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 probably 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 ~1mg/day of 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.

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

Reasons to get off low-fat diets...

Part 1. Increased risk of Coronary Heart Disease due to a lack of gamma-tocopherol in the diet. See Antioxidant state and mortality from coronary heart disease in Lithuanian and Swedish men: concomitant cross sectional study of men aged 50.

See 300 foods highest in Gamma Tocopherol per 100g serving. Low-fat dieters are discouraged from eating foods high in fat. There is no gamma-tocopherol in most Vitamin E supplements. There is gamma-tocopherol in nuts & seeds. Only use Vitamin E supplements that contain mixed tocopherols.

Ditto for beta-carotene, found in coloured veggies and poorly absorbed without dietary fat.
Ditto for lycopene, found in tomatoes and poorly absorbed without dietary fat.


Part 2. Increased risk of tooth decay due to a lack of Vitamin K2. If you listen to Denise Minger's talk, starting at 8 minutes in, she discusses her poor oral health at a young age brought on by a lack of Vitamin K2. Richard Nikoley also discusses the effect of Vitamin K2 on his oral health.

See Vitamin K.


Part 3. Increased risk of gallbladder disease when losing weight. This applies to people (particularly Fair Fat Females in their Forties) who are losing weight rapidly, as this concentrates cholesterol in their bile. I find it rather odd that some people are obsessed with doing exercise, but they fail to exercise their gallbladders by eating at least 5 grams of fat in a meal.

See The Protein-Sparing Modified Fast (PSMF).

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".

The latest "wonder" drugs.

You may have read Aspirin 'cuts cancer death risk by 37 per cent'. 37 per cent, I tell ya!

Or even The £1.40 heart pill lifesaver: 10,000 patients a year could be saved by newly-licensed drug. Ivabradine cuts heart failure deaths by 39 per cent. 39 per cent, I tell ya!

Impressive, huh? Well, not really.

If you read Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial, you'll see that, taking the results from years 2 to 5 inclusive (to eliminate women who had cancer before the start of the study), there's a 77 per cent reduction in cancer deaths in the intervention group. Funny how that fact isn't trumpeted in the press.

If you read Dietary Intake of Menaquinone Is Associated with a Reduced Risk of Coronary Heart Disease: The Rotterdam Study, you'll see that a modest intake (greater than 32.7ug/day) of Vitamin K2 is associated with a 57 per cent reduction in heart attack deaths. There are far more heart attacks than heart failures. Funny how that fact isn't trumpeted in the press.

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. It can cause:-

High fasting serum glucose, which increases the risk factor for Coronary Heart Disease.
High post-prandial serum glucose, which increases the risk factor for Coronary Heart Disease, Retinopathy, Neuropathy & Nephropathy (Kidney failure) amongst other things.
High serum cholesterol.
High serum triglycerides, which in conjunction with high serum cholesterol 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 & urate Kidney stones.
Hypertension, which raises the risk factor for Coronary Heart Disease, Strokes & Kidney failure.
Excessive appetite after eating high-GL carbohydrates, due to rebound low serum blood glucose, leading to overeating & obesity.
Lethargy after eating almost anything, but especially after eating high-GL carbohydrates, due to compensatory hyperinsulinaemia.
If IR is left untreated, it can deteriorate into type 2 diabetes. See Type 2 diabetes in the UK.

The cause and solutions:
1) "Bad" genes. My genes aren't particularly good, but it is possible to change the expression of your genes.

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. NEFAs, 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 uses Glu-T5 transporters which are insulin-independent & 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.

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 serum 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 exercise is compulsory. I have been in denial for years. Then, Uh-oh! There may be trouble ahead... happened. See Increased Glucose Transport–Phosphorylation and Muscle Glycogen Synthesis after Exercise Training in Insulin-Resistant Subjects and Improvement in Glucose Tolerance After 1 Wk of Exercise in Patients With Mild NIDDM (hat-tip to Go Kaleo). See also Move More: Solutions to problems.

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. NEFAs & 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. NEFAs & 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. I go for a 30 minute walk each evening.

3) 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 (fasting serum glucose = 6.8mmol/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 hyperinsulinaemic drowsiness. I was also about the same weight that I was in 2003, so the improvement was not due to weight loss.

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.

4) Deficiency in Magnesium.
For the top 999 foods highest in Magnesium per 100g serving, see HERE. I take ~4g of Epsom Salts/day (~400mg Mg/day). 

