Supplement Alert! Carlson Labs Vitamin K2 MK-4 (Menatetrenone).

In 2003, I started supplementing with one a day of Ultra K2 Menatetrenone (MK-4) 15mg (plus 1.5g/day of Ca plus 400mg/day of Mg plus ~1,000iu/day of Vitamin D3) to reverse osteoporosis in my lumbar spine (bone density by DEXA went from -2SD to 0SD) in 3 years. I then used a maintenance dose of 15mg per week (~2,200ug per day). Everything was fine.

At some point, I switched to one a day of Vitacost Ultra Vitamin K with Advanced K2 Complex. Everything was fine.

Around 2012, I switched to one a day of Carlson Labs, Vitamin K2, 5 mg, in order to use-up my remaining iHerb rewards from the use of my discount code NIG935. I'd lost ~$300 of rewards through non-use. Everything was fine - for a while.

In ~2014, my right hip joint, which had previously caused me pain due to iliotibial band impingement on a bony/calcified outgrowth (cured when I began K2 supplementation), began to cause me pain again. As sleeping on my right side worsened the pain, I began to sleep on my left side. My GP felt my right hip joint and declared that there was some "wear & tear" in it and to use topical analgesics. This helped a bit.

In ~2015, my left shoulder joint, which had previously caused me pain due to impingement on a bony/calcified outgrowth (cured when I began K2 supplementation), began to cause me pain again. I assumed that it was "wear & tear", so I put up with it and applied topical analgesics. This helped a bit.

I recently looked-up rotator cuff pain and was perplexed to see that it was usually caused by impingement on a bony/calcified outgrowth. This of course is quite impossible, if taking 5mg/day of K2!

I took a look at the product reviews on iHerb.com, and noticed comments about joint pains from some reviewers, so I ordered a pot of Ultra K2 Menatetrenone (MK-4) 15mg.

Within a week of switching from Carlson Labs to Vitamin Research Products, my joint pains had virtually* all gone.

EDIT: The pain reduction was accompanied by a feeling of great relief and an increased tolerance to loud music & dazzling headlights. I think my cortisol level has dropped.

Therefore, there's something wrong with Carlson Labs, Vitamin K2, 5 mg. DO NOT USE!

*As the rotator cuff is damaged, there will always be some shoulder pain. As a herniated disk in my lumbar spine (before my osteoporosis was reversed) damaged nerves to/from my right leg, I walk lop-sidedly which means that there will always be some hip & knee joint pain.

Calcium shift: An interesting hypothesis.

More serendipity! Billy the k left a comment that piqued my curiosity.

From http://www.health-heart.org/acceuil.htm The atheroma 'junk' in the media is cholesterol + calcium in older people.

From Aging and calcium as an environmental factor. (emphasis mine)
"The consequences of calcium deficiency might thus include not only osteoporosis, but also arteriosclerosis and hypertension due to the increase of calcium in the vascular wall, amyotrophic lateral sclerosis and senile dementia due to calcium deposition in the central nervous system, and a decrease in cellular function, because of blunting of the difference in extracellular-intracellular calcium, leading to diabetes mellitus, immune deficiency and others.

I highlighted amyotrophic lateral sclerosis in red, as many Facebook friends have been having buckets of water & ice cubes tipped over themselves to raise money for research into this horrible & ultimately fatal condition.

So, what prevents & reverses migration of calcium from hard tissues to soft tissues?
Clue: It carboxylates osteocalcin in bone matrix Gla proteins. Yes, it's Vitamin K2.

See also Calcium, parathyroids and aging. N.B. 50iu/kg bodyweight/day of Vitamin D3 significantly lowers parathyroid hormone.

A "discussion" with Dr. Garth Davis M.D.

I put "discussion" in quotes, for reasons which will become obvious.

The Pyramid of Disagreement. You should be using the top 3 levels at all times.

I've written this because Dr. Davis has blocked me from leaving comments on his Facebook page, and I really need to reply to his last reply to me.

See https://www.facebook.com/drgarth/posts/834305339923709
I was acutely aware as an omnivore, of "walking into the lion's den", by posting a dissenting comment on a vegan's thread, but it was necessary as I had evidence of harm of vegan diets. The evidence on Denise Minger's teeth is supported by her own blog. The evidence on Jay Dinshah's fatal heart attack at the age of 66 is supported by a YouTube video by Dr Michael Greger, the vegan M.D. Dr Greger's video showed evidence of other harms caused by vegan diets that were lacking in vegan DHA & Vitamin B12.

EDIT: Dr. Davis has deleted all of my comments. However, he hasn't deleted his replies to them.

It's impossible to prove a hypothesis, even with n=1,000,000, as the 1,000,001th subject could be the "Black Swan" that disproves it. On the other hand, it only takes 1 "Black Swan" to disprove it. Therefore, n=1 evidence of harm is sufficient to disprove a hypothesis that something is harmless. See Falsifiability.

I provided n=2 evidence of harm.

Dr Davis's final comment to me:-
" Nigel Kinbrum really? You are giving me a n of 2. There is no data that vegans teeth fall out. If she was vitamin K deficient then she was eating a crappy diet lacking greens. It so stupid it's just silly. I also laugh at the idea that authority is some how bad. I have written a book with thousands of references. I give lectures on the topic and have treated thousands of patients yet Denise knows more than me. Silly."

My reply:-
1. As stated above, an n of 2 is double the n needed to disprove your hypothesis that there is no evidence of harm for vegan diets. I'd already pointed that out to you in a previous comment that you've since deleted.

2. I said that Denise's teeth were disintegrating. I didn't say that they fell out. That's a strawman fallacy.

3. Greens contain phylloquinone (Vitamin K1), not menatetrenone (Vitamin K2). Only Vitamin K2 carboxylates osteocalcin in MGP's. The only vegan source of Vitamin K2 is Nattō, a.k.a. pungent beans in a snot sauce.

