Guess who didn't look after his brain?

Due to the sudden deterioration in my mum's physical & mental health and also due to struggling to come to terms with her having to spend the rest of her life in a nursing home (not the happiest of places), my diet went completely to pot.

I "went off" salmon, sardines & powdered linseeds and started to eat carbohydrate/fat-based comfort foods. A black cloud slowly descended over me. I lost the motivation to do anything, including updating this blog. I also slept a lot. This continued for several months.

Then, for no apparent reason, a few weeks ago I got an urge to eat smoked salmon. I added 200g of smoked salmon twice a week back into my diet and after a few weeks, the black cloud started to lift.

Before I started supplementing with Vitamin D3, I used to eat lots of oily fish but did not function correctly mentally. This time, my Vitamin D3 status was good (I never stopped taking supplements even when I had the black cloud over me) but my EPA (Eicosapentaenoic Acid) and DHA (Docosahexaenoic Acid) intakes were near zero.

In conclusion, it would appear that my brain needs adequate Vitamin D3 and EPA and DHA to function correctly mentally.

I won't be blogging as much as I have been previously, as I've now dumped the vast majority of the nutritional knowledge within my brain into this blog. If I come across anything new, I'll post it here.

Finally, I've found the cheapest source yet of 5,000iu Vitamin D3 gelcaps. See http://www.iherb.com/Vitamin-D3-5-000-IU-360-Softgels/18335 That's a 1 year supply for about £10. First-time buyers can use discount code WAB666 to get $5 off the first order.

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 (amyloid plaques 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 very 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. 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 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 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 ,
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 quite impressive considering that a) she was taking half the dose of Aricept that previously gave her that score, b) there were no adverse side-effects from the supplements and c) she was about 8 months older and progressive, degenerative brain diseases worsen with the passing of 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 and
Substantial sulfatide deficiency and ceramide elevation in very early Alzheimer's disease: potential role in disease pathogenesis

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 also no evidence that these substances are of any harm.

There is a herbal extract called Huperzine A which has an effect like Aricept (i.e. it's also an acetylcholinesterase inhibitor) which I am considering for future use. See Potential therapeutic targets of huperzine A for Alzheimer's disease and vascular dementia ,
Alternative medicine and Alzheimer disease and
Efficacy and safety of natural acetylcholinesterase inhibitor huperzine A in the treatment of Alzheimer's disease: an updated meta-analysis

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

I will supply the nursing home with Effercitrate (potassium citrate + citric acid tablets) to be added to mum's drinks if the staff are unable to get her to drink enough. I use this and find that it significantly increases my urinary output.

The future: I just saw it.

Today is Thursday 19th February 2009. I've just read an article in The New York Review of Books 'Drug Companies & Doctors': An Exchange dated 26th February 2009. I don't even possess a Flux Capacitor!

The above article was linked from Drug Companies & Doctors: A Story of Corruption which I found on The International Network of Cholesterol Skeptics (THINCS).

"Because drug companies insist as a condition of providing funding that they be intimately involved in all aspects of the research they sponsor, they can easily introduce bias in order to make their drugs look better and safer than they are. Before the 1980s, they generally gave faculty investigators total responsibility for the conduct of the work, but now company employees or their agents often design the studies, perform the analysis, write the papers, and decide whether and in what form to publish the results. Sometimes the medical faculty who serve as investigators are little more than hired hands, supplying patients and collecting data according to instructions from the company.

In view of this control and the conflicts of interest that permeate the enterprise, it is not surprising that industry-sponsored trials published in medical journals consistently favor sponsors' drugs—largely because negative results are not published, positive results are repeatedly published in slightly different forms, and a positive spin is put on even negative results. A review of seventy-four clinical trials of antidepressants, for example, found that thirty-seven of thirty-eight positive studies were published. But of the thirty-six negative studies, thirty-three were either not published or published in a form that conveyed a positive outcome. It is not unusual for a published paper to shift the focus from the drug's intended effect to a secondary effect that seems more favorable."

Oh dear!

A slight hitch.

On Friday 13th February, my mum collapsed and had to go to hospital. She's stable but completely incoherent at the moment, due to a combination of a) having a Urinary Tract Infection (UTI) and b) discontinuing her anti-dementia medication last week in the (mistaken) belief that it was giving her hallucinations.

It's hard to believe just how rapidly mental function in an old person can decline due to a UTI, but mum had a Mini Mental State Examination (MMSE) score of 26 out of 30 on Monday 12th January. It would have been 0 last Friday.

Normal Blogging will be resumed when mum's infection has been treated and she is back on her medication. I will be getting mum to use D-mannose in her juice in future, as this is effective against E. coli and Klebsiella.

Cancer.

By request, I'm writing about cancer. I didn't know this, but cancer is now the No.1 killer of men in the UK. I previously thought that coronary heart disease was the No.1 killer.

Cancer is such a huge subject that, rather than oversimplify it, I'll put a link to Wikipedia. Warning: Pictures of tumours.

Vitamins get a mention, particularly Vitamin D, but EFAs aren't mentioned. This is odd, as typing "Omega-3 Cancer" into PubMed produces 1,230 results going back to the 1980s. Here are some of the results, ignoring animal studies:-

Some effects of the essential fatty acids linoleic acid and alpha-linolenic acid and of their metabolites gamma-linolenic acid, arachidonic acid, eicosapentaenoic acid, docosahexaenoic acid, and of prostaglandins A1 and E1 on the proliferation of human osteogenic sarcoma cells in culture.

Selective killing of human cancer cells by polyunsaturated fatty acids.

Chronic arachidonic acid eicosanoid imbalance: a common feature in coronary artery disease, hypercholesterolemia, cancer and other important diseases. Significance of desaturase enzyme inhibition and of the arachidonic acid desaturase-independent pathway.

n-3 fatty acids and cancer.

Fish consumption and breast cancer risk: an ecological study.

Effect of docosahexaenoic acid on rate of differentiation of HL-60 human leukemia.

N-3 and N-6 fatty acids in breast adipose tissue and relative risk of breast cancer in a case-control study in Tours, France.

Opposing effects of dietary n-3 and n-6 fatty acids on mammary carcinogenesis: The Singapore Chinese Health Study.

Induction of apoptosis in human pancreatic cancer cells by docosahexaenoic acid.

Dietary intakes of omega-6 and omega-3 polyunsaturated fatty acids and the risk of breast cancer.

And, at No.1 in the list:-

Nutritional knowledge of primary health care physicians in Jeddah, Saudi Arabia.

"These results showed that physicians need more training on nutrition. Nutrition should be an essential part in the curriculum of medical schools and continuing medical education for primary health care physicians."

Hear-hear!

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, probably everybody. Due to changes in 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) We are more sedentary than we used to be. This means that we require less food than we used to in order to not get fat. Less food, coupled with less nutrients in our food = dietary deficiencies.

b) We don't get as much sun on our skin as we used to. This results in hypovitaminosis D, as only an Eskimo's diet contains enough dietary Vitamin D. The RDA of 400iu/day is woefully inadequate and out of touch with modern research.

