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Writer's pictureDr. Thomas J. Lewis

Oreo Cookies Outperform Statin Drugs

This is taken directly from Epoch Times (EPOCH HEALTH) with some editorials to clarify statements made by "regular" clueless doctors.



A Harvard researcher specializing in metabolism and nutrition has explored uncharted territory in cholesterol management through an innovative experiment.


Nicholas Norwitz, a Harvard medical student with a doctorate from the University of Oxford, had an ambitious goal: to validate the lipid energy model, a theory poised to transform our comprehension of human fat or “lipid” metabolism. To that end, Mr. Norwitz investigated the contrasting effects of Oreo cookies and statins on cholesterol levels.


Within the esteemed environments of Harvard and Oxford, the 28-year-old researcher faced the daunting challenge of being a “little fish with a big idea,” he said, adding that he intended to make a substantial scientific contribution while operating without the backing of multimillion-dollar grants.


“Everyone knows the feeling of being so engrossed by a question that it occupies your mind,” he told The Epoch Times. “What do you do when that question challenges everything you’ve been taught? For me, that’s the essence of this experiment.”


Understanding Cholesterol

Cholesterol is a term that often ignites passionate debate in health care. Viewed by many as a primary factor in heart disease, cholesterol also plays a critical role in multiple bodily functions.


 

Lewis: Read this from Harvard Medical School:


"Cholesterol is the building block of steroid hormones, including the stress hormone cortisol and the male and female sex hormones, including testosterone and the estrogens. Cholesterol is also an essential component of the membranes that surround all human cells. More than simply holding cells together, these membranes have a crucial role in regulating cell function and allowing chemicals to pass into and out of cells.

Because cholesterol is so vital, the body does not rely on diet to provide it. In fact, most of the cholesterol in the blood is manufactured in the liver."

 

Central to this discussion is LDL-C, or low-density lipoprotein cholesterol, which is commonly labeled as “bad” cholesterol. The protein component, LDL, acts as a transporter of cholesterol. LDL particles are like delivery trucks, circulating fat fuel and cellular building blocks throughout the body.


 

LEWIS: I don't know why "C" is put at the end of "LDL," because LDL is a lipoprotein and cholesterol is a constituent. Why aren't the other constituents called out? Because it supports the failed dogma.

 

Traditionally, medical professionals have linked an excess of LDL “trucks” to arterial plaque accumulation, which elevates one’s risk of heart attack and stroke. And given that nearly 94 million U.S. adults are said to have high cholesterol, the importance of understanding these risks is undeniable.

 

LEWIS: "are said to have high cholesterol." How were the ranges established? They are NOT based on increasing mortality risk.

 

In the American Medical Association (AMA) series “What Doctors Wish Patients Knew,” Kate Kirley, a family physician and director of chronic disease prevention at AMA, debunks a prevalent cholesterol myth. “The amount of cholesterol that you eat doesn’t actually impact your own cholesterol very much,” she writes. Dr. Kirley underlines that the body’s cholesterol production is mostly separate from dietary cholesterol, countering a common misconception.


The battle against high LDL-C has long been fought with statins—drugs that cut down cholesterol production in the liver. As of 2021, the global statins market was estimated at about  $15 billion, and it is expected to reach $22 billion by 2032.


Lean Mass Hyper-Responders: A Unique Group


Cholesterol levels are unusually high among a specific group of otherwise healthy people, called lean mass hyper-responders (LMHRs).

 

LEWIS: What is "unusually high?" Mine is 240, which is perfect based on early all-cause mortality data.

 

These are typically active, athletic people with little body fat who eat a low carbohydrate, ketogenic diet. They are named for their lean physiques and high cholesterol levels. In fact, in what Mr. Norwitz calls the LMHR phenomenon, these individuals are known to experience dramatic escalations in their LDL-C levels, which can reach as high as 500 to 600 milligrams per deciliter (mg/dL).