4. See 3. Denise Minger was not eating a "crappy diet". That's an extremely insulting & uninformed comment for a medical professional to make about someone.

5. I never claimed that authority is bad. When you say "I am an expert in "X", therefore I am never wrong about "X".", that's an "Appeal to authority" fallacy. Jeez!

6. See 5. I never claimed that Denise Minger knows more than you. That's another strawman fallacy.


So, there you have it. Comments will only be approved if they meet my Moderation Policy. As long as I am blocked from commenting on Dr. Davis' Facebook page, Dr. Davis is blocked from commenting on my blog.

Why do some people have trouble doing things in moderation?

This is related to my previous post.

From http://www.kindredcommunity.com/2013/01/xtreme-eating-awards-2013-extremism-running-amok-at-americas-restaurant-chains/

Some people take low-carbing to an extreme, 'cos if reducing carbohydrate intake has benefits, reducing it to zero must be better. Oy!


We're told that eating 5 portions of fruit and vegetables a day is good for us. One patient who was admitted to St George's with malnutrition, had been eating more than 50 portions of fruit and vegetables a day, 'cos if 5 portions of fruit and vegetables a day is good for us, 50 portions of fruit and vegetables a day must be better. Oy!


People who are taking the anti-clotting medication Warfarin need to maintain an accurate balance between their warfarin dose and their Vitamin K intake to keep their INR between 2 and 3, as warfarin antagonizes vitamin K₁ recycling, depleting active vitamin K₁.
"Between 2003 and 2004, the UK Committee on Safety of Medicines received several reports of increased INR and risk of haemorrhage in people taking warfarin and cranberry juice. Data establishing a causal relationship is still lacking, and a 2006 review found no cases of this interaction reported to the FDA; nevertheless, several authors have recommended that both doctors and patients be made aware of its possibility. The mechanism behind the interaction is still unclear." Here's a clue...

From Possible interaction between warfarin and cranberry juice (emphasis, mine):-
"After a chest infection (treated with cefalexin), a man in his 70s had a poor appetite for two weeks and ate next to nothing, taking only cranberry juice as well as his regular drugs (digoxin, phenytoin, and Warfarin). Six weeks after starting cranberry juice he had been admitted to hospital with an INR (international normalised ratio) > 50. Before, his control of INR had been stable. He died of a gastrointestinal and pericardial haemorrhage. He had not taken any over the counter preparations or herbal medicines, and he had been taking his drugs correctly." Cranberry juice contains no Vitamin K. Oy!

"The Committee on Safety of Medicines has received seven other reports through the yellow card reporting scheme about a possible interaction between warfarin and cranberry juice leading to changes in INR or bleeding. In four cases, the increase in INR or bleeding after patients had drunk cranberry juice was less dramatic. In two cases, INR was generally unstable, and in another case INR decreased. Limited information is available about whether patients complied with their treatment in these cases.

Cranberry juice (Vaccinium macrocarpon) is popular and is also used to prevent cystitis. Interaction with warfarin is biologically plausible, because cranberry juice contains antioxidants, including flavonoids, which are known to inhibit cytochrome P450 enzymes, and warfarin is predominantly metabolised by P450 CYP2C9. The constituents of different brands of cranberry juice may vary, and this might affect their potential for interacting with drugs. Whether the constituents of cranberry juice inhibit CYP2C9 and therefore the metabolism of warfarin or interact in another way needs further investigation. Until then, patients taking warfarin would be prudent to limit their intake of this drink." Oy!

So, one man's inadvertent (his doctor should have warned him about eating next to nothing while taking warfarin) dietary extremism resulted in his own death and the restricted intake of cranberry juice for everybody else taking warfarin. Oy. :-(


P.S. It's about time an alternative to warfarin was found. It's difficult to maintain an accurate balance between warfarin dose and Vitamin K intake.

Siri-Tarino et al, Forests & Trees and "Eureka!" moments.

Here's Fig. 2 from Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease:-

Risk ratios and 95% CIs for fully adjusted random-effects models examining associations between saturated fat intake in relation to coronary heart disease and stroke.

The above "Forest" plot has a subtotal RR of 1.07 (95% CI 0.96 1.19). The overall conclusion is that there's no association between saturated fat intake and the RR for CHD. Hmmm.

I looked at the data in Table 3. Of the 16 studies contributing to the CHD results, only 3 of them specify high sat fat intakes over a wide range. The results from these 3 studies are as follows:-

Pietinen et al: RR=0.93 (95% CI 0.6, 1.44).
Mann et al: RR=2.77 (95% CI 1.25, 6.13).
Boniface et al: Pooled RR = 1.37 (95% CI 1.17, 1.65).

The results from Pietinen et al are statistically-insignificant (95% CI values are way above & below 1) with an overall slight protective effect. The results from Mann et al have a RR >> 1 with both 95% CI's >1 and the results from Boniface et al have a RR >1 with both 95% CI's >1.

Other studies either have sat fat intakes varying from very low to low, or specify mean/median sat fat intakes without values for highest & lowest tertiles/quartiles/quintiles etc. Other studies have results that are statistically-insignificant.

However, there are some studies that show a slight protective effect of small amounts of sat fats. How come?

Thanks to George Henderson, I had a "Eureka!" moment. He posted a link to Dietary intake of saturated fat by food source and incident cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis.

Here's Fig. 1 from that study.

HRs and 95% CI's of CVD risk according to quintiles of energy-adjusted SF from different sources (n = 5209).

The Meat SF plot has a net positive slope (bad news, but the range of intake is very small), the Butter & Plant SF plots are random, but the Dairy SF plot has a net negative slope (good news). Dairy saturated fats in amounts of up to 10g/day are protective against CHD. As the Dairy sat fat intake is too small to have a significant effect on lipids, what's the mechanism? I think that it's Vitamin K2. See Chowdhury et al, More forests & more trees and more "Eureka!" moments with cheese.

