Cholesterol on keto?
One of the biggest concerns I hear from people wanting to begin A Ketogenic lifestyle is that of cholesterol. One thing I hate is beating around the bush, so I’ll hit you with this up front...
The 2015 Dietary Guidelines Advisory Committee Report Concerning Dietary Cholesterol Consistent with the American Heart Association Deemed That...
‘CHOLESTEROL IS NOT A NUTRIENT OF CONCERN FOR OVER-CONSUMPTION’
Cholesterol is imperative for life!
Cholesterol is produced by the liver and is also made by most cells within the body. It is carried around in the blood by little couriers called lipoproteins. We need blood cholesterol because the body uses it to:
- Build the structure of cell membranes. Cholesterol is an essential component of cell membranes, which are the structures that border every cell in the human body. Without cholesterol, T-cells (A type of white blood cell) for example, would not maintain their cell membrane, leading to rupturing of the cells.
- Cholesterol makes hormones like estrogen, testosterone and adrenal hormones.
- It also helps your metabolism work efficiently, for example, cholesterol is essential for your body to produce vitamin D. Vitamin D is required for a good immune system.
- It produces bile acids, which help the body digest fat and absorb important nutrients. In addition, triglycerides are an important source of energy for the body, particularly when glucose is deficient, a ketogenic state for example.
- Cholesterol allows the arteries and veins to withstand the pressure of the blood flowing through them and heals them after injury.
- It is ESSENTIAL for the IMMUNE SYSTEM! Immune cells rely on cholesterol, it fights off infections. LDL binds and deactivates bacterial toxins, for example, the MRSA bacterial toxin does not destroy red blood cells when LDL is present.
- And it has been found that higher cholesterol levels in the blood increase post-surgery aiding in the healing process! Something I can attest to personally!
After an operation requiring the wound to be left open, I was told to expect a 12 week healing period. Below are the images post operation and I think you’ll agree that these are quite exceptional, in-fact, the nurses packing this for me each day said that in the 30 years of nursing, they had never seen an injury heal so quickly...
My body had almost healed 9 weeks quicker than expected! 9 WEEKS!
Guess what my cholesterol profile looks like? You guessed it!
My cholesterol is double figures and yes, mostly LDL, the so called 'Bad Cholesterol'
So...Why Are We Told to Fear Cholesterol?
It was once believed (and unfortunately still is by many) that high cholesterol would build up on the walls of the arteries causing a process called atherosclerosis, a form of heart disease. Now, where this in some sense is true, we need to look deeper.
The body is a highly efficient machine that wants to be fit, healthy and heal... why would it produce something that would damage itself?? It wouldn’t!
LDL Cholesterol is often touted as ‘Bad cholesterol’ but why? LDL is protective, LDL is sent to repair damage to the arterial wall to protect the body. That doesn’t sound so bad to me! The question is, ‘What is causing the damage in the first place?’
The image below by Chemical Engineer and Nutrition Expert Ivor Cummins shows the damage caused to the glycocalyx (the arterial wall’s first line of defence) following a high carbohydrate meal. The glycocalyx has been completely destroyed by blood glucose from the carbohydrates exposing the endothelium allowing LDL to access for REPAIR.
We’re told to eat little and often, but this image shows it takes 8-12 hours to recover from a high carbohydrate meal, meaning we are constantly causing damage which requires more LDL to enable repair.
The above graph from a study on the endothelial glycocalyx eposure to elevated blood glucose for 6 hours shows a significant drop in glycocalyx volume (**)
The liver produces and releases LDL, but it begins it's journey as VLDL (very low density lipoprotein). VLDL circulate the body, releasing their lipid cargo along their travels, in the same way a bus would with passengers, becoming smaller and smaller along the way resulting in the VLDL particle becoming IDL (intermediate density lipoprotein) and eventually LDL (low density lipoprotein).
Once the bus (LDL particle) has finished it's route by releasing it's cargo, it will return to the liver for recycling. Each LDL particle contains an APOB100 protein, which is a receptor that is recognised by the liver, it is this receptor that allows the LDL particle access to the liver, without it, LDL cannot be recycled.
The consumption of carbohydrates leads to glucose in the blood, excess glucose causes this APOB100 protein to become glycated (sticky) by binding to this receptor site, blocking the receptor and with it the liver's ability to recognise it, meaning it won't allow it access for recycling, it continues to circulate in the blood, growing in number.
As well as glycated LDL particles we can get oxidised LDL particles. This again can be caused by insulin resistance, high blood glucose levels and through things like oxidised linoleic acid from vegetable / seed oils. Fully oxidised cells also lose their ability to be recognised by the liver as this also blocks the APOB100 receptor.
Like glucose, these oxidised particles also damage the glycocalyx lining the arterial wall, this damage causes a widening of the tight junction proteins between the epithelial cells, this allows oxidsed and glycated LDL particles to travel to the sub-endothelial space. Within this space are cells called macrophages. These macrophages contain a receptor called a scavenger receptor. This scavenger receptor will recognise the glycated / oxidised APOB100 receptor when the liver could not and allow them access. The macrophage will take in the oxidised LDL particles and cram them in until they increase greatly in size leading to the creation of a foam cell. Foam cells are the creation of calcification in atherosclerotic plaques.