Because of this, I supplement with the following:-
300mg/day of Magnesium as Amino Acid Chelate, or 450mg/day as Oxide.
500mg/day of Vitamin C + 25mg/day of Citrus Bioflavonoids.
5,000iu/day of Vitamin D3.
15mg/week of Vitamin K2.
I also use Losalt, which provides 2 parts Potassium to 1 part Sodium.

Research shows.....

....that people who eat a low-fat breakfast like Special K are more likely to be slimmer than those who don't.

So states the Special K advert. I wonder whether the researchers used a control group who ate a high-fat breakfast? Somehow, I doubt it. I eat a high-fat breakfast, if you look at the Blog post immediately below this one and I am slimmer than when I didn't eat breakfast. Skipping breakfast causes low blood glucose, which encourages over-eating later-on. Therefore, people who eat breakfast are more likely to be slimmer than those who don't.

That's the problem with "Research". It usually shows what people want it to show. By omitting control groups, such research is utterly worthless. While I'm on a mini-rant, "Clinically proven" is another phrase often bandied about in advertisements. I have news for you. Clinical studies can only disprove something. The best that a clinical study can do is provide evidence that something is beneficial to some or most of the people in the study only. It cannot be extrapolated to the rest of the population.

Food Porn.

It's the only porn you're going to get on this Blog!

I was looking at Richard Nikoley's Blog at http://www.freetheanimal.com/ and I couldn't help but notice all of the pictures of yummy food on it. When I mention to people that I am on an "Atkins-style" diet, they usually say "Oh, so all you eat is bacon & eggs and those expensive low-carb bars, right?" I have yet to buy a low-carb bar.

This post should give you an idea of what I eat. Some of my meals contain Burgen soya & linseed bread and even sweetcorn. These foods are relatively high in starchy carbohydrate, but my body can tolerate them thanks to Vitamin D.

The first picture is what I often (but not always, as variety is important) have in the morning. It's basically coffee with extra oomph provided by a 60cc scoop of powdered linseeds (in the storage jar) and a 60cc scoop of unflavoured whey protein (a milk protein). Vanilla flavouring, brown sugar & Splenda improve the flavour of this concoction, which has the consistency of wallpaper paste!


I do eat bacon & eggs but not for breakfast. I usually have it for lunch, accompanied by chopped onions & mushrooms microwaved with Losalt, Lee & Perrins & Extra-Virgin Olive oil. A big squirt of tomato ketchup gives me my third portion of vegetables! The whole lot sits on top of a slice of Burgen toast.


For afternoon tea, I may have something salmony. Here's a simple smoked salmon sarnie made with ~100g of smoked salmon and a couple of slices of raw onion.


I have a friend who hates the skin & bones in tinned salmon. As this is where a lot of the omega-3 fat & minerals are, I tried an experiment to see if I could disguise them. I blended a 213g tin of wild red salmon with a couple of dollops of Hellman's Real Mayonnaise & a little "juice" from a tin of sweetcorn. I then mixed sweetcorn with the salmon mayonnaise. I dumped a load of the salmon & sweetcorn mayonnaise mix onto a slice of Burgen buttered with Anchor. A little sliced tomato & cucumber completed the ensemble.


Sometimes. I just dump everything on a plate!


For supper, I usually microwave something meaty with something vegetably. Here are some Somerfield "Best Ever" Pork & Chorizo sausages microwaved with chopped onions & mushrooms in a Lea & Perrins-based gravy.


Here's an Aldi quarter-pounder beefburger with microwaved chopped onions, mushrooms & English mustard.


Here's an Aldi chicken jambonette in a sun-dried tomato, balsamic & sweet basil sauce microwaved with peas & mixed veg. The sauce went everywhere!


Here's an Aldi lamb shank in a mint & red wine-flavoured sauce. The shank was in a bag, so the sauce didn't go everywhere when I microwaved it on the plate alongside the peas & mixed veg. The vegetables look a little strange as I microwaved them as they were with a little Losalt (and no added water), but they tasted just fine. Not adding any water means that there is no loss of minerals.


And finally, here's an Aldi pork shank in sweet & sour sauce cooked as per the lamb shank. Aldi have a lot of different varieties of chicken jambonettes, lamb & pork shanks and I will be trying them out as they are very reasonably priced.


So, can I spend the rest of my life on this sort of diet? Oh, yes yes yes yes yes!

The Firefox a.k.a. Red Panda.

My browser is named after this little fella (or girl, I can't tell!).



I left Red Pandas out of my previous Blog post as they are not Bears (Ursidae), but are in a family of their own (Ailuridae).

Like Giant Pandas, Red Pandas have a false thumb which helps them to grip bamboo shoots & leaves. They also spend most of their lives eating, pooing (as they also can't digest cellulose) and sleeping!



That's how I used to spend a lot of my life when I ate a high-carb diet. Since I've been eating more salmon, I've been more active than usual. It's not yet 8am and I'm on-line, typing this.

The Bear Essentials.

I'm writing about bears. Why? I was having a discussion, oh alright then, argument with a vegan lady. There was a thread on a message board about the slaughter of pigs and she argued that humans are not designed/evolved/w.h.y. to eat meat based on the following list:

Meat-eaters: have claws
Herbivores: no claws
Humans: no claws

Meat-eaters: have no skin pores and perspire through the tongue
Herbivores: perspire through skin pores
Humans: perspire through skin pores

Meat-eaters: have sharp front teeth for tearing, with no flat molar teeth for grinding
Herbivores: no sharp front teeth, but flat rear molars for grinding
Humans: no sharp front teeth, but flat rear molars for grinding

Meat-eaters: have intestinal tract that is only 3 times their body length so that rapidly decaying meat can pass through quickly
Herbivores: have intestinal tract 10-12 times their body length.
Humans: have intestinal tract 10-12 times their body length.

Meat-eaters: have strong hydrochloric acid in stomach to digest meat
Herbivores: have stomach acid that is 20 times weaker than that of a meat-eater
Humans: have stomach acid that is 20 times weaker than that of a meat-eater

Meat-eaters: salivary glands in mouth not needed to pre-digest grains and fruits.
Herbivores: well-developed salivary glands which are necessary to pre-digest grains and fruits
Humans: well-developed salivary glands, which are necessary to pre-digest, grains and fruits

Meat-eaters: have acid saliva with no enzyme ptyalin to pre-digest grains
Herbivores: have alkaline saliva with ptyalin to pre-digest grains
Humans: have alkaline saliva with ptyalin to pre-digest grains

Based on a chart by A.D. Andrews, Fit Food for Men, (Chicago: American Hygiene Society, 1970)

The fact that humans can't digest cellulose (the stuff that plant cell walls are made of) seemed to have been conveniently left off the above list, so I pointed out that if she wanted to play the list game, perhaps she should read http://www.second-opinions.co.uk/carn_herb_comparison.html. Someone then posted a link to Humans are Omnivores. Humans are omnivores. End of.

Then I had a thought. Bears have a digestive system similar to ours. Here's a list of some bears and their characteristics:

Polar Bears: Body composition: Variable (they have a layer of blubber for thermal insulation and they gain body fat when food is plentiful to sustain them through times when food is unavailable). Activity: Very active (pregnant females hibernate). Fertility: On average 2 cubs every year. Diet: 99% meat (there may be some vegetable matter in the guts of the animals that they eat).