When you average out the results from all studies, the result is null. This is data dilution statistics.

EDIT: See also Study: Saturated Fat as Bad as Sugar!

Ultra-high-fat (~80%) diets: The good, the bad and the ugly.

The good:

Here's a plot of mean (±SEM) plasma glucose concentrations during an oral-glucose-tolerance test (OGTT) when preceded by either a high-fat (▪) or a high-carbohydrate (□) evening meal and during an oral-fat-tolerance test (OFTT) when also preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal (Fig. 1).

Fig. 1 from Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism

An OGTT (100g of glucose dissolved in water) causes a short-term increase in blood glucose level. Ditto for insulin (see Fig. 2 ▪ & □ below).

Fig. 2 from Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism

An OFTT (40g of fat as cream) doesn't cause a significant increase in blood glucose level (see Fig. 1 • & ○ above). Ditto for blood insulin (see Fig. 2 • & ○ above).

The bad:

Here's a plot of mean (±SEM) plasma triacylglycerol concentrations during an oral-fat-tolerance test (OFTT) when preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal (Fig. 3).

Fig. 3 from Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism

An OFTT (40g of fat as cream) causes a significant increase in blood triacylglycerol (a.k.a. TAG a.k.a. triglyceride a.k.a. TG) level for 3 hours. Note that the effect of a preceding high-carbohydrate meal on fasting TG is only +0.1mmol/L. Is high postprandial TG a problem? Definitely, maybe. From Cholesterol And Coronary Heart Disease , "Cholesterol-depleted particles oxidise faster than large, cholesterol-rich ones." Chylomicrons, chylomicron remnants & VLDL-C are triglyceride-rich, cholesterol-poor, as that's the composition of the fat in the diet.

The ugly:

Here's evidence that high postprandial TG is atherogenic. See Fig. 1 in Fasting Compared With Nonfasting Triglycerides and Risk of Cardiovascular Events in Women.

People who have Insulin Resistance &/or type 2 diabetes have impaired postprandial clearance of glucose and TG, which is atherogenic. Lifestyle Intervention Leading to Moderate Weight Loss Normalizes Postprandial Triacylglycerolemia Despite Persisting Obesity.

Here's evidence that postprandial saturated fat TG is atherogenic. Postprandial triglyceride-rich lipoproteins promote invasion of human coronary artery smooth muscle cells in a fatty-acid manner through PI3k-Rac1-JNK signaling.

See also:-
Postprandial triglyceride-rich lipoprotein changes in elderly and young subjects.,
Effect of a single high-fat meal on endothelial function in healthy subjects.,
Postprandial lipemia: emerging evidence for atherogenicity of remnant lipoproteins.,
Alimentary lipemia, postprandial triglyceride-rich lipoproteins, and common carotid intima-media thickness in healthy, middle-aged men.,
Evidence for a cholesteryl ester donor activity of LDL particles during alimentary lipemia in normolipidemic subjects.,
Association of postprandial hypertriglyceridemia and carotid intima-media thickness in patients with type 2 diabetes.,
Postprandial hypertriglyceridemia impairs endothelial function by enhanced oxidant stress.,
High-energy diets, fatty acids and endothelial cell function: implications for atherosclerosis.,
Impact of postprandial hypertriglyceridemia on vascular responses in patients with coronary artery disease: effects of ACE inhibitors and fibrates.,
[Influence of postprandial hypertriglyceridemia on the endothelial function in elderly patients with coronary heart disease].,
Impact of postprandial variation in triglyceridemia on low-density lipoprotein particle size.,
Association between fasting and postprandial triglyceride levels and carotid intima-media thickness in type 2 diabetes patients.,
[Correlation of lipemia level after fat loading with manifestation of atherosclerosis in coronary arteries].,
Postprandial hypertriglyceridemia and carotid intima-media thickness in north Indian type 2 diabetic subjects.,
Association between postprandial remnant-like particle triglyceride (RLP-TG) levels and carotid intima-media thickness (IMT) in Japanese patients with type 2 diabetes: assessment by meal tolerance tests (MTT).,
Postprandial lipemia and remnant lipoproteins., 
Elevated levels of platelet microparticles in carotid atherosclerosis and during the postprandial state.,
Postprandial metabolic and hormonal responses of obese dyslipidemic subjects with metabolic syndrome to test meals, rich in carbohydrate, fat or protein.,
Atherosclerosis, diabetes and lipoproteins., 
Clinical relevance of non-fasting and postprandial hypertriglyceridemia and remnant cholesterol.,
Post-prandial hypertriglyceridemia in patients with type 2 diabetes mellitus with and without macrovascular disease.,
A hypertriglyceridemic state increases high sensitivity C-reactive protein of Japanese men with normal glucose tolerance.,
CD36 inhibitors reduce postprandial hypertriglyceridemia and protect against diabetic dyslipidemia and atherosclerosis., 
[Trends of evaluation of hypertriglyceridemia -from fasting to postprandial hypertriglyceridemia-].,
The effects of dietary fatty acids on the postprandial triglyceride-rich lipoprotein/apoB48 receptor axis in human monocyte/macrophage cells.

See also What Is the Significance of Postprandial Triglycerides Compared With Fasting Triglycerides? and Uncovering a Hidden Source of Cardiovascular Disease Risk.

A counter-argument is that the subjects in the above studies were eating carbohydrate, and that postprandial TG isn't atherogenic if you're not eating much carbohydrate. Definitely, maybe. In the absence of carbohydrates, there is still glucose in the blood, thanks to the liver and kidneys. Also, some carbohydrates don't spike blood glucose (or fructose) level. It's pure speculation that the subjects in the above studies had high blood glucose at the same time as high postprandial TG. As Insulin Resistance/Metabolic Syndrome and/or a high-sugar diet raise fasting TG, and there was no significant association between fasting TG and the risk factor for CHD, this suggests that the subjects had no significant metabolic derangement and were not eating excessive amounts of sugar.

