Why (LDL particle) size matters.

Having gone through the math(s) with several people, I thought I'd stick it in a blog post for posterity.

This is a diagram of a chylomicron or VLDL-c (high TG/C ratio) 'cos I couldn't find one for LDL-c!

Cholesterol synthesised in the liver is exported in LDL particles. The more cholesterol that's synthesised, the more particles there need to be to carry it.

∴ LDL-P (particle number) ∝ LDL-C (total amount of cholesterol)

The particles are roughly spherical with a very thin wall (consisting of a phospholipid mono-layer, the yellow wiggly lines with a green end bit in the above diagram).

Volume of a sphere = 4/3 * π * r³, where r = half the diameter.

If there's a 10% reduction in LDL particle size, the volume reduces to 0.729, relative to the original size. Therefore, to carry the same amount of cholesterol requires 1/0.729 = 1.37 times more particles, which is a 37% increase in the number of LDL particles, relative to the original size.

∴ LDL-P (particle number) ∝ 1/LDLsize³

As it's LDL particle number that determines the infiltration of LDL cholesterol into the media of artery walls (see image below), it's advisable to keep cholesterol synthesis to a reasonable level by keeping fat intake to a reasonable level (i.e. not Nutritional Ketosis!) and keeping LDL particle size to a reasonable level by keeping added sugar (e.g. sucrose & fructose) intake and rapidly hydrolysed/overcooked starches (e.g. amylopectin & maltodextrin) intake to a reasonable level (i.e. a level that's oxidised by the body without having a chronic excess). An acute excess of carbohydrate can be stored as liver/muscle glycogen, provided that mean carbohydrate intake is less than mean carbohydrate oxidation.

How COULD I write a post about LDL-P and forget to include THIS?

Historical perspectives on the impact of n-3 and n-6 nutrients on health, by Bill Lands.

Here's Fig. 1. from https://www.sciencedirect.com/science/article/pii/S0163782714000253

Relating tissue HUFA balance with blood cholesterol and heart attacks. Results from the 25-year follow-up in the Seven Countries Study [35] were discussed in an earlier review [10] which noted that “Food energy imbalances which elevate blood cholesterol may be fatal only to the degree that omega-6 (n-6) exceeds omega-3 (n-3) in tissue HUFA. Such evidence raises questions about the hypothesis that blood cholesterol levels cause CHD.” Northern Europe and Southern Europe have abbreviations “No.” and “So.”, respectively. The Figure is reprinted with permission of the publisher.

Hat-tip to Dr. Thomas Dayspring for Tweeting this review.

Fig. 1 is interesting, as it shows a significant association between 25-year CHD mortality and Serum Total Cholesterol for every region except Japan. What's different about Japan, compared to Northern Europe, USA, Serbia, Southern Europe & Crete?

According to Measuring Blood Fatty Acids as a Surrogate Indicator for Coronary Heart Disease Risk in Population Studies , Philippines & Iceland have lower % linoleic acid than Japan. Where's the CHD vs TC data?

Could another difference be that the Japanese eat rice, a relatively intact grain, instead of foods made from wheat grain dust (i.e. flour) as their main source of dietary carbohydrates?

See also Using 3–6 differences in essential fatty acids rather than 3/6 ratios gives useful food balance scores , and Omega 3-6 Balance Score.

Another tasty analogy.

Here's a tasty analogy.

From https://grannychoe.com/recipe3_Soup.php

In Ultra-high-fat (~80%) diets: Fat storage, and a delicious analogy, I analogised the effect of carbohydrate consumption on mean serum glucose level with the effect of fat consumption on mean serum triglyceride level. Here's another one.

Chronic excessive consumption of carbohydrates relative to what are being burned results in excessive fat synthesis in the liver, resulting in excessively-high fasting serum triglyceride level, which is harmful.

Chronic excessive consumption of fats relative to what are being burned results in excessive cholesterol synthesis in the liver, resulting in excessively-high fasting VLDL, LDL & IDL level, which is harmful.

Seems legit.