American Black Bears: Body composition: Leaner than Polar Bears as ambient temperatures are higher. Activity: Very active (even active when hibernating). Fertility: 2-3 cubs every 2 years. Diet: 10-15% meat, insects & plants.

Brown Bears: Body composition: Leaner than Polar Bears as ambient temperatures are higher. Activity: Very active (even active when hibernating). Fertility: On average 2 cubs every year. Diet: 90% plants, insects, fish and small mammals.

Giant Pandas: Body composition: Quite high body fat. Activity: Quite sedentary. Fertility: 1 cub every 2 years (if the mother has 2, she lets 1 of them die as she can only raise 1 at a time). Diet: 99% bamboo shoots but will eat meat, fish and eggs when available.

Do you see a pattern, here?

Ignorance, apathy & bone-idleness...

...are not attractive traits in people. But do you know what? I don't know, I don't care and quite frankly, I can't be bothered!

Each day, I surf a lot of message boards and I read a lot of messages. People who post messages on message boards obviously have access to the Internet. So when I saw:
"Didn't Atkins die from a heart attack with high cholesterol?", I just had to reply:
"Yeah! Course he did. Everybody knows that. See Everybody knows.........Part 1" to which I got the reply:
"There's no need for your sarcasm, Nigeepoo - pack it in. I was only asking a question" to which I replied:
"Sorry. Did I come across as sarcastic? This is sarcasm Let me Google that for you"

When I saw "Asparagus. How good is it for you and why?", I just had to reply:
"Let me Google that for you"

And when I saw "What is PSMF?", well I'm sure you can guess what I replied. I am such a bad boy!

So, next time you want to find out something, try Google, Wikipedia or (if it's a study) PubMed.

Anyway, here is a picture with a caption that makes me wet myself laughing.

There was this Cleveland dentist...

...and his name was Weston A. Price MS., D.D.S., F.A.G.D.

He was a dentist, so he got to see inside a lot of mouths. What he saw worried him - a lot. There's no point in me copying and pasting stuff that someone else has written, so read all about it at http://www.westonaprice.org/brochures/wapfbrochure.html

To sum-up. Mr Price travelled around the world with his wife looking inside the mouths of relatively primitive people, compared to the residents of Cleveland. What he saw impressed him - a lot. Considering that primitive people don't have access to clean water, food, medicine and other modern aids to living, they had hardly any tooth decay, gum disease or overcrowded teeth.

So he took lots of photographs, made lots of measurements and asked lots of questions. When he finished his travels, he wrote a book called Nutrition and Physical Degeneration A Comparison of Primitive and Modern Diets and Their Effects. You can read it at http://www.journeytoforever.org/farm_library/price/pricetoc.html

It's worth your while reading this book. The conclusions:-

Don't eat food that's been "buggered about with". Eat as much natural food as you can and prepare it in a way that maximises the nutrients and minimises the anti-nutrients. Don't worry about the fat in it, as fat contains the fat-soluble Vitamins A, D, E & K (but not enough D unless you live on a diet of oily fish, seals & beluga whales). For more information, see http://www.westonaprice.org/

That is all.

So, when & where did it all go wrong?

No, I'm not talking about Demand Five! I'm talking about us, modern man & woman. We have improved hygiene, clean water & food, modern medicine, anti-biotics, anti-virals etc. We should be enjoying good health and vitality into our nineties. We're not, though. Degenerative diseases like Type 2 Diabetes, Coronary Heart Disease, Cancer, Dementia, IBS etc are afflicting increasing numbers of people (including youngsters) and are even starting to reduce our longevity statistics. Why?

On one side of the fence are the anti-animal fat brigade who claim that animal fats are the cause of all our health problems and that we should all be eating more vegetable fats and reducing our cholesterol.

On the other side of the fence are the anti-carb brigade who claim that carbohydrates are the cause of all our health problems and that we should all be eating less carbohydrates and increasing our fat consumption.

I'm sure you can guess where I am. I have the splinters to prove it!

In 1911, hydrogenated vegetable oil (Crisco) entered the marketplace. So, in 1911, fat turned bad! See http://www.westonaprice.org/motherlinda/fats_crisco.html

Interestingly, rates of Coronary Heart Disease started to rise from 1920, 9 years later. Co-incidence?

Our genes may have not changed much in the last few hundred thousand years, but our lifestyles certainly have. We now live mostly sedentary lives (which makes our muscles less sensitive to insulin). We now live and work mostly indoors (which makes us deficient in Vitamin D).

We now don't eat much oily fish. Our vegetables contain much less omega-3 fat than they used to (to make them stay fresh for longer). Our meat now contains much more omega-6 and much less omega-3 fat than it used to (due to feeding animals on grains). These changes make us deficient in omega-3 fat (which makes our muscles less sensitive to insulin).

We now eat loads of refined carbohydrate (which causes unstable blood glucose & insulin levels) and loads of processed foods (which makes us deficient in Magnesium and fibre).

As a result of all of the above changes, we have many modern diseases. We can't blame it on one factor only. So, what can we do? Here's one suggestion....



























Good health!

I do NOT believe they wanted to be doing that!

As Harry Enfield's "It's only meee!" character used to say. I'm talking about Demand Five, Channel 5 TV's on-line "watch television on demand" service.

Up until last Friday, I was watching Neighbours using Firefox 3. Yes, I know that's really sad! On Monday, I went to watch Neighbours and was greeted by a new Media Player window displaying:
"Your flash plug-in is out of date
Please download the latest version here"
No problemo, thought I. I updated my flash plug-in and went back to watch Neighbours, to be greeted by the new Media Player window displaying:
"Your flash plug-in is out of date
Please download the latest version here"
Uh-oh! I contacted the Demand Five Support Team informing them of my problem. I got the following reply:

"Greetings,
Thank you for contacting the Demand Five Support Team.
Please try to access with Internet Explorer..."

I stopped reading at that point as I don't use Internet Explorer. I e-mailed the Support Team informing them of that fact. I got the following reply:

"Greetings,
We apologize for the inconvenience, since our contents are related with DRM therefore our service is only compatible with Internet Explorer. All other browsers (e.g., Firefox, Opera, Safari, etc...) are not compatible at this time..."