Chronic consumption of carbohydrates can cause insulin resistance and a large increase in inflammation, this inflammation causes further damage to the arterial wall requiring more LDL for repair, further allowing these oxidised and glycated particles to be consumed by the macrophages leading to further calcification.
The different types of LDL can be split into 2 categories.
PATTERN A - Non oxidised (Healthy LDL)
PATTERN B - Oxidised (Damaging LDL)
How can we tell if our LDL is Pattern A or Pattern B? Your Doctor should be able to tell you this, but if they don't, you can get a pretty good idea by following this simple flowchart.
Still not convinced about LDL?
This study here released by the BMJ (**) looked at 19 cohort studies with a total of 68,094 elderly people and the relationship between LDL and all cause mortality (death).
The result from the study showed an inverse association between all-cause mortality and LDL, representing a massive 92% of the participants.
What does this mean? This means the LOWER your LDL, the HIGHER your risk of death!
Now the interesting thing here is that this study didn't account for pattern A & B LDL just LDL. So if we can assume that most people in the study with higher level of LDL consume lots of carbohydrates which would result in the PATTERN B LDL, we could assume lots of these participants had oxidised (bad) LDL, yet even their chance of living longer with this LDL was still statically significant.
Our view on LDL has to change, A non-glycated and non-oxidised LDL particle causes no harm, in-fact, a healthy LDL particle is very good for us, a healthy LDL particle is protective and heals the body. We shouldn't fear high LDL, we should promote it!
Do Not Fear Saturated Fats
Many of us still fear the consumption of saturated fats in fear of raising LDL cholesterol, would you believe despite this notion being around for over 50 years, there is very little scientific backing for this! HOWEVER, there is an abundant amount of studies to show the opposite!
This double blinded, ramdomised controlled trial (**) looked at heart disease in 3 groups. Vegetable oil & olive oil intervention groups and a control group consuming mostly saturated fat. The trial lasted 2 years and the results showed that 5 people died in the vegetable oil group, 3 in the olive oil group and only 1 in the saturated fat group
This next study (**) included 2412 patients (2412 patients so not a small study!!!) on a meta-analyses to question the association between dietary intake of saturated fatty acids (SFAs) and risk of cardiovascular disease.
The conclusion of this study reads ‘There was no association between dietary intake of SFAs and incident coronary events or mortality in patients with established CAD.’
Just to reiterate that... THERE WAS NO ASSOCIATION BETWEEN DIETARY INTAKE OF SATURATED FATS AND INCIDENT CORONARY EVENTS OR MORTALITY IN PATIENTS WITH ESTABLISHED CARDIOVASCULAR DISEASE!
Still not convinced? Let’s take a look at another...
The Minnesota Coronary Experiment Re-evaluation published by the BMJ (**)
Is a highly compelling report. This was a double blind randomised controlled trial designed to test whether replacing saturated fat with vegetable oil rich in linoleic acid reduces coronary heart disease. This trial took place in 6 mental hospitals so consumption of food was monitored exactly. The study included 9423 people, the patients were split into 2 groups :
- One group had high saturated fat in their diet
- The other group replaced saturated fats for vegetable oils.
The idea was to lower cholesterol and improve cardiovascular disease. Now, what the study reveals was hidden for many years because those performing the study didn’t like the results the study showed.
The study did indeed show that the group using the vegetable oil had lower serum cholesterol, but this group had a higher mortality rate than saturated fat group. This study shows that lower cholesterol increased risk of death.
Blaming cholesterol for cardiovascular disease is like blaming the firefighter for starting the fire, as there’s a Fire Fighter at the scene of every fire... just like cholesterol at the site of atherosclerosis.
DON’T FEAR YOUR CHOLESTEROL OR SATURATED FATS!
Saturated fats do NOT clog arteries! (**) Heart disease is a chronic inflammatory condition. Inflammation and Insulin resistance caused from the over consumption of carbohydrates and vegetable / seed oils which can easily be reversed & controlled through a HEALTHY diet.
“In my opinion and as the science tells us, eating the way our ancestors did and living a Ketogenic Lifestyle, consuming lots of saturated fats and proteins from high quality grass fed animal sources, while heavily restricting, or completing removing processed foods, grain, vegetable / seed oils high in oxidised linolenic acid is the best way to keep a healthy immune system and prevent chronic illness / autoimmune issues, inflammation, glycation, oxidative stress and cardiovascular disease.“ R.Smith
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Jo Ann S. Carson, Alice H. Lichtenstein, Cheryl A.M. Anderson, Lawrence J. Appel, Penny M. Kris-Etherton, Katie A. Meyer, Kristina Petersen, Tamar Polonsky, Linda Van Horn, and on behalf of the American Heart Association Nutrition Committee of the Council on Lifestyle and Cardiometabolic Health; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular and Stroke Nursing; Council on Clinical Cardiology; Council on Peripheral Vascular Disease; and Stroke Council (**)
Maxfield FR, Tabas I. Nature. 2005; 438(7068): 612-21 (**)
France M. Abnormalities of lipid metabolism. In: Ahmed N Clinical Biochemistry. Oxford University Press, Oxford. 2011.
Dr. Paul Mason MD