically see high HDL, low triglycerides, low insulin, and higher LDL, and he frames this cluster as a favorable profile rather than a dangerous one. His final slide poses the provocative question of whether we should celebrate high LDL instead of mourning it, especially when high LDL coexists with low triglycerides and low insulin in metabolically healthy, fat-adapted individuals. He argues that this pattern may promote longevity, better cognitive function, lower infection rates, and lower cancer risk, and he thanks the audience for the opportunity to present his views.