According to Very Low-Carbohydrate and Low-Fat Diets Affect Fasting Lipids and Postprandial Lipemia Differently in Overweight Men, there's a ~50% reduction in postprandial TG after adaptation to a low-carb, high-fat diet. However, mean energy intake was 1,850kcals/day, the subjects were in a 500kcal/day energy deficit and %E from fat was 60%.

Some people's LDL becomes very high on low-carbohydrate high-fat diets. See Some Metabolic Changes Induced by Low Carbohydrate Diets.

It's possible to get Coronary Artery Calcium (CAC) scans, to measure the amount of calcified plaque in coronary arteries. While a high CAC value means lots of plaque, a zero CAC value doesn't necessarily mean zero plaque, as young people and people with a high Vitamin K2 intake don't have significant calcification. See Stenosis Can Still Exist in Absence of Coronary Calcium.

See also Page 10 of  HIGH CARBOHYDRATE DIETS: MALIGNED AND MISUNDERSTOOD - Nathan Pritikin.
"Could such a cream meal precipitate an angina attack because the oxygen-carrying capacity of the blood is lowered?"
The answer is "Yes."

Rigid diets & taking loadsa supplements to compensate for them.

I do not believe you want to be doing that!

This post was inspired by a recently-published study by Alan Aragon & Brad Schoenfeld, as bodybuilders are a group of people who often eat a rigid diet (some eat skinless chicken breasts, broccoli & brown rice for several meals each day).

See Nutrient timing revisited: is there a post-exercise anabolic window?
"Collectively, these data indicate an increased potential for dietary flexibility while maintaining the pursuit of optimal timing."

This post is also aimed at people who eat severely restricted diets in the (often mistaken) belief that something's making them ill.

People with type 1 diabetes who struggle to keep their blood glucose within reasonable limits (3 to 8mmol/L, or 24 to 144mg/dL) benefit from restricting their intake of high-GL carbohydrates, so this post is not aimed at them. See The problem with Diabetes.

People with type 2 diabetes who severely restrict their intake of carbohydrates must be in caloric deficit, otherwise the physiological insulin resistance caused by high serum NEFAs will mess up just about everything in their body if they are in caloric balance or caloric excess. I've read (so it could be false) that a certain non-skinny blogger who I'm in conflict with (who has type 2 diabetes and who eats a VLC diet) has heart problems and is taking medication(s) for high blood pressure. Hmmm.

People who suffer from gastrointestinal problems after eating gluten-containing foods, or mucus after eating casein-containing foods may have impaired gut integrity. See Gluten - more than just a pain in the guts?

Supplements that I consider of positive value are:-

Fish oils: If the diet is low in oily fish (tinned tuna is not an oily fish), there may be insufficient EPA & DHA (especially in men, children & post-menopausal women). Women of reproductive age can get away with taking flaxseed oil.

Magnesium: If the diet is low in veg/high in dairy, there may be too much Calcium relative to Magnesium.

Vitamin D3: If the lifestyle results in sun-avoidance, insufficiency in Vitamin D is highly likely.

Vitamin K2: If the diet is low in animal fats and/or fermented foods, insufficiency in Vitamin K2 is highly likely.

Supplements that I consider of negative value are:-

Vitamin A: If there's an insufficiency in Vitamin D, supplementing with Vitamin A/β-carotene may exacerbate it. As Vitamin D + Calcium may reduce cancer risk, supplementing with Vitamin A absent Vitamin D3 may increase cancer risk.

Vitamin E: If there's an insufficiency in γ-tocopherol, supplementing with α-tocopherol may exacerbate it. As γ-tocopherol may reduce CHD mortality risk, supplementing with α-tocopherol absent γ-tocopherol may increase CHD mortality risk. Most Vitamin E supplements contain α-tocopherol only. Some Vitamin E supplements contain mixed tocopherols and these are O.K.

\ curves and U curves: Vitamins D3 and K2 again.

Here are some curves relating to Vitamin D. Ref: http://www.ncbi.nlm.nih.gov/pubmed/23601272

Hazard Ratios (HRs) vs serum Vitamin D level

The solid lines are the 95% confidence intervals (CI) & mean for all-cause mortality. 95% CI's are the values within which 95% of the subjects tested fall. 2.5% fall below the lower CI and 2.5% fall above the upper CI. The dashed lines are the 95% CIs & mean for coronary heart disease (CHD) mortality. Most of the curves follow a \ curve, indicating that more Vitamin D is better, up to 66ng/mL (150nmol/L, the level that I'm at). The interesting curve is the upper dashed line, which follows a U curve.

The U curve indicates that a Vitamin D level of greater than 30ng/mL (75nmol/L) increases the Hazard Ratio (HR) for CHD in the top 2.5% of subjects only, relative to 30ng/mL, even though the mean HRs for CHD & all-cause mortality (the more important parameter) are decreasing, up to 66ng/mL. What's occurring?

See Vitamin K. The increase in HR for CHD mortality above 30ng/mL in the top 2.5% of subjects only is almost certainly due to calcification within artery walls, due to under-carboxylation of osteocalcin in bone Matrix Gla Proteins, caused by insufficient Vitamin K2 rather than excessive Vitamin D. This is why I supplement with Vitamin K2. See also Vitamin D toxicity redefined: vitamin K and the molecular mechanism.

Cancer, part 2.

In cancer, I discussed omega-3 and methylglyoxal.

Methylglyoxal

This time, I'm just going to do a Research Review, by publishing a list of PubMed searches with the following Filters activated: Abstract available, published in the last 10 years, Humans.

Cancer AND "Dichloroacetic Acid".

Cancer AND "Magnesium".

Cancer AND "Methylglyoxal".

Cancer AND "Omega-3".

Cancer AND "Vitamin D3".

Cancer AND "Vitamin K2".

I added searches for Magnesium and Vitamin K2, as I supplement with those and want to see if they have a positive or negative effect on Cancer. I added Dichloroacetic Acid (DCA), as I've read about it.