Lipoproteins & apolipoproteins: E, by 'eck.

In December 2008, I wrote about Cholesterol And Coronary Heart Disease , where I used a limousine metaphor to describe how cholesterol & fat are transported around the body. Here's a diagram of a chylomicron lipoprotein "limousine". Chylomicrons transport dietary fat (triglycerides) & cholesterol from the gut to the liver & other tissues. As there's much more dietary fat than dietary cholesterol, the contents are mostly fat.

A chylomicron. T=Triglyceride C=Cholesterol. From https://en.wikipedia.org/wiki/Lipoprotein

The lipoprotein "limousines" vary a lot in size.

(a) VLDL (b) chylomicrons (c) LDL (d) HDL. 
From https://healthcorrelator.blogspot.co.uk/2011/11/triglycerides-vldl-and-industrial.html

Apolipoproteins are the "chauffeurs" which determine to where lipoproteins transport stuff.
Apo A is found mainly on HDL, which transports fat & cholesterol from tissues to the liver.
Apo B is found mainly on LDL, which transports cholesterol from the liver to tissues.
Apo C is found on HDL when fasted, but moves to chylomicrons & VLDL when fat is eaten.
Apo D is found mainly on HDL and is is associated with an enzyme involved in lipoprotein metabolism.
Apo E is found mainly on chylomicrons & IDL and transports lipoproteins, fat-soluble vitamins, and cholesterol into the lymph system and into the blood. In the CNS, Apo E transports cholesterol to neurons. Defects in Apo E result in hyperlipidaemia , cardiovascular & neurological diseases, and is the E referred to in the title.

There's also Apo H, which is a β-glycoprotein involved in the binding of cardiolipin. It has nothing to do with the above lipoproteins.

False dichotomies: serum cholesterol level vs all-cause mortality. Cause or effect?

Here are some plots from the MRFIT study.

From https://sph.bu.edu/otlt/MPH-Modules/PH/PH709_Heart/PH709_Heart5.html

Although the relative risk (RR) for coronary heart disease (CHD) and cardiovascular disease (CVD) mortalities increase with serum total cholesterol (TC) level, all-cause mortality follows a U-curve.

According to Low Serum Cholesterol and Mortality: Which Is the Cause and Which Is the Effect?, certain illnesses that increase mortality lower TC levels. This is the Iribarren hypothesis.

According to Cholesterol and all-cause mortality in elderly people from the Honolulu Heart Program: a cohort study, TC that's low and is still low 20 years later results in a 64% increase in the RR for mortality relative to TC that's intermediate and is still intermediate 20 years later.

Table 4 Relative risk for mortality based on change in cholesterol between examinations three and four

Is low TC level the cause of, or the effect of fatal illnesses? I think that it's both. Cholesterol is an important substance, as a severe lack of it is bad news, as per Smith–Lemli–Opitz syndrome. If certain illnesses result in a depletion of cholesterol and cholesterol synthesis is too low, there's insufficient cholesterol to allow recovery.

Interestingly, TC that's low but is intermediate 20 years later results in a 30% increase in the RR for mortality, whereas TC that's low but is high 20 years later results in a 5% increase in the RR for mortality.

P.S. There's a false dichotomy for vitamin D level vs illness. Ditto for carbohydrates vs calories.

FAO the over-fat and/or those with metabolic syndrome: Big breakfast, medium lunch & small dinner is beneficial.

Breakfast like a King/Queen.

Go to work on an egg.

According to High caloric intake at breakfast vs. dinner differentially influences weight loss of overweight and obese women.
"High-calorie breakfast with reduced intake at dinner is beneficial and might be a useful alternative for the management of obesity and metabolic syndrome." See the other PubMed studies listed in the above study, which corroborate it.

What about all the "artery-clogging" cholesterol in egg yolks? See Eat Whole Eggs All Day and Throw Your Statins Away? 375x Increased Dietary Cholesterol Intake From Eggs Reduces Visceral Fat & Promotes Healthy Cholesterol Metabolism.

Mum's Proposed Ketogenic Diet for Dementia.