They left out Google Chrome! So basically, Demand Five just alienated a large number of their users by making their site incompatible with every browser except Internet Explorer. Thanks a bunch! (That's an ironic thank you, for the benefit of foreign readers).
As I really wanted to watch Neighbours, I ran Internet Explorer, updated my flash plug-in and off I went. Monday's episode played O.K. but Tuesday's episode stopped after the 15 second Weight-Watcher's intro'. I e-mailed the Support Team informing them of that fact. I got the following reply:

"Greetings,
Please upgrade your DRM security at the following site:
http://go.microsoft.com/FWLink?LinkID=34506

The Demand Five Support Team
downloadsupport@five.tv
AM"

I clicked the link and pressed the Upgrade button. It didn't work. I e-mailed the Support Team informing them of that fact. I got the following reply:

"Greetings,
Thank you for contacting the Demand Five Support Team.
Please follow the instructions given below:

Please open Windows Media Player (WMP)
In the menu area at the top of the WMP window, click "Tools"
If "Tools" is not visible, Right-click on the upper bar area on WMP and a Menu-list will appear
In the list that appears, choose "Options"
In the window that opens, the "Player" tab will be the first tab displayed
Please ensure that both "Download codecs automatically" and "Connect to the Internet" are selected
Please select the "File Types" tab
Click "Select All", located below and to the right of the list
Click "Apply", located at the bottom of the "Options" window
Please select the "Network" tab
In the "Protocols for MMS URLs" section, un-check "RTSP/UDP" and "RTSP/TCP"
Now, re-check "RTSP/UDP" and "RTSP/TCP"
All three protocols should now be selected
Click "OK" at the bottom of the "Options" Window
Please close Windows Media Player."

It worked. I e-mailed the Support Team informing them of that fact and also asked them why Demand Five couldn't be as easy to use as BBC iPlayer. I didn't get a reply. I have posted the above information so that you too can watch Neighbours....everybody needs good Neighbours....

UPDATE: The Demand Five media player now works with Firefox 3.
According to the support page it's not compatible, so don't tell Demand Five otherwise they might mess it up again.

The Protein-Sparing Modified Fast (PSMF)

As promised, I shall discuss the PSMF (I was going to have a whinge about the sudden loss of ability to watch "Neighbours" on Demand Five using Firefox, but I'll save that for another time if Demand Five Support don't fix the problem!)

What's a PSMF?

A standard PSMF is ~1g of protein for every kg bodyweight a day plus lots of green leafy vegetables plus six to ten fish oil capsules a day plus vitamin & mineral supplements plus unlimited water AND NOTHING ELSE. You may find this quite literally hard to swallow! PSMF may also stand for Protein Strictly, Mother-F***er! A 100kg person (e.g. me) may get to eat ~400kcals from protein + ~100kcals from incidental carbohydrates & fats = ~500kcals a day. Hear that rumbling noise? It's my tummy! A well-known (to me, anyway) PSMF is Lyle McDonald's Rapid Fat Loss Handbook. For information on that, see http://forums.lylemcdonald.com/forumdisplay.php?f=7 and Is Rapid Fat Loss Right For You?

To make a PSMF easier to manage (but have a slower rate of weight loss), here are some modifications.

1) Instead of six to ten fish oil capsules a day, stir ~25g of powdered linseeds into a large glass of drink and swallow the lot. Do this at breakfast-time. 25g of linseeds contains ~10g of fat (of which ~6g is Alpha-Linolenic Acid, an omega-3 fatty acid) which does the following:-

a) It stimulates the gall-bladder to empty, thus reducing the risk of gallstones.
b) It usually results in a bowel movement some time later. The ~10g of soluble fibre in the linseeds + accompanying fluid guarantees regularity.
c) It provides women (but not men) with all of the omega-3 fat they need each day.

Men need to eat either half a 213g tin of wild red salmon a day or six to ten fish oil capsules a day as their bodies don't produce enough DHA from Alpha-Linolenic Acid. See Extremely Limited Synthesis of Long Chain Polyunsaturates in Adults: Implications for their Dietary Essentiality and use as Supplements

2) Eat about 100g of protein a day. As meat, poultry & fish contains 20-25% protein, this means that you can eat ~1lb of meat, poultry & fish a day. 100g of protein a day is well within the capabilities of your liver and kidneys.

3) Eat about 44g of fat a day. This allows you to choose less lean cuts of meat & poultry and you can even eat the skin on chicken as long as you factor it into your total fat allowance. It also allows you to use vinaigrette salad dressings or a knob of butter or a dollop of real mayonnaise to make your vegetables taste nicer.

4) Eat about 50g of carbohydrate a day. This allows you to eat shed-loads of leafy green vegetables and also an onion. It also allows you to eat a portion of fruit e.g. an apple or a bowl of berries/cherries with Splenda & a dollop of double cream each day.

5) If you do any intense exercise (e.g. HIIT or resistance training with weights), you can eat an extra 50g of slow-release carbohydrates a couple of hours beforehand to fuel it.

6) Supplement with 5,000iu/day of Vitamin D3. Nowadays, many of us spend our lives mostly indoors and this causes many of us to become deficient in Vitamin D. Please read the Vitamin D Blog.

In conclusion:

100g of protein provides 400kcals, 44g of fat provides 400kcals and 50g of carbohydrate provides 200kcals, making a grand total of 1,000kcals a day. Hopefully, this will be enough to stop your tummy from rumbling. If you weigh over 100lbs and don't lose weight on 1,000kcals a day, see your GP as you may have a thyroid problem.

I believe that the above diet tackles the problems of gallstones, constipation, dry skin, dry hair, depression and dietary deficiencies. You get to eat real food and quite a lot of it too, for a Rapid Fat Loss diet.

Very Low Calorie Diets (VLCDs)

A well-known VLCD is The Cambridge Diet. Lighter Life is another VLCD.

The VLCD is, as its name suggests, very low in Calories and is aimed at morbidly obese people i.e. people who have a Body Mass Index (BMI) of over 40. Such people are at a very high risk of dropping dead of a heart attack and they are also at a high risk of complications caused by high blood pressure, high blood glucose, high blood triglycerides, high blood cholesterol, high blood LDL-c, low blood HDL-c and high blood uric acid. In addition, morbidly obese people have breathing problems e.g. sleep apnoea and they are also at a high risk of dying while under anaesthetic if they need to be operated on. Such people need to lose weight rapidly. However, people who are overweight (BMI 25-29.9) or obese (BMI 30-39.9) or who are just unhappy with their bodies should not embark on a VLCD as the risks outweigh the benefits.

1) VLCDs result in rapid weight loss. You may think that this is a good thing, but rapid weight loss brings with it problems.

a) Excessive loss of muscle. This is more of a problem for women who, because they have naturally-low testosterone levels, have great difficulty regaining any lost muscle.

b) High risk of developing Gallstones. Rapid weight loss results in an increase in the concentration of cholesterol in bile. This increases the risk factor for gallstones, something that women have a higher risk factor for than men. There's an acronym FFFF for people who are at a high risk of developing gallstones. It stands for Female, Forty, Fat, Fair. What makes the situation even worse is that VLCDs are very low in fat. The gallbladder is a muscular bag which stores bile. When >=5g of dietary fat is eaten, this stimulates the secretion of cholecystokinin, which then stimulates contraction of the gallbladder muscle, which expels bile from inside the gallbladder into the duodenum. The lower the fat content of a meal, the less the gallbladder contracts and gallbladder stasis can result. See The role of gallbladder emptying in gallstone formation during diet-induced rapid weight loss. The problem with this study is that the two groups of subjects were not eating the same number of calories. See Gallbladder motility and gallstone formation in obese patients following very low calorie diets. Use it (fat) to lose it (well). and Similarity in gallstone formation from 900 kcal/day diets containing 16 g vs 30 g of daily fat: evidence that fat restriction is not the main culprit of cholelithiasis during rapid weight reduction.
In these studies, both groups were on the same calorie intake. In the second study, 17% of the low-fat group developed gallstones whereas only 11.2% of the higher-fat group developed gallstones.