 

LEWIS: Sadly, the doctors don't understand physiological mechanisms so cannot explain this so-called "hyper-responder" phenomenon. Athletic people break down tissue. We all know that. It's called "the burn." This is the breakdown of weak tissue in preparation of rebuilding it stronger/better/faster.


Every cell membrane (and beyond) are composed of phospholipid bilayers. Translation: phospho FAT bilayers. LDL carries fats to rebuild tissue. Thus, it makes sense that athletic people will have higher LDL values - they require more repair. And, the very high levels may be observed if blood is obtained right after a heavy or long workout.

 

These people provide a unique metabolic profile to test an almost ridiculous hypothesis: Can you lower cholesterol with Oreos instead of medication?


This was the core of Mr. Norwitz’s experiment. He investigated whether incorporating Oreo cookies into his low-carb, ketogenic diet could decrease his LDL-C levels and how it would compare to taking conventional statins.


Dr. William Cromwell, a seasoned lipidologist and physician, said people within the LMHR phenotype tend to have very high levels of LDL-C, high-density lipoprotein cholesterol (HDL-C), and low triglycerides. (see my note above - between the dividers)


These traits craft a distinctive lipid profile that is rare in the general population but relatively prevalent among lean individuals on low-carb diets.


 

LEWIS: It's rare in the general population because of their sedentary nature. "No Pain - No Gain" - including LDL

 

“This case study adds to our understanding of an atypical group of people—lean individuals who have a substantial increase in LDL cholesterol on a ketogenic/very low-carb diet,” he told The Epoch Times.


The explanation of this phenotype originates from the lipid energy model (LEM), which proposes that reduced carbohydrate intake changes the way fats are processed, which in turn may influence cholesterol levels in otherwise metabolically healthy people.


 

LEWIS: If you are metabolically flexible and thus burn fats more efficiently, you still need to transport them to cells adapted to burn them. You need the LDL trains and taxis to bring them to the cells.


 

For lean people, cutting down on carbs means their bodies use more fat for energy. This change primarily happens in the liver, which produces more very-low-density lipoprotein, a type of particle that carries fats in our blood. Once these particles deliver their fat cargo, they become LDL-C (the so-called “bad” cholesterol) and HDL-C (the “good” cholesterol). This process explains why LDL-C and HDL-C levels in these individuals can rise while triglycerides (another type of fat) drop.


 

LEWIS: Really? When I burn fat fuel, suddenly LDL turns "toxic" after delivering its cargo? When something doesn't make sense - it doesn't make sense.

 

“Based on the lipid energy model, adding back carbs and repleting the store of glycogen in the liver should bring LDL-C back down in a lean-mass hyper-responder,” Mr. Norwitz said. His study suggests that the carbohydrate source, whether it’s bananas, potatoes, or even Oreo cookies, can substantially decrease LDL cholesterol.


 

LEWIS: Of course it does, because sugars can flow through your blood without a taxi called LDL - daah!

 

Oreos Versus Statins


In this dietary trial, Mr. Norwitz adhered to his typical ketogenic diet, which is low in carbohydrates (20 grams per day). Subsequently, he introduced a unique variable—eating 12 Oreo cookies per day for 16 days, adding 100 grams of carbohydrates to his diet. During this phase, he maintained ketosis with ketone supplements, ruling out ketosis as a factor in any increase in his LDL-C levels.


After a three-month break to reset his weight and health markers to their original state, he embarked on the second phase of the experiment. This time, he took 20 milligrams of rosuvastatin, a statin drug used for lowering cholesterol, every day for six weeks, all while sticking to his ketogenic diet.


The results were striking. Initially, Mr. Norwitz’s LDL-C level was 384 mg/dl. After the Oreo supplementation, it plummeted to 111 mg/dl, a 71 percent reduction. In the second phase of the experiment, adding statin therapy, his LDL-C levels rose to 421 mg/dl but were only reduced to 284 mg/dl, a 32.5 percent reduction.