Quality >> Quantity.

Mum passed away peacefully in the middle of the night. I'm waiting for paperwork to be done.

"And the best you can hope for is to die in your sleep."

On the internet, I read that Dementia with Lewy bodies has a mean survival time of 6 years from the onset of symptoms. Mum first became confused in mid-July 2007, so it's been just under 6 years. Does this mean that all of the supplements I gave her were worthless. Hell, no!

As mentioned in Look after your brain., mum's MMSE score increased from 14 to 26 out of 30 after taking medication and supplements. The medication gave a 3 point increase in MMSE score on average, so the rest of the increase in MMSE score was probably due to the supplements, which had no undesirable side-effects.

On Christmas day 2008, mum was capable of preparing Brussels sprouts for cooking, though she got the knives, forks & spoons mixed up when she tried to lay the table. Here's her final Christmas at home. Roast duck with all of the trimmings. Om, nom, nom!

Mum's last Christmas at home.

People commented on how happy mum always was. Even though she probably didn't know who she was or I was, when I said "Fancy a cup of tea, mum?", she'd reply "Ooh yes, please!" That was the last part of her speech to go.

In conclusion, I believe that quality of life trumps quantity of life, so supplementation for the win.

At first I was afraid, I was petrified...

My titles are becoming increasingly blatantly song-orientated. No YouTube video, this time.

I just read Hans Wu's latest post Alzheimer's and Dementia and had a few thoughts.

1) In the early stages of mental decline, there is still self-awareness and the process is frightening. Constant reassurance is the best thing for somebody in this state. As self-awareness fades, one becomes happy. An example of this is HAL-9000 as his memory modules were being unplugged in the film "2001 a space odyssey". My mum is in this state, thank goodness.

I entered this state temporarily during an Insulin Shock Test on my pituitary gland, when my serum glucose fell to 1.5mmol/L (27mg/dL) under medical supervision. I was blissfully unaware of my confusion. Too much alcohol in the blood also causes loss of self-awareness. I entered this state last week while socialising with a friend. After half a bottle of White Zinfandel, I was blissfully unaware of my merriness!

2) When I see "arterial stiffness", I think "inappropriate calcification" and "Vitamin K2".

3) Transient Ischaemic Attacks (TIAs a.k.a. mini-strokes) cause loss of blood flow to parts of the brain, resulting in amnesia. There may be some permanent brain damage, depending on how long the TIAs last. TIAs can be caused by spasms in arteries within the brain. Ditto migraines.

When I see "spasm", I think "magnesium".

Insulin Resistance: Solutions to problems.

Before I start on what may be the most important thing that I've ever written, here's Don't Stop Movin' by S Club 7. It's a clue to what's coming.


The problem:

Insulin Resistance (IR) is a major problem for a significant percentage of the population in the developed world. If left untreated, it can deteriorate into Type 2 Diabetes (T2D). See Type 2 diabetes in the UK.

IR & T2D can cause:-

High fasting & postprandial serum glucose, which increases the risk factor for Coronary Heart Disease, Retinopathy, Neuropathy & Nephropathy (Kidney failure), amongst other things. 
High fasting & postprandial serum triglycerides, which increases the risk factor for Coronary Heart Disease. See Lifestyle Intervention Leading to Moderate Weight Loss Normalizes Postprandial Triacylglycerolemia Despite Persisting Obesity.
High serum cholesterol, which increases the risk factor for Coronary Heart Disease.
High serum Free Fatty Acids (a.k.a. FFAs a.k.a. NEFAs) from IR fat cells, which increases the risk factor for Sudden cardiac death and also worsens IR in liver & muscle cells. 
High serum uric acid, which increases the risk factor for Gout & Uric acid Kidney stones.
Hypertension, which raises the risk factor for Coronary Heart Disease, Strokes & Kidney failure.
Excessive appetite after eating high-GL carbohydrates, leading to overeating & obesity.
Lethargy/sleepiness after eating almost anything, but especially after eating high-GL carbohydrates, due to postprandial hyperinsulinaemia.


Possible causes (IR is multi-factorial) and solutions:

1. "Bad" genes. My genes aren't particularly good, but it is possible to change the expression of genes. See below.

2. Full cells. A full cell is an IR cell. Consider Liver, Muscle and Fat cells:-

a) Liver cells: Liver cells are a 2-way street. "Stuff" (e.g. FFAs, Glucose & Fructose) goes in and "stuff" (e.g. Ketones & Glucose) comes out. Glucose normally comes out of the liver at a rate of ~5g/hour to fuel the brain, but this can increase a lot under the control of Insulin, Glucagon & Cortisol. If more stuff goes in than comes out, liver glycogen stores fill up and vice-versa. When liver glycogen stores become full, liver cells down-regulate processes that produce liver glycogen e.g. hexokinase & Glu-T2 transporters. Liver cells effectively become IR, to stop more stuff from going in.

However, fructose is transported by Glu-T5 transporters which are insulin-independent & taken up by fructokinase which has a high affinity for fructose, so fructose effectively "barges its way in" to the liver. This is why fructose is a problem for people who have permanently full liver glycogen stores.

The Protein-Sparing Modified Fast (PSMF) depletes liver glycogen and liver & pancreatic fat rapidly. See also Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.

b) Muscle cells: Muscle cells are a 1-way street as far as Glucose is concerned, though Amino Acids can go in & come out. Muscle glycogen cannot be used to produce blood glucose - it can only be used by muscles. When muscle glycogen stores become full, muscle cells down-regulate processes that produce muscle glycogen e.g. hexokinase & Glu-T4 transporters. Muscle cells effectively become IR to stop more stuff from going in.