The other problem with a very low fat intake is EFA deficiency. Essential Fatty Acids are called that for a reason....they are essential for us to live. Dry skin & hair are common on VLCDs. The small amount of fat that there is in a VLCD almost certainly contains mostly omega-6 polyunsaturates. A lack of omega-3 EFAs can adversely affect mental function. Depression is common on VLCDs. See Omega-3 fatty acids and major depression: A primer for the mental health professional. Another problem with very low fat intakes is a lack of fat-soluble vitamins, particularly Vitamins D3 and K. See Vitamin D and Vitamin K.

2) VLCDs contain excessive amounts of sugars. This has two problems.

a) Unstable blood glucose levels. See Blood Glucose, Insulin & Diabetes. You don't notice peaks in blood glucose. However, dips cause severe hunger pangs and, in some people, neurosis. See Hypoglycemia & Neurosis.

b) Carbohydrates fill glycogen stores. As glycogen stores become filled, fat-burning decreases. When glycogen stores become full, fat-burning falls to zero. Fat-burning increases again as glycogen stores deplete between meals - but you feel hungry.

Sedentary people's bodies don't burn much carbohydrate. See Everyone is Different. At rest, on average a fasted person derives ~65% of energy from fats and ~35% from carbohydrate, although there are extremes of 93% fat-burning to 20% fat-burning. Even if someone who has full glycogen stores derives 100% of their energy at rest from carbohydrate, as they are only burning ~1kcal/minute at rest, their body is only burning 0.25g of carbohydrate/minute. So why feed someone carbohydrate when their body doesn't need it?

c) People with excess belly fat almost certainly have The Metabolic Syndrome. This causes various problems including high serum triglycerides (TGs). Eating carbohydrate that isn't burned and can't be stored raises TGs. I know about this as I have blood test results which showed TGs increasing with increasing carbohydrate intake. High TGs are bad news for your arteries. See Cholesterol And Coronary Heart Disease.

3) VLCDs don't contain enough protein. Protein supplies Amino Acids (AAs) to the body. These are used to preserve muscle mass. AAs can also be used to generate blood glucose in the liver by a process called Gluconeogenesis (GNG), which makes the consumption of carbohydrates redundant for most sedentary people.

4) VLCDs don't contain enough fibre. Constipation is common on VLCDs.

In my next Blog post, I will discuss a Rapid Fat Loss alternative to the VLCD that overcomes all of the above problems and is therefore much safer and more pleasant to be on.

For a discussion of VLCDs, see What do you think of Very Low Energy Diets?

Why exercise may or may not help you to lose weight.

Exercise. I hate it. I'm about as active as a Brazilian 2-toed Sloth. The problem that I have with exercise is that it makes me feel really hungry and I end up eating more Calories than I burned by exercising. This is due to the effect of AMPk on my brain.

The thing about exercise in moderation is that it's good for health and fitness. The problem is that some people think that lots more is better. That ain't necessarily so. The 38 year old lady sitting near me at karaoke last night used to run a lot when she was at school. She now needs a replacement knee joint due to damaged cartilage and she had her knee wired up to a TENS machine.

Too much early morning exercise can also make you ill, by raising serum Cortisol levels. Excessive Cortisol is immunosuppressive. See Early morning exercise could make you ill. Excessive Cortisol also causes water retention, so people who over-exercise can gain (water) weight. Excessive Cortisol can also cause muscle loss, thin skin and osteoporosis.

Starving yourself and over-exercising just makes things even worse. From WHY is the combination of high intensity and/or long duration activity a mistake when calories are being severely restricted?

"Water retention: cortisol binds to the mineralocorticoid receptor (the receptor involved in water retention, well one of them). And although cortisol has 1/100th of the effect on water balance of the primary hormones (aldosterone and a couple of others), since there is like 8000 times as much of it, it can cause a major effect." and

"Excessive cortisol, especially chronic elevations cause other problems not the least of which is leptin resistance. Which only magnifies the drop in leptin from dieting. This could be another mechanism behind the greater drop in metabolic rate for the study I mentioned above."

So, what's the best thing to do for maximum fat loss with minimal muscle loss? A mixture of high-intensity exercise (resistance training with weights, or sprinting) and medium-intensity exercise (jogging) is better than just medium-intensity exercise. See Resistance Weight Training With Endurance Training Enhances Fat Loss, Impact of Exercise Intensity on Body Fatness and Skeletal Muscle Metabolism and HIIT & Run.

One theory to try and explain the improved fat loss is that Calories are burned after the high-intensity exercise is finished. However, the Excess Post-exercise Oxygen Consumption (EPOC) only amounts to about 35kcals so it isn't significant. What is significant is the appetite reduction produced by high-intensity exercise, the opposite effect from low and medium-intensity exercise.

Magnesium: Just as important as Calcium.

Feeling stressed-out? Suffering from night cramps? You're probably deficient in Magnesium. After Vitamin D and Omega-3 fats, Magnesium is the third thing that people are most likely to be deficient in. Processed foods are low in Magnesium. For a list of the 999 richest sources of Magnesium per 100g serving, see http://www.nutritiondata.com/foods-000120000000000000000-w.html

An optimum intake of Magnesium is approximately 50% of your Calcium intake. Other sources of Magnesium are Milk of Magnesia and Epsom Salts. Too much Magnesium gives you loose bowel movements, but it takes >3g/day to do this. Because of this, Milk of Magnesia and Epsom Salts are used as remedies for constipation.

Magnesium is also available as a dietary supplement. Magnesium oxide (Magnesia) isn't as well-absorbed as Citrate/Amino Acid Chelate forms, so take 50% extra if using oxide. Magnesium is absorbed through the skin, so adding Epsom Salts to your bathwater is another option.

I've got a lovely bunch of coconuts!

Coconut Oil is the No. 1 most stable oil for cooking at high temperatures.

What’s in coconut oil?

According to http://www.manitobaharvest.com/nutrition/index.asp?itemID=183 , coconut oil is ~91% saturated fatty acids, ~7% monounsaturated fatty acids, ~2% omega-6 fatty acids and zero omega-3 fatty acids.

According to McCance and Widdowson's “The Composition of Foods”, the fatty acid composition of coconut oil is as follows:-

Name(:0=sat, :1=mono, :2=poly, n6=omega-6) Quantity (%)
Caprylic Acid (C8:0)___________________________7.5
Capric Acid (C10:0)____________________________7.1
Lauric Acid (C12:0)___________________________47.7
Myristic Acid (C14:0)_________________________15.8
Palmitic Acid (C16:0)__________________________9.0
Stearic Acid (C18:0)___________________________2.4
Arachidic Acid (C20:0)_________________________1.0
Palmitoleic Acid (C16:1)_______________________0.4
Oleic Acid (C18:1)_____________________________6.6
Linoleic Acid (C18:2 n6)_______________________1.8

Won’t all that saturated fat give me a heart attack?