The following diet is not intended to induce deep ketosis. It's intended to be a trade-off between ketosis, palatability & simplicity.



Feedback from the nurse on duty:- "Eggs shouldn't be in the "unlimited" list. You're not supposed to eat more than two eggs a week because of the cholesterol". God Bless the NHS! The British Heart Foundation doesn't impose a restriction on egg consumption.

Eggs can be eaten as part of a balanced diet.

Mum's currently eating two eggs a day in her cooked breakfasts.

Effect of dietary egg on human serum cholesterol and triglycerides.

Old people have the lowest mortality when their serum cholesterol is higher than average.

Total cholesterol and risk of mortality in the oldest old.
Cholesterol and all-cause mortality in elderly people from the Honolulu Heart Program: a cohort study.
Low total cholesterol and increased risk of dying: are low levels clinical warning signs in the elderly? Results from the Italian Longitudinal Study on Aging.
Higher total serum cholesterol levels are associated with less severe strokes and lower all-cause mortality: ten-year follow-up of ischemic strokes in the Copenhagen Stroke Study.
Serum total cholesterol levels and all-cause mortality in a home-dwelling elderly population: a six-year follow-up.
Lipid-lowering treatment to the end? A review of observational studies and RCTs on cholesterol and mortality in 80+-year olds.

Paul Jaminet has done a series on ketogenic diets.
Ketogenic Diets, I: Ways to Make a Diet Ketogenic
Ketogenic Diets 2: Preventing Muscle and Bone Loss on Ketogenic Diets

Also: See Branched chain amino acids as adjunctive therapy to ketogenic diet in epilepsy: pilot study and hypothesis.

Uh-oh! There may be trouble ahead...

I won't deny that I'm not very active. On days that I don't visit my mum, I spend many hours reclining on a sofa with a lap-top on a small table, surfing the internet. I make sloths look hyperactive!

I thought that this wasn't a problem as I also don't eat very much (as I'm so engrossed rummaging through the vast amount of information out there) and I'm maintaining a relatively stable weight.

Then I read Sedentary Physiology at Obesity Panacea which lead me to Sedentary Physiology Part 1 – Not Just The Lack of Physical Activity , full study HERE.

"Hamburg et al. (2007) examined the effect of 5 days of complete bed rest on metabolic health in 22 adult volunteers. Study participants remained in bed for over 23.5 h per day, rising only for matters of personal hygiene. At the completion of the study, despite no changes in body weight, they experienced significant increases in total cholesterol, plasma triglycerides, glucose, and insulin resistance. The changes in carbohydrate metabolism were particularly pronounced, with participants experiencing a 67% greater insulin response to a glucose load following the 5-day intervention."

The thing is, I've never liked sports & formal exercise. In infant school, exercise involved running around in the playground. That, I could do. In primary school, exercise involved running around in the playground, some PE and some outdoor sports (rounders & cricket, using a tennis ball). That, I could also do, although my short legs made me rubbish at running. In secondary school, in addition to PE, there were sports such as football, rugby, cricket, hockey, tennis, swimming & cross-country running. That, I utterly hated (tennis was just about bearable) and so to avoid doing them, I developed an art for forging sick notes in my mum's handwriting. This improved my normal handwriting, so some good came of it. So, what to do?

As toilet breaks force me off the sofa, I shall drink more to make me wee more often. I shall also use the upstairs toilet during the day and the downstairs toilet during the night. See also Eat Less, Move More: Solutions to problems.

Whatever happened to...Lapaquistat?

By now, you've probably noticed that I'm a bit anti-statin. The "problem" with statins is that they reduce cholesterol synthesis in the liver by reducing the conversion of HydroxyMethylGlutaryl (HMG) Co-enzyme A (CoA) into Mevalonate by inhibiting the enzyme HMG CoA reductase.