As per It's all in a day's work (as measured in Joules), muscle cells use mostly fat at rest & lowish-intensity exercise. Glycogen usage increases rapidly as exercise intensity increases. Now do you see the significance of the music video above? Intense exercise (e.g. Running, Sprinting, Resistance training with weights, parts of High-Intensity Interval Training a.k.a. HIIT, parts of Tabata & parts of Zumba) depletes your muscle cells and makes them Insulin Sensitive.

This means that activity is compulsory. See Physiological and health implications of a sedentary lifestyle.

See also Increased Glucose Transport–Phosphorylation and Muscle Glycogen Synthesis after Exercise Training in Insulin-Resistant Subjects , 
Improvement in Glucose Tolerance After 1 Wk of Exercise in Patients With Mild NIDDM (hat-tip to Go Kaleo) and
Move More: Solutions to problems. Excessive sedentariness was a secondary contributor to my IR.

However, don't overdo it! You may have a funny turn, keel over & hurt yourself. See "Funny turns": What they aren't and what they might be.

c) Fat cells: Fat cells are a 2-way street. Fat cells are a bit like balloons that are full of holes. As stuff (e.g. FFAs & glucose) goes in, the balloon expands to accommodate it. As more stuff goes in and the balloon gets bigger, the internal pressure increases and the holes get bigger, so stuff (e.g. FFAs & glycerol) comes out at a faster rate. At some level of fullness, stuff comes out as fast as it goes in. At that point, fat cells are effectively IR. So, don't overstuff your fat cells by getting too fat. If you are already too fat, medium intensity exercise (e.g. Walking, Power Walking, Jogging, "Aerobics", parts of High-Intensity Interval Training a.k.a. HIIT, parts of Tabata & parts of Zumba) depletes your fat cells and makes them Insulin Sensitive.

Dress appropriately so that you don't feel cold. Feeling cold is what stimulates your appetite, not exercise. See Influence of resistance and aerobic exercise on hunger, circulating levels of acylated ghrelin, and peptide YY in healthy males.

3. Empty (of glycogen) cells.
If carbohydrate intake is too low (say, less than 50g/day), physiological Insulin Resistance develops in order to spare glucose for the brain (as parts of the brain run on glucose only) and red blood cells. This is reversible on increasing carbohydrate intake. People who are on ketogenic diets are advised to increase their carbohydrate intake for a few days prior to taking an Oral Glucose Tolerance Test. See HIGH CARBOHYDRATE DIETS AND INSULIN EFFICIENCY.

4. Deficiency in Vitamin D3.
See Hypovitaminosis D is associated with insulin resistance and ß cell dysfunction.
The effects of calcium and vitamin D supplementation on blood glucose and markers of inflammation in nondiabetic adults.
The role of vitamin D and calcium in type 2 diabetes. A systematic review and meta-analysis.
A double-blind, randomized, placebo-controlled trial of the short-term effect of vitamin D3 supplementation on insulin sensitivity in apparently healthy, middle-aged, centrally obese men.
Plasma 25-hydroxyvitamin D concentration and metabolic syndrome among middle-aged and elderly Chinese individuals.
Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient - a randomised, placebo-controlled trial.

In January 2003, I had Impaired Glucose Tolerance/Metabolic Syndrome/Prediabetes (fasting serum glucose = 5.8mmol/L & 2 hours post-75g glucose load serum glucose = 8.7mmol/L). A sandwich used to send me to sleep.

By September 2008, I had Normal Glucose Tolerance (fasting serum glucose = 5.0mmol/L & 2 hours post-75g glucose load serum glucose = 3.7mmol/L). I also no longer suffered from carbohydrate-induced comas. I was also about the same weight that I was in 2003, so the improvement wasn't due to weight loss. Hypovitaminosis D was the primary contributor to my IR.

So, either use a UVB sun-lamp as per instructions to receive a sub-erythemal dose (not quite going pink) or get tested by your GP and supplement with Vitamin D3 accordingly. I take 5,000iu of Vitamin D3/day.

5. Deficiency in Magnesium.
See Magnesium and type 2 diabetes. For the top 999 foods highest in Magnesium per 200kcal serving, see HERE. I've been taking ~4g of Epsom Salts/day (~400mg Mg/day, dissolved in 2 litres of fluids that I drink each day, to avoid laxative effects) since 2003 as it reversed osteoporosis in my lumbar spine.

6. Deficiency in Vitamin K2.
See Vitamin K2 Supplementation Improves Insulin Sensitivity via Osteocalcin Metabolism: A Placebo-Controlled Trial and Vitamin K₂ prevents hyperglycemia and cancellous osteopenia in rats with streptozotocin-induced type 1 diabetes.
Good sources of Vitamin K2 can be found HERE. I was taking 15mg/day of MK-4 since 2003, as it reversed osteoporosis in my lumbar spine. I'm now 15mg of MK-4 three times a week as a maintenance dose.
Note: Warfarin/Coumadin works by depleting Vitamin K, so lots of Vitamin K2 makes Warfarin/Coumadin ineffective.

7. Deficiency in Manganese.
See Manganese supplementation protects against diet-induced diabetes in wild type mice by enhancing insulin secretion. For the top 999 foods highest in Manganese per 100g serving, see HERE.

8. Deficiency in, or excess of Copper w.r.t. Zinc. See Dietary copper supplementation restores β-cell function of Cohen diabetic rats: a link between mitochondrial function and glucose stimulated insulin secretion. For the top 468 foods highest in Copper per 100g serving, see HERE.

9. Deficiency in, or excess of Zinc w.r.t. Copper. See Zinc, pancreatic islet cell function and diabetes: new insights into an old story. For the top 999 foods highest in Zinc per 100g serving, see HERE.

10. Excessive intake of man-made trans-fats.
Base your diet on minimally refined produce rather than over-refined &/or moreish food products.

11. Excessive intake of chemicals.
Don't swallow toothpaste (fluoride) or disclosing tablets (as they may contain iodine). Don't hold till receipts between your lips (may be coated in BPA).

12. More than one of the above. See A tale of the unexpected & an analogy.

Any other ideas?