Whether or not you get coronary heart disease depends on your whole diet. According to http://www.ajcn.org/cgi/reprint/34/8/1552.pdf , Pukapukans got 26% (male) to 30% (female) of their total Calories from saturated fats. Tokelauans got 47% (male) to 49% (female) of their total Calories from saturated fats. Tokelauans had total serum cholesterol 35-40mg/dL (0.9- 1.03mmol/L) higher than Pukapukans.

As Tokelauans were getting about seven times more energy from saturated fats than the 7% that current healthy eating guidelines recommend, they must have been dropping like flies from coronary heart disease or strokes, right? Wrong! To quote:-
“Vascular disease is uncommon is both populations and there is no evidence of the high saturated fat intake having a harmful effect in these populations.”
How come? Well, if you look at the rest of the Tokelauans’ diet, you’ll see virtually no refined sugar or cereal products. Basically, they weren’t eating any junk. When Tokelauans migrated to New Zealand, their sat fat intake fell to ~41% of total calories but as they were eating more refined carbs & sugar, their lipid profile got worse.

What are the benefits of coconut oil?

Medium-chain fatty acids are metabolised rapidly without passing through the liver and they provide a quick source of energy for muscles. There is some evidence that medium-chain fatty acids stimulate the thyroid gland to secrete more T4 & T3 which can be an aid when cutting. There is also some evidence that Lauric Acid has anti-bacterial & anti-viral properties. Coconut oil is also good for the skin when rubbed in.

Where can I buy coconut oil?

Don’t buy cheap coconut oil. It’s almost certainly Refined, Bleached & Deodorised which detracts from its health benefits. The best coconut oils are Organic Virgin Oils. Some good on-line sources are
http://www.fresh-coconut.com/ ,
Coconut Oil UK and
http://www.revital.co.uk/product_search.cfm?searchString="Nutiva+Organic+Extra+Virgin+Coconut+Oil"

In addition, check-out Rosso's Blog on Saturated oils.

As sure as Eggs is Eggs.....

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

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

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

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

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

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

Can I drink eggs raw to save time?

There are three potential problems with this:

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

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

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

What about all that cholesterol in egg yolks?

Current “Healthy Eating” guidelines state that we should eat no more than 3 egg yolks/whole eggs per week. This is based on the erroneous assumption that dietary cholesterol always increases serum cholesterol and that this is always a bad thing. According to http://www.ajcn.org/cgi/reprint/32/5/1051.pdf , adding or not adding 500mg of dietary cholesterol from two large eggs per day made no significant difference to serum cholesterol or triglycerides in 116 healthy male subjects. Some went up and some went down. Eddie Vos at http://www.health-heart.org/cholesterol.htm reckons that you’d have to eat 20 whole eggs per day to get as much dietary cholesterol as the liver produces each day (5g). Egg yolks do contain some fat and this should be factored into your total diet. If you happen to have the genes for familial hypercholesterolaemia, then you need to keep a close eye on dietary cholesterol intake.

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

Linseeds/Flaxseeds & Flaxseed oil.

"Where flax is eaten...health abounds!" - Mahatma Ghandi.
These little seeds pack a quadruple-whammy of protein, omega-3 essential fatty acids (EFAs), soluble fibre, and minerals, vitamins & co-factors.


What's in flaxseeds & flaxseed oil?

Click http://www.nutritiondata.com/facts/nut-and-seed-products/3163/2 and set serving size to 100g to see what nutrients there are in flaxseeds.
Click http://www.nutritiondata.com/facts/fats-and-oils/7554/2 and set serving size to 100g to see what nutrients there are in flaxseed oil.


How do I eat flaxseeds & flaxseed oil?

Flaxseeds have a fibrous seed coat which swells-up when wet and passes through our guts undigested. To get the benefit of the protein, omega-3 essential fatty acids and minerals in flaxseeds, the seeds need to be crushed, cracked, chopped-up, sliced-up or ground-up using a coffee grinder, adjustable pepper grinder or most simply, a blender with a sharp blade. The resulting powder can be mixed with liquids or sprinkled on foods, though extra fluid must be drunk as the soluble fibre absorbs lots of water. Although whole flaxseeds will keep fresh at room temperature, once powdered, it's advisable to keep them in a cool dark place to minimise oxidation of any exposed fat*. Flaxseed oil must be kept refrigerated with the cap screwed on the bottle at all times after opening and it must never be used for cooking. It's O.K. sprinkled over hot food as long as the food is eaten shortly afterwards. Oxidised flaxseed oil tastes bitter and has lost any health benefits it had when fresh, so it should be discarded or used to varnish something or thin down putty. Unoxidised flaxseed oil has a nutty taste or it may taste slightly like tea. Ground-up flaxseeds hardly taste of anything.
*NEW! Milled flaxseed stability information.


How much flaxseeds & flaxseed oil do I need to eat each day?

Men are much poorer converters of alpha-linolenic acid (the omega-3 fatty acid in flaxseeds) into the longer-chain omega-3 fatty acids than women. See http://www.nutritionsociety.org.uk/bjn/088/bjn0880355.htm and http://www.nutritionsociety.org.uk/bjn/088/bjn0880411.htm. Therefore, vegetarian and vegan men need to eat ~50g of ground flaxseeds a day and women need to eat ~25g a day. The daily amount of flaxseed oil for men is ~20g and the daily amount for women is ~10g.


Where can I buy flaxseeds & flaxseed oil?

Flaxseeds/linseeds come in different colours. The cheapest linseeds are brown/bronze ones which are often sold as bird seed in pet shops, but they can also be found in small independent health food shops. There are also golden linseeds, which is the type most often found in supermarkets. Linusit & Granovita are two well-known brands. Granovita organic flaxseed oil is a good brand and it comes in dark bottles to keep the light out as light causes photo-oxidation of omega-3 fatty acids.

Food Combining: What's THAT all about?

Some people believe in food combining, as per The Hay Diet i.e. don't eat protein with carbohydrate as protein needs acid conditions to digest and carbohydrate needs alkaline conditions to digest. This theory assumes that the human digestion system is like a big barrel where all foods get digested at the same time. This isn't the case.

The following is cribbed (with edits) from the bodybuilding.com message board (you didn't think I wrote all this, did ya?)

DIGESTION 101

The order you eat foods in does not make a difference to how they are digested. Once foods hit your stomach, the peristaltic motion (that is - the muscles in your stomach wall contracting) mix it all together regardless. In addition, the different enzymes that are released are released regardless of the order that you eat your food.

In your stomach:-
The presence of food in your stomach stimulates:-

1) Gastrin - this is what is responsible for the eventual release of Hydrochloric Acid (HCl) - stomach acid.
2) Pepsinogen - this is converted to pepsin by the acid in your stomach. Pepsin is important in the digestion of proteins.

In the small intestine:-
Once food hits the small intestine the pancreas and gall bladder are stimulated:-

1) Pancreas - It secretes many enzymes which help digest proteins, starches and triglycerides (fats).
2) Liver/gall-bladder - This is responsible for making and secreting bile. This is important in fat digestion. It is stimulated more when you eat fatty foods. The small intestine itself is also important, but it actually does not secrete anything. It acts to further digest the carbohydrates, proteins and fats, due to enzymes that are bound to the wall of the intestines, and then acts to absorb these things.