Reducing Mevalonate reduces lots of other things e.g. Coenzyme Q10 synthesis, terpenoid synthesis, protein prenylation, cell membrane maintenance, hormones, protein anchoring, N-glycosylation and steroid biosynthesis which leads to cholesterol synthesis. Paradoxically, although cholesterol synthesis is reduced, Vitamin D level is increased. See also Atorvastatin increases 25-hydroxy vitamin D concentrations in patients with polycystic ovary syndrome.

Some of the above changes are undesirable in terms of all-cause mortality, so what would be ideal is a drug that just reduces serum cholesterol without doing anything else. Enter....Squalestatin a.k.a. Zaragozic Acid. This reduces the conversion of Farnesyl Pyrophosphate into Squalene by inhibiting the enzyme Squalene synthase. This has no effect on Mevalonate, or any of the substances listed in the above paragraph. Perfect!

A Squalene synthase inhibitor called Lapaquistat (a.k.a. TAK-475) was developed and tested by Takeda Pharmaceutical Company Limited in 2008. So, why is this wonder drug not on the market today? According to Limited press release - Discontinuation of Development of TAK-475, A Compound for Treatment of Hypercholesterolemia:- " the profile of the compound is not superior to existing marketed drugs from both efficacy and safety viewpoints".

So, just reducing serum cholesterol without changing anything else is not superior to reducing serum cholesterol and changing loads of other things. Maybe statins reduce CHD mortality a bit because they change loads of other things, not because they reduce serum cholesterol. See Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein.

Statins are anti-inflammatory. So is Vitamin D3. I'd take Vitamin D3 instead of statins any day.

We are not all the same.

Cont'd from Everyone is Different.

Lyle (McDonald) brought the following study to my attention to illustrate that "We are not all the same":- Some Metabolic Changes Induced by Low Carbohydrate Diets. On a very-low-carb diet, one subject’s total cholesterol rose to 12.9mmol/L (500mg/dL in US units). The others didn't.
See also LDL cholesterol goes sky high on fatty diet.

I posted the study in various blogs to make the above point. Here are some of the replies I got:-
"Lyle? Lyle McDonald? Is that where you got that study, Nigel?" and... "I’m usually a pretty polite guy, Nigel. But based on this quote from the beginning of the study you mentioned, the people who wrote this study were a bunch of f**kwads, and really don’t deserve our attention. It’s a hatchet job."
"That was a weird study (1967) what I could make of it." and... "The men did all the stages but the women only did 3 stages of the diet."
"The fats were mostly omega-6 PUFA 13-35 grams worth..."
"The report you cite is so old and out of date that it makes me cry..."

My point was well & truly missed. I got the distinct impression that people thought I was criticising very-low-carb, high-fat diets. I wasn't. The simple fact is that there is no "One True Diet" that suits absolutely everybody. In the olden days everywhere & in poor countries nowadays, people that ate/eat the wrong diet for their body died/die young. Nowadays in rich countries, they get put on drugs e.g. oral hypoglycaemics (to lower blood glucose) & hypolipidaemics (to lower blood cholesterol/triglycerides).

Please note that omega-6 PUFAs tend to lower serum cholesterol rather than raise it, as per Figure. 1 below from Individual fatty acid effects on plasma lipids and lipoproteins: human studies.

However, don't rush off and eat shed-loads of omega-6 PUFA (e.g. corn oil) in the mistaken belief that it will make you live any longer.

Cont'd on Everyone is Different, Part 2.

As sure as Eggs is Eggs.....

...is grammatically incorrect! Rumour has it that it's a corruption of "As sure as x = x". But anyway....

Eggs are very nutritious and should be eaten freely as part of a healthy diet.

Click https://www.nutritiondata.com/facts/dairy-and-egg-products/111/2 and set the serving size to 1 large (50g) to see what nutrients there are in a raw whole egg.

Click https://www.nutritiondata.com/facts/dairy-and-egg-products/112/2 and set the serving size to 1 large (33g) to see what nutrients there are in a raw egg white.

Click https://www.nutritiondata.com/facts/dairy-and-egg-products/113/2 and set serving size to 1 large (17g) to see what nutrients there are in a raw egg yolk.