Finally, the obligatory picture. Hannah Spearritt is rather nice. :-p

I nearly forgot! Today, when I arrived at mum's nursing home, I found her reading a book. She hasn't done that for over a year. She even knew that it was Wednesday. Ketogenic diet for the win. Mum now has a dual-fuel brain. EDIT: Mum passed away in April 2013, so although it's possible to slow the progression of Lewy Body Dementia and reduce the symptoms of it, it wasn't possible to cure it.

Look after your brain.

"One in three people over 65 will die with dementia..." said Dr Susanne Sorensen, head of research at the Alzheimer's Society. I read this in a recent BBC News article Vitamin D 'is mental health aid' which referred to the study Serum 25-Hydroxyvitamin D Concentration and Cognitive Impairment.
The article contained the usual phrase "...more work was needed..."

The above article also led to Parkinson's linked to vitamin D which referred to the study Prevalence of vitamin d insufficiency in patients with Parkinson disease and Alzheimer disease. "However, the Emory University researchers do not yet know if the vitamin deficiency is a cause or the result of having Parkinson's". "Further research is required...." yet again.

It's like someone standing by their broken-down car wondering whether it's the empty fuel tank that's made the car stop or whether it's the car stopping that's made the fuel tank empty. Does it matter? Just put some fuel in the tank and see what happens! See also Higher serum vitamin D3 levels are associated with better cognitive test performance in patients with Alzheimer's disease.

Severe Mental Impairment blights the lives of many old people and their loved ones. My mum developed Parkinson's Disease a few years ago. I didn't know anything about the condition at the time, but it's caused by the formation of Lewy Bodies (blobs of abnormally-folded alpha-synuclein protein) in the substantia nigra part of the brain, which controls movement. This part of the brain has high levels of the Vitamin D receptor. I don't know why the brain contains Vitamin D receptors, but I think that they'd like to receive some Vitamin D!

As Lewy Bodies form in other parts of the brain, mental faculties decline. The hippocampus is involved with short-term memory. The neocortex is involved with concious thought.

Mum started showing obvious signs of mental impairment in August 2007. She was assessed by a Community Psychiatric Nurse (CPN) in January 2008 when she scored 14/30 in a MMSE. She was unable to remember 3 words or follow 2 simple instructions in a row (e.g. fold this piece of paper in half and put it on the floor). I started her on 5,000iu/day of Vitamin D3, as it was having a positive effect on my mental function. She was prescribed Aricept, starting at 5mg/day for a month then increasing to 10mg/day. In May 2008 she was re-assessed and scored 26/30 in a MMSE. EDIT: In 2010, Mum's consultant told me that Aricept increases MMSE score by 3 points on average.

Unfortunately, Aricept has side-effects including severe diarrhoea and worsening of the symptoms of Parkinson's Disease, which she complained about, so her Aricept dose was reduced back down to 5mg/day.

Unsurprisingly, this resulted in a slight decline in mum's mental faculties. In November 2008, I increased her intake of smoked salmon to about 400g/week, as the consumption of long-chain omega-3 pufas have benefits. See
Low Plasma N-3 Fatty Acids and Dementia in Older Persons: The InCHIANTI Study.

After about four weeks, this had a noticeable (by myself and mum's friend) positive effect on her mental faculties so, inspired by Dr Art Ayers, I started her on Turmeric (curcumin) extract and Goldenseal (berberine) extract. See
Curcumin inhibits aggregation of alpha-synuclein
Neuroprotective effects of curcumin
Alpha-synuclein assembly as a therapeutic target of Parkinson's disease and related disorders
Curcumin labels amyloid pathology in vivo, disrupts existing plaques, and partially restores distorted neurites in an Alzheimer mouse model
Influence of piperine on the pharmacokinetics of curcumin in animals and human volunteers
Research on the mechanism of neuronal apoptosis in Alzheimer's disease and the effects of tetrohydroberberine on the apoptosis... and
Berberine chloride can ameliorate the spatial memory impairment and increase the expression of interleukin-1beta and inducible nitric oxide synthase in the rat model of Alzheimer's disease.

On January 12th 2009, mum was re-assessed and still scored 26/30 in a MMSE. I thought that this was impressive considering that 1) she was taking half the dose of Aricept, compared to when she previously got that score, 2) she had no adverse effects from any of the supplements and 3) she was eight months older and degenerative brain diseases always worsen with increasing age.

I mentioned to the CPN who did the MMSE that I was starting mum on 15mg/week Vitamin K2 as there were benefits. See
Menaquinone-4 concentration is correlated with sphingolipid concentrations in rat brain ,
Vitamin K status influences brain sulfatide metabolism in young mice and rats ,
Substantial sulfatide deficiency and ceramide elevation in very early Alzheimer's disease: potential role in disease pathogenesis and
The possible role of vitamin K deficiency in the pathogenesis of Alzheimer's disease and in augmenting brain damage associated with cardiovascular disease
New Vitamin K, an emerging nutrient in brain function
New The Science of Brain Health and Cognitive Decline | Eric Kandel
New Vitamin K2, Intelligence and the Aging Brain

I don't anything about sphingolipids, but sulfatides are good and ceramides are bad.

Around the time that mum collapsed, I received a copy of a letter from the CPN to mum's GP which stated "I have informed him (i.e. me) that I am unaware of any robust evidence that these substances are of any benefit." However, there is no evidence that these substances are of any harm.

And finally......
What started the cascade of confusion and collapse leading to hospitalisation and discharge to a nursing home was a simple Urinary Tract Infection UTI) of e. coli. I don't know why UTIs cause so much confusion in elderly people, but elderly females are at a high risk of developing UTIs because a) elderly people don't drink enough so they don't pass enough urine, b) females have insufficient spacing between anus & urethra and c) elderly females who have any urinary/faecal leakage wear a Tena disposable "nappy/diaper", which increases the likelihood of faeces entering the urethra.