So - digestion occurs in two parts - the Luminal phase - which involves all of the enzymes that are secreted by the stomach, pancreas and liver. And the Membranous phase which is that which occurs because of the enzymes attached to the intestinal wall. It does not matter when you eat carbohydrates or proteins or fats during a meal, because the simple stimulus of food in your digestive tract will cause the secretion of the luminal enzymes (although as you increase your fat, you will stimulate more fat enzymes to be released).

Carbohydrates:-
Starches are the only type of carbohydrates to undergo luminal phase of digestion. This results from enzymes (called amylases) that are released from the pancreas. These act to break down the long starches into shorter polysaccharides (intermediate chains called dextrins). These are then cleaved again to form Disaccharides or trisaccharides (such as maltose or maltotriose). Sugars and the trisaccharides and disaccharides from the starches are then further digested in the Membranous phase. This involves enzymes (such as lactase - for the breakdown of lactose, sucrase for the digestion of sucrose and maltase for the breakdown of maltose) that are bound to the intestinal wall. So - these enzymes act on lactose, sucrose and the di and trisaccharides from the breakdown of starch to form glucose, galactose and fructose. These are then absorbed across the intestinal wall and enter the blood to go to the liver. The liver then takes up most of the glucose/galactose and all of the fructose and converts it into glycogen or fats while the rest stays in the blood for the rest of the body.

Proteins:-
These are broken down in a similar fashion as carbs. But - the enzymes involved in protein breakdown are secreted by the stomach (pepsin and chymosin) and the pancreas. There are lots of different enzymes involved in protein breakdown (because of the large variety of amino acids). So - digestion of proteins begins in the stomach with the secretion of HCl and pepsin which begin to cleave the long protein molecules. This then continues in the small intestines with the secretion of pancreatic enzymes. These smaller chains of amino acids (called peptides) are then either broken down by membranous phase enzymes on the intestine cells to form amino acids or are absorbed as dipeptides or tripeptides and then convert to simple amino acids by the cells. The amino acids are then released into the blood and are taken to the liver. In the liver, some of the amino acids go straight into circulation for the muscles, some are used directly for protein synthesis, but the rest are processed to enter the pathway of energy metabolism, carbohydrate formation or fatty acid formation.

Fats:-
This is a little different. Fat is harder to digest because it does not dissolve in the fluids in your gut. The digestion of fat is divided into four stages:-

1) Emulsification - This begins in the stomach and involves the warming and mixing of the fats. This breaks the fats into globules. The bile acids from the liver are then secreted into the intestines and make the fat droplets even smaller.
2) Hydrolysis - Enzymes from the pancreas (lipases) then act on the fats to form smaller molecules.
3) Micelle formation - These smaller molecules (free fatty acids, cholesterol, single chain fats etc) combine with bile to form tiny, droplets called micelles.
4) Absorption - The micelles then attach to the intestinal wall and all the components (except the bile) are then absorbed. These are then packaged (into things called chylomicrons) and secreted by the intestinal cells into tiny tubes in your intestinal wall called lacteals which take the fats to your heart, which then enters the back of your heart, which then pumps it around the body. These are then taken up by the liver or the fat cells. These processes in the intestine take a while to complete (depending on what you eat) and so eating one thing 5 minutes after the other will make no difference.

That said, there are certain combinations of food which are less desirable than others, but not for reasons of digestion.

Don't eat high-GI carbs together with whey, saturated, monounsaturated or omega-6 fats. High-GI carbs produce a large glucose and insulin response. Whey, saturated, monounsaturated and omega-6 fats magnify that insulin response. This results in unstable blood glucose levels and increased appetite. Virtually all junk foods are a combination of high-GI carbs and fats. The only time that an insulin spike is desirable is if you have just finished a workout. That particular insulin spike is obtained by swallowing whey with glucose and/or maltodextrin not usually accompanied by fat.

Don't eat fruit and protein foods at the same time. Fruit passes through the gut very quickly (possibly due to the fibre and simple sugar content stimulating peristalsis) and if eaten with or just after slow-digesting foods like meat or eggs, makes the protein pass through the small intestine faster than normal resulting in incomplete protein absorption and subsequent fermentation in the colon, producing smelly flatulence!

Vegetarians & vegans, listen up!

Firstly, by vegetarian I mean someone who does not eat the flesh of animals. This includes fish and chicken.

Dr. Michael Greger M.D. ("The Vegan MD") has a very informative and witty lecture Optimum Vegetarian Nutrition: Surprising New Research on Omega 3's and B12.

In a nutshell, vegetarians & vegans don't live any longer than omnivores – as shown in a study of 28,000 subjects. Vegetarians & vegans have the same rates of coronary heart disease as omnivores but double the rates of Alzheimer's Disease. WHY? There are two reasons.

1) Vegetarians and vegans don't eat oily fish and most don't eat cracked or ground-up linseeds either. This means that the ratio of omega-6 to omega-3 fats in their diet is way too high. This increases the risk of diabetes, certain cancers and heart disease.

2) Only animal produce naturally contains Vitamin B12. Lack of B12 in the diet raises the level of homocysteine in the blood, which attacks artery walls. This raises the risk of heart disease and Alzheimer's Disease. What to do?

1) Eat 25g (women) or 50g (men) of powdered brown or golden linseeds per day or add 10g (women) or 20g (men) of flax-seed oil to food per day or take 10 (women) or 20 (men) 1000mg flax-seed oil capsules per day. Or supplement with ~1000mg/day vegan DHA.

2) Eat foods fortified with vegan B12 or supplement with vegan B12.

'Nuff said?

Gluten - more than just a pain in the guts?

Remember the advert "I'm feeling a bit bloated". "Here, have some Bifidus Digestivum!"? I wonder what percentage of the population suffers from bloating, gas pains, constipation, IBS or some degree of failure to absorb the nutrients from their food?

People with Coeliac Disease (CD) or Dermatitis Herpetiformis (DH) (intensely itchy spots on pressure points) have to avoid gluten as much as possible, as it produces an auto-immune response with antibodies that attack their own bodies. However, gluten is also implicated in other conditions due to molecular mimicry. Sjogren's syndrome (dry eyes & other bits) and cerebellar ataxia (brain damage) are mentioned in a huge article by Loren Cordain Cereal Grains: Humanity’s Double-Edged Sword.

This article suggests that there are conditions other than CD & DH which can be helped by switching from gluten-containing grains (wheat, rye, oats, barley & spelt) to non gluten-containing ones (rice, corn, quinoa, buckwheat, millet & amaranth). Luckily, supermarkets like Tesco, Waitrose and Sainsbury's now have a large "Free from" section, which makes finding gluten-free substitutes for breads, cakes, biscuits & breakfast cereals etc a lot easier.

I was just thinking......

On a messageboard in a galaxy far far away, someone suggested that as many as one in three people in the UK could have impaired carbohydrate metabolism. This set me thinking.

London is 51degrees North of the Equator, so the sun has to pass through ~45% more atmosphere to reach us, compared to the Equator.