The amino acid scores for whole egg , white and yolk are 136, 145 and 146 respectively. Eggs are a good source of complete proteins. This is because the yolk and white need to contain everything necessary for a growing chick embryo.


Can I drink eggs raw to save time?There are three potential problems with this:

1) Salmonella poisoning. Unless you’re pretty sure of the hens that the eggs came from, there is a risk of poisoning from raw eggs. This doesn’t apply to pasteurised eggs from suppliers like https://www.eggnation.co.uk/ for example.

2) Poor absorption of egg white protein. According to https://jn.nutrition.org/cgi/content/full/128/10/1716 , only 51% of raw egg white protein is absorbed during digestion compared to 91% for cooked egg white protein. According to https://ajpgi.physiology.org/cgi/content/full/277/5/G935 , the figures are 65% and 94% respectively. The second study used 200g of white and one yolk. I don’t believe that there is a problem with the absorption of raw egg yolk, though problem 1 still remains. Pasteurised egg white protein is well absorbed.

3) Poor biotin absorption. Raw egg white contains a glycoprotein called avidin which binds to biotin (Vit. B7) in the yolk and prevents its absorption. Cooking or pasteurisation denatures (changes the 3-D structure of) the avidin and renders it harmless.


What about all that cholesterol in egg yolks?

Current “Healthy Eating” guidelines state that we should eat no more than 3 egg yolks/whole eggs per week. This is based on the erroneous assumption that dietary cholesterol always increases serum cholesterol and that this is always a bad thing. According to Effect of dietary egg on human serum cholesterol and triglycerides, adding or not adding 500mg of dietary cholesterol from two large eggs per day made no significant difference to serum cholesterol or triglycerides in 116 healthy male subjects. Some went up and some went down. Eddie Vos at https://www.health-heart.org/cholesterol.htm reckons that you’d have to eat 20 whole eggs per day to get as much dietary cholesterol as the liver produces each day (5g). Egg yolks do contain some fat and this should be factored into your total diet. If you happen to have the genes for familial hypercholesterolaemia, then you need to keep a close eye on dietary cholesterol intake. See also Eat Whole Eggs All Day and Throw Your Statins Away? 375x Increased Dietary Cholesterol Intake From Eggs Reduces Visceral Fat & Promotes Healthy Cholesterol Metabolism.

There is a problem with modern eggs though, and it’s caused by the food that’s fed to the hens. Grains contain about 50 times more Linoleic acid (omega-6) than Alpha-Linolenic acid (omega-3) and this raises the omega-6:omega-3 ratio of the eggs that the hens lay. Hens eating a natural diet of bugs, grubs and vegetation lay eggs with a 1:1 ratio of omega-6:omega-3, but grain-fed hens lay eggs with an omega-6:omega-3 ratio of >10:1. A high omega-6:omega-3 ratio in the diet is associated with increased risk factors for heart disease, cancer and Insulin Resistance (pre-type 2 diabetes). Therefore, if large numbers of cheapo eggs are eaten, it’s advisable to eat other foods that are rich in omega-3 fats.

Cholesterol And Coronary Heart Disease

From https://www.health-heart.org/

Cholesterol & coronary heart disease are mentioned a lot in the media. Unfortunately, most of what you see & hear is either completely wrong, or dumbed-down so much that it's inaccurate.

Fat & cholesterol don't stick to the insides of artery walls like grease on the inside of a drainpipe. This article explains what cholesterol is, how arteries get blocked and how to minimise the risk of having a heart attack or ischaemic stroke.


What is cholesterol?

Cholesterol is a large, waxy molecule (C₂₇H₄₅OH) consisting of a hydrocarbon (fat-soluble) tail, a middle section consisting of four carbon rings (the steroid bit) and an alcohol (water-soluble) group on the end. Cholesterol is a powerful anti-oxidant and is what bile acids, mineralcorticoids, glucocorticoids and sex hormones are made from.