5) Deficiency in Vitamin K2.
See 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 take a Vitacost Ultra Vitamin K with Advanced K2 Complex/day. Note: Warfarin/Coumadin works by depleting Vitamin K, so lots of Vitamin K2 makes Warfarin/Coumadin ineffective. 

6) 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.

7) 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.

8) 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.

9) Excessive intake of man-made trans-fats.
Base your diet on Real Food rather than manufactured food products.

10) Excessive intake of chemicals.
Don't swallow toothpaste (fluoride) or disclosing tablets (may contain iodine). Don't hold till receipts between your lips (may be coated in BPA). Don't slather too many chemicals on your skin.

Any other ideas for normalising insulin sensitivity?

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.

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. Why does the brain contain Vitamin D receptors?

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 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 pufas have benefits. See
Low Plasma N-3 Fatty Acids and Dementia in Older Persons: The InCHIANTI Study and
Disruption of glial (oligodendrocyte and astrocyte) cellular function leads to carnosine (b-alanyl-L-histidine) synthesis failure, and nutrient and protective factor deficiency in neurons with secondary development of oxidative stress and amyloid toxicity, with subsequent neuronal dysfunction and development of dementia which stated "Measures which reduce toxicity to vascular endothelium and glia, such as fish oil, may have potential for reducing the likelihood of development of the disease..."

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 scored 26/30 in a MMSE. I thought that this was impressive considering that a) she was taking half the dose of Aricept compared to when she previously got that score, b) she had no adverse effects from taking any of the supplements and c) she was 8 months older and degenerative brain diseases worsen with time.

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 ,
Vitamin K and sphingolipid metabolism: evidence to date ,
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
I don't know what sphingolipids are (I know who probably does) 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 and
Natural approaches to prevention and treatment of infections of the lower urinary tract

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) Most 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) Most 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) Most people don't eat much oily fish. Also, animal & vegetable produce now contains more omega-6 & less omega-3 than it used to. This results in an imbalance.

d) Diets low in vegetable & fruits lack Potassium & Magnesium.

e) Diets low in fermented products lack Vitamin K2.

Because of the above, I supplement with:-
300mg/day of Magnesium as Citrate/Amino Acid Chelate, or 600mg/day as Oxide.
5,000iu/day of Vitamin D3.
15mg/week of Vitamin K2.
I also use Losalt, which provides 2 parts Potassium to 1 part Sodium.

Vitamin K

After Vitamin D, Vitamin K will be the "next big thing" you hear about in the media. Why? Just Google "Vitamin K" and see what comes up. At the top of the list is good ol' Wikipedia.

Vitamin K used to be thought of as only the blood clotting vitamin. Some new-borns have to be given Vitamin K injections to ensure proper clotting. However, Vitamin K is 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, brain etc. A lack of Vitamin K can cause osteoporosis. To prevent/treat osteoporosis, either Vitamin K1 (phylloquinone) or Vitamin K2 (menaquinone or menatetrenone) will do. I used 15mg/day K2 (plus Calcium plus Magnesium plus Vitamin D3) to reverse osteoporosis (bone density -2SD) in my lumbar spine.

However, only Vitamin K2 is effective at removing calcium from the media of artery walls. In The Rotterdam Study, "The relative risk (RR) of CHD mortality was reduced in the upper tertile of dietary menaquinone (K2) compared to the lower tertile (RR 0.43, 95% CI: 0.24, 0.77). Phylloquinone (K1) intake was not related to any of the outcomes." An RR of 0.43 means, on average, a 57% reduction in heart attack deaths. I've now put K2 in Cholesterol & Coronary Heart Disease.

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

See also Vitamin K₂ prevents hyperglycemia and cancellous osteopenia in rats with streptozotocin-induced type 1 diabetes and Vitamins D and K as Pleiotropic Nutrients.

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.

Cholesterol And Coronary Heart Disease

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, small cholesterol-depleted particles (Type B) oxidise faster than large 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, click HERE and scroll down to the bottom of the 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, 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. Eventually, the cap covering the plaque can 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 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. See The unusual suspects.

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 virtually zero 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 arteries, 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 the oxidation of these particles.

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 should supplement 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, and Eat Whole Eggs All Day and Throw Your Statins Away? 375x Increased Dietary Cholesterol Intake From Eggs Reduces Visceral Fat & Promotes Healthy Cholesterol Metabolism. People with ApoE4/E4 are more sensitive to dietary cholesterol raising serum LDL, and cannot eat 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. Note that CVD mortality isn't the same thing as overall mortality. Higher than "normal" total cholesterol level is associated with lower overall mortality, according to Research finds ‘raised’ cholesterol to be associated with a reduced risk of death.