 

LEWIS: I believe in the effect but there is something fishy about these high LDL numbers. It might have to do with when the blood was drawn.

 

“The results in this case study are consistent with changes expected from the LEM, and demonstrate the potential for substantial and rapid LDL cholesterol lowering by increasing dietary carbohydrates in selected individuals,” Dr. Cromwell said.

“This study is helpful for lean individuals who experience a significant increase in LDL cholesterol on a ketogenic/low-carb diet. For such people, diet modification (increasing carbohydrates), rather than medications, should be considered as the first line of treatment if LDL lowering is needed.”


 

LEWIS: Why "treatment?" Your body is efficient—like a flex-fuel vehicle or, more appropriately, a hybrid. I just completed a 12-hour trip in my hybrid, averaging 70 MPH and getting 49.3 MPG.


SHOULD I HAVE SHUT OFF THE HYBRID AND JUST USED THE GAS ENGINE SO I WOULD HAVE GOT 29 MPG?

 

The study is meant to be a head-turner. New research has shown that low body-mass index, not saturated fat, is a key factor in the sharp rise of LDL-C for those on low-carb diets. This insight challenges previous beliefs, as it points to leaner body mass—rather than dietary fat—being the primary driver behind the LMHR phenomenon.


 

LEWIS COMMENT: It's neither. It's activity/movement that requires fats for repair and also often relies on fats as a back-up fuel. Many people who exercise, especially endurance exercise, become metabolically flexible, and thus, their LDL will elevate to accommodate the fat-as-fuel (ketosis) pathway.


It's NOT a head-turner for those who understand how soap works - and lipoproteins (LDL, etc) ARE SOAPS!

 

Constraints of the Oreo Experiment


While Mr. Norwitz’s experiment has garnered interest, its limitations must be acknowledged. The study reflects the singular experience of Mr. Norwitz, who is categorized as an LMHR individual. The results of his experiment can’t be broadly applied to the general population.


“This was a metabolic demonstration. I sincerely hope nobody takes this to mean Oreos are good for heart health,” Mr. Norwitz said. “Nevertheless, the experiment raises an uncomfortable implicit question about the consequences ... and I love uncomfortable questions in science.”


The core concept of Mr. Norwitz’s study, the LEM, is an evolving model yet to gain scientific consensus. While it sheds light on how low-carb diets may influence cholesterol levels in particular cases, it doesn’t account for all variables influencing those levels across different diets and populations. “It’s not meant to be all-encompassing,” Mr. Norwitz said. “No models are complete, but some are useful.”


The hope, however, is that his approach will inspire further research. By spotlighting the LMHR phenotype and the complex dynamics of human lipid metabolism, this study could pave the way for more detailed investigations. Such research could lead to a better understanding of dietary effects on health, potentially transforming personalized nutrition and medical treatment.


Challenging the Status Quo

The pursuit of knowledge in academic medicine frequently encounters significant hurdles, notably in securing funding. Many studies are backed by the pharmaceutical and food industries, which can lead to conflicts of interest, especially when research might contradict industry agendas. For independent researchers, finding support for unconventional research can be daunting.


“I think funding is the greatest hurdle in conducting this type of research,” Dr. Cromwell said.


Mr. Norwitz agreed, pointing out the challenges faced by researchers with innovative ideas but limited resources. “I’m in an environment surrounded by the world’s top experts. How could I see something they don’t? How can I pursue this question without the established academic muscle or the funding to make a large-scale experiment happen?” he said.


Mr. Norwitz believes this experiment is more than just a scientific inquiry; it’s a call to attention within the medical field about a model that could revolutionize our understanding of cholesterol management for the general population, he said.


“What I want people to walk away with is a feeling of curiosity,” he said. “One of the greatest pleasures in life is when reality defies your expectations, and you’re like an infant seeing the world anew.”

 

LEWIS: The real-world limitation is a lack of understanding of physiological mechanisms!

 
 

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