Cholesterol is "chauffeured" around the body in lipoprotein "limousines". Lipoproteins are lipo (fat-soluble) at one end, protein (water-soluble) at the other end and they form a spherical shell around their contents with the lipo end pointing inwards and the protein end pointing outwards. The shell is like the body of the limousine. In the shell, there are apo(lipo)proteins which are like the chauffeur, as they determine where the particles are taken up. HDL has apo A in its shell which makes it get taken up by receptors in the liver. LDL has apo B in its shell which makes it get taken up by receptors in cells, artery walls etc. The passengers are cholesterol, cholesteryl esters, phospholipids and triglycerides. These limousines have different types, like chylomicrons, VLDL, LDL, IDL & HDL, the difference being the type & amount of apo(lipo)protein and the relative proportions of cholesterol & the other passengers. There are also sub-groups of each type.

The different variants are affected by serum triglycerides. High serum triglycerides (caused by a chronic over-consumption of sugary & starchy carbohydrates for activity level) result in cholesterol-depleted, triglyceride-rich particles and low serum triglycerides result in cholesterol-rich, triglyceride-depleted particles. As cholesterol is a powerful antioxidant, smaller cholesterol-depleted particles (Type B) oxidise faster than larger cholesterol-rich ones (Type A).

Oxidised LDL particles are "bad cholesterol" and are swallowed by scavenger macrophages. These expand into foam cells, which become embedded in the intima of artery walls. Other processes occur which cause cholesterol & calcium to accumulate as a plaque inside the media of artery walls. To see a cross-section through an artery wall, see the top of this page. Unoxidised LDL particles are not swallowed by scavenger macrophages, so unoxidised LDL particles are not "bad cholesterol". In young people, plaques of cholesterol with no calcium can accumulate within artery walls, making Coronary Artery Calcium (CAC) scans ineffective. See Stenosis Can Still Exist in Absence of Coronary Calcium.

Plaques force the inner artery wall inwards, making the artery narrower, impeding the flow of blood through it. This can cause angina pectoris (pain in the chest) as the heart is starved of oxygen, or vascular dementia as the brain is starved of blood. The cap covering the plaque may rupture, causing chunks of plaque to circulate and block coronary arteries (causing a heart attack), or cerebral arteries (causing an ischaemic stroke).

It's possible to reduce serum triglycerides significantly by eating lots of long-chain omega-3 fats from oily fish. These inhibit the conversion of glucose into triglycerides. Inhibiting the conversion of glucose into triglycerides can result in increased blood glucose levels (not good - see below) if sugary/starchy carbohydrate intake is too high. Solution? Reduce sugary/starchy carbohydrate intake to suit activity level.


Why do foam cells embed themselves into the intima of artery walls?

Arteries are elastic, muscular tubes which stretch a bit each time the heart pumps and contract again between beats. They also relax & constrict to control the flow of blood through them. When you get cold, they constrict to reduce the flow of blood to the skin to prevent excessive heat loss. When you get hot, they open to increase the flow of blood to the skin to increase heat loss.

Foam cells don't go just anywhere. They embed themselves into damaged areas of artery walls. This is a good thing, otherwise damaged artery walls could rupture, causing a haemorrhage.


What damages artery walls?

Chronically high blood pressure.
Chronically high blood glucose.
Chronically high blood free radicals.
Chronically high blood homocysteine.
Chronically low blood antioxidants.
Chronically high blood pro-oxidants.
Chronically low blood anti-inflammatories.
Chronically low Vitamin K2.
Chronically high LDL due to hypothyroidism or other factors.


How can I reduce damage to my artery walls?

1) Have blood pressure (BP) tested regularly. There's one problem with having your BP taken in a GP's surgery and that is 'white-coat hypertension' where the stress of having your arm squeezed by the cuff sends your BP up! If you buy your own BP monitor (Lloyds pharmacy sell a fully automatic BP monitor with standard cuff for £9.99), you can become accustomed to using it and overcome white-coat hypertension. 5,000iu/day of Vitamin D3 can reduce BP by making artery walls more elastic. 4g/day of Epsom Salts provides 400mg/day of Magnesium, which acts as a smooth muscle relaxant, reducing BP & cardiac arrhythmias.