To reduce the risk of further UTIs, I have supplied the nursing home with a pot of D-mannose Plus, which contains D-mannose and cranberry extract, with instructions to add a heaped teaspoonful to a glass of juice once a week. See Intervening with urinary tract infections using anti-adhesives based on the crystal structure of the FimH-oligomannose-3 complex,
Natural approaches to prevention and treatment of infections of the lower urinary tract and
Vitamin D Induction of the Human Antimicrobial Peptide Cathelicidin in the Urinary Bladder.


EDIT: Thanks to Galina L for bringing the following study to my attention.
Magnesium supplementation in the treatment of dementia patients.
It's probably of no help to Lewy Body Dementia sufferers, as they already have high Mg levels in their CSF. See CSF Mg and Ca as diagnostic markers for dementia with Lewy bodies.

Continued on Look after your brain, Part 2.

Supplements: Who needs 'em?

According to Health Professionals, nobody. Apparently, we get all of the vitamins, minerals & other nutrients that we need from a "Healthy Balanced Diet" (whatever that is!).

According to me, just about everybody. Due to modern farming methods, food ain't what it used to be. Dammit, even nostalgia ain't what it used to be! Due to changes in lifestyle:-

a) People are more sedentary than they used to be. This means that they require less food than they used to in order to not get fat. Less food, coupled with less nutrients in the food = dietary deficiencies.

b) People don't get as much sun on their skin as they used to, as they now work, play & live mostly indoors and when they do go outside, they are encouraged to Slip Slop Slap (slip on a shirt, slop on sunscreen and slap on a hat). This results in hypovitaminosis D, as only an Eskimo's diet contains enough dietary Vitamin D. The RDA of 200/400/600iu/day (depending on age) is woefully inadequate and totally out of touch with modern research.

c) Many people don't eat much oily fish. Also, animal & vegetable produce now contains more omega-6 & less omega-3 than it used to. This can result in a large imbalance. I eat two 120g cans of mackerel in spicy sauce a day. This also provides protein.

d) Diets low in dark green vegetables & fruits lack Magnesium & Potassium.

e) Diets low in fermented foods lack Vitamin K2.

I currently supplement with:-
400mg/day of Magnesium, as 4g/day Epsom Salts dissolved in water & the solution added to drinks.
5,000iu/day of Vitamin D3.
15mg/day of Vitamin K2.

See also The usual suspects.

Vitamin K(2)

From http://www.health-heart.org/acceuil.htm The atheroma 'junk' in the media is cholesterol + calcium in older people.

Vitamin K used to be thought of as only the blood clotting (Koagulation) vitamin, as the liver needs it in order to synthesise Factor X. Some new-borns need Vitamin K injections, to achieve proper blood clotting.

However, Vitamin K is also needed for the carboxylation of osteocalcin in Bone Matrix Gla Proteins. The what of what in what? In simple terms, Vitamin K is needed to ensure that dietary calcium goes into your bones, rather than into your artery walls, kidneys, nervous system, brain, pancreas etc. A lack of Vitamin K can cause osteoporosis. To prevent/treat osteoporosis, either Vitamin K1 (phylloquinone) or Vitamin K2 (menaquinone or menatetrenone) will suffice. Only Vitamin K2 can remove calcium from the media of artery walls.

I used 15mg/day of Vitamin K2 (plus 750mg/day of Ca plus 400mg/day of Mg plus ~1,000iu/day of Vitamin D3) to reverse osteoporosis in my lumbar spine (bone density by DEXA went from -2SD to 0SD) in 3 years. I didn't take Fosamax, as it damages the oesophagus if it's not swallowed while standing up & washed down with shed-loads of water. It also kills osteoclasts. My endocrinologist told me that what I did was impossible. The impossible, I can do. Miracles take a little longer! :-)

From The Rotterdam Study:-"The relative risk (RR) of CHD mortality was reduced in the upper tertile (~40.9ug/d) of dietary menaquinone (K2) compared to the lower tertile (~15.1ug/d), RR 0.43, 95% CI: 0.24, 0.77.
Phylloquinone (K1) intake was not related to any of the outcomes."

RR 0.43 means, on average, 57% reduction in heart attack deaths. I've now put K2 in Cholesterol & Coronary Heart Disease.

Vitamin K2 is required for blood glucose regulation. See Vitamin K₂ prevents hyperglycemia and cancellous osteopenia in rats with streptozotocin-induced type 1 diabetes.

Vitamin K2 is required for brain health. See Look after your brain.

Good food sources of Vitamin K2 can be found here.

Warfarin antagonises Vitamin K, so it can result in arterial calcification. Anyone taking warfarin should ask their GP for regular check-ups to keep an eye on this potential problem. Taking Vitamin K supplements makes warfarin ineffective.

As we age, arteries can harden, bones can soften and joints can become painfully calcified. See Calcium shift: An interesting hypothesis for an hypothesis explaining how this can happen, a list of other diseases caused by Calcium Shift, and how to prevent and/or reverse it (the answer's in this post!).

Speculations on vitamin K, VKORC1 genotype and autism.
"Recent research has documented the protective effect of Vitamin K on neural cells and its role in maintaining normal neural development. Of interest, specific neural effects of Vitamin K overlap with key brain development aberrations, including those associated with autism. Furthermore, Vitamin K protects against oxidative stress associated with toxic exposure."

"...a small sample of severely autistic children of Somali descent residing in the Minneapolis/St. Paul area of Minnesota were genotyped and found to have a higher than expected genetic substitution that results in reduction in the efficiency of the Vitamin K cycle."

NEW!  Current trends and recent advances in diagnosis, therapy, and prevention of hepatocellular carcinoma. Hepatocellular carcinoma (HCC) is Liver cancer.
"Sorafenib is currently the only approved systemic treatment for HCC."

"Interestingly, coffee and vitamin K2 have been proven to provide protective effects against HCC."

Cholesterol And Coronary Heart Disease

From http://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.