2) Have blood glucose (BG) tested regularly. If you're lucky, you may be able to get a HbA1c test. This shows accumulated damage to red blood cells by blood glucose.

3) Don't smoke! Apart from lung cancer, chronic obstructive pulmonary disease & emphysema, smoking speeds the oxidation of LDL.

4) Take a B-complex containing B6, B12 & folic acid, which lowers serum homocysteine levels.

5) Eat a diet rich in anti-oxidants from coloured veggies (beta-carotene), fruits (Vitamin C + bioflavonoids), tomatoes (lycopene), nuts & seeds (gamma-tocopherol & copper), Brazil nuts (selenium), beer/wine in moderation (muscle relaxant), green tea (polyphenols), cocoa/dark chocolate (polyphenols & copper), onions/garlic (quercetin) etc. See Antioxidant state and mortality from coronary heart disease in Lithuanian and Swedish men: concomitant cross sectional study of men aged 50.

6) In men and non-menstruating women, too much iron in the blood relative to copper is pro-oxidant, so don't supplement with iron. Menstruating women have the opposite problem.

7) Take about 2g/day of long-chain omega-3 fats from oily fish, or about 20g/day of flaxseed oil if male, or about 10g/day of flaxseed oil if female. Please note that tinned tuna contains very little omega-3 fats. See Clinical nutrition: 4. Omega-3 fatty acids in cardiovascular care.

8) Eat a diet rich in Vitamin K2, to make calcium go into bones & teeth, instead of into artery walls, kidneys & brain. For good sources of Vitamin K2, see HERE. Note: Warfarin/Coumadin works by depleting Vitamin K, so lots of Vitamin K2 makes Warfarin/Coumadin ineffective.

9) If you're feeling tired and are gaining weight for no obvious reason, get serum thyroid hormone levels tested (TSH, FT4 & FT3 preferably), as low thyroid hormones down-regulate LDL receptors, resulting in LDL particles lingering in the blood for longer than usual. This increases LDL-C, LDL-P (particle count) and the oxidation of the particles. See Neovascularization of coronary tunica intima (DIT) is the cause of coronary atherosclerosis. Lipoproteins invade coronary intima via neovascularization from adventitial vasa vasorum, but not from the arterial lumen: a hypothesis.


What about Benecol & Flora Pro-Activ?

These yoghurts & spreads contain plant sterols/stanols, which reduce total serum cholesterol by up to 15%. However, LDL quality is more important than LDL quantity (up to a point) and there is no evidence that these foods save lives.


What about statins?

Statins (HydroxyMethylGlutarate Coenzyme-A Reductase inhibitors) reduce serum cholesterol. They also have anti-inflammatory & anti-clotting effects by reducing levels of the non-sterol derivative mevalonate and subsequent products. Click HERE to see the cholesterol synthesis pathway. Statins save lives in people who have had a heart attack and in men between the ages of 30 and 60. However, younger & older men and women do not get a significant reduction in deaths, (though heart-attack deaths may be reduced) and there can be undesirable side-effects (muscle pains, memory loss etc). I strongly recommend that anyone taking statins, supplements with at least 100mg/day of Co-Q10, as the synthesis of this vital substance is reduced. Note that fish oils have anti-inflammatory, anti-clotting and anti-arrhythmia actions, but don't suppress the production of Co-Q10.


What about dietary cholesterol?

When cholesterol is eaten, the liver produces less cholesterol. An average egg contains about 250mg of cholesterol. The vast majority of people (who don't have genes for familial hypercholesterolaemia) can eat two eggs a day without significantly affecting their serum cholesterol & triglyceride levels. See Effect of dietary egg on human serum cholesterol and triglycerides. People with the ApoE4/E4 polymorphism are more sensitive to dietary fat & cholesterol raising serum LDL, and cannot eat fat & cholesterol willy-nilly.

There are a couple of sites that have CVD risk calculators, JBS2 and QRISK®2-2013. The National Institute for Clinical Excellence (NICE) no longer recommends the use of JBS2, as it's overly-pessimistic.