According to Elina Hyppönen & Chris Power, (edited) "The prevalence of hypovitaminosis D was highest during the winter and spring, when 25(OH)D concentrations less than 75nmol/L were found in 87.1% of participants, respectively; the proportion was 60.9%, respectively, during the summer and autumn."

Note that 75nmol/L was insufficient to give me normal Insulin Sensitivity. See Chiu, Chu, Go & Saad. However, greater than 160nmol/L was sufficient, but that was only obtained after I supplemented with 5,000iu/day of Vitamin D3 (25 x RDA).

A deficiency of omega-3 EFAs can cause Insulin Resistance (poor Insulin Sensitivity). See Ghafoorunissa, Ahamed Ibrahim, Laxmi Rajkumar & Vani Acharya, Storlien LH, Kraegen EW, Chisholm DJ, Ford GL, Bruce DG & Pascoe WS and Yam D, Bott-Kanner G, Friedman J, Genin I, Klainman E & Shinitzky M.

The typical omega-6:omega-3 ratio in the British diet is ~15:1. This is partly due to the fact that animal produce from grain-fed animals contains a lot more omega-6 and a lot less omega-3 than it used to. See Is food less nutritious than it used to be? Andre Purvis investigates. In addition, people eat grains, nuts, seeds, oils & spreads high in omega-6 and don't eat much oily fish, powdered Flax-seeds (a.k.a. Linseeds) or Purslane (a plant that's relatively high in omega-3).

With all of these problems, I wonder what percentage of the UK population actually do have some degree of impaired carbohydrate metabolism? It might be more than one in three.

According to The eatwell plate, one third of our total Calories are supposed to come from bread, rice, potatoes, pasta and other starchy foods. All of these foods raise blood glucose. Impaired carbohydrate metabolism makes for roller-coaster blood glucose levels which encourages over-eating (see my Blog post on Blood Glucose, Insulin & Diabetes.)

I think that that's enough thinking for now.

Everybody knows.........Part 2

.........that ketogenic diets like the Atkins diet destroy your kidneys and rot your bones, right? Wrong!
.........that the Atkins diet causes ketoacidosis which is a very dangerous condition requiring urgent hospital treatment, right? Wrong!

There's a lot of nonsense spoken about ketogenic diets by people who really should know better. I suspect that they have been taught wrongly at uni or med school as per the quote in Everybody knows.........Part 1.

Benign Dietary Ketosis is NOT Ketoacidosis.

Consider the following four cases:- Note: Figures are from "Introduction to Nutrition and Metabolism" By David A Bender (Senior Lecturer in Biochemistry, UCL)

1) Healthy human, fed state: Glycogen stores are replete. Serum glucose = ~5.5mmol/L. Serum fatty acids = ~0.3mmol/L. Serum ketones = 0mmol/L. No gluconeogenesis is taking place. Amino acid pool is replete. Cortisol level is normal so there is no loss of muscle mass.

2) Healthy human, fasting for 7 days: Glycogen stores are depleted. Serum glucose falls to ~3.5mmol/L. Serum fatty acids rise to ~1.2mmol/L. Serum ketones (mainly D-3-hydroxybutyrate) rise to ~4.5mmol/L (not high enough to cause acidosis). Gluconeogenesis is occurring. Amino acid pool is depleted. Cortisol level is high, causing slow loss of muscle mass. This is bad ketosis.

3) Healthy human, low-carbohydrate diet: Glycogen stores are depleted. Serum glucose falls to ~5mmol/L.
Serum fatty acids rise to ~1.2mmol/L. Serum ketones (mainly D-3-hydroxybutyrate) rise to ~4.5mmol/L (not high enough to cause acidosis). Gluconeogenesis is occurring. Amino acid pool is replete (due to protein intake). Cortisol level is normal so there is no loss of muscle mass. This is good ketosis.

4) Human with untreated type 1 diabetes: Glycogen stores are depleted. Due to lack of insulin, the Glu-T4 transporters in cells cannot move to the surface so glucose cannot enter cells. Serum glucose = >20mmol/L. This causes major damage to kidneys, arteries, eyes, nerves etc by cross-linking with proteins (glycation) resulting in major disability and eventual death. As the body is forced to run on fatty acids & ketones, metabolic processes are out of control and ketones rise to much higher levels than in 2) or 3) (I don't know how high exactly) resulting in acidosis and eventual death. This is ketoacidosis.

Conclusion: Low-carbohydrate dieting is similar to fasting in that serum glucose levels are lower than normal and glycogen stores are depleted. The body is encouraged to burn less glucose and more fatty acids & ketones, but the metabolic processes are all under control. The big difference between low-carbohydrate dieting and fasting is in the amino acid pool and cortisol levels.

Everybody knows.........Part 1

Yesterday, on a messageboard in a galaxy far far away, I was informed by a Nutritionist with letters after her name:-

"As a health and fitness scientist, I have to agree with the overwhelming body of peer reviewed evidence that shows high fat diets are dangerous over a long period of time, and that an athletic diet includes complex carbs taken regularly throughout the day."

To which I replied:-

"Apart from epidemiological evidence (which is highly suspect as there are too many variables), can you show me some solid evidence that "high fat" hypocaloric or isocaloric diets are dangerous over a long period of time? Obviously, high fat hypercaloric diets are dangerous as they cause weight gain.....as do all hypercaloric diets."

Followed by:-

"What if what you were taught was wrong? Read Dr. Schwarzbein's Personal Experiences - Background to first book.

"In medical training, I was taught that a low-fat diet high in complex carbohydrates prevented weight gain and disease. I believed what my professors said. Early on, I advocated low-fat diets. But this soon changed."

Practical experience showed that what she'd been taught was wrong. Just bear that in mind. Obviously, athletes have different dietary requirements to fat people with type 2 diabetes. However, suggesting that all athletes eat "complex carbs" (you shouldn't use the expression "complex carbs" as amylopectin & maltodextrin are complex carbs that turn into blood glucose as quickly as glucose) regularly throughout the day, whether bulking or cutting is wrong.

Cheers, Nige."

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 just 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 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 K2 (menaquinone/menatetrenone) will suffice.

However, Vitamin K2 (menaquinone/menatetrenone) alone 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 56% reduction in heart attack deaths. I've now put a mention of K2 in my Cholesterol & Coronary Heart Disease Blog.

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.

Elvis lives!

This bloke said he saw Elvis down the chip shop. What? You mean he was mistaken or lying? Surely not!
Every day, you read or hear: Aspartame gives you cancer! Meat gives you cancer! Crisps give you cancer! Coffee gives you cancer! Coffee doesn't give you cancer! Coffee gives you cancer! And so on and so on......

In terms of Diet & Nutritional information, there's a hierarchy of credibility. Here's a rough list of credibility, starting with least credible and ending with most credible.

Inexpert opinion. Basically, anyone can say anything but that doesn't make it true! This includes anything that I say, which is why I try to back up what I say with evidence from higher up the pile.

Anecdotal data/testimonials. Just because it worked for Joe or Josephine doesn't mean that it'll work for anyone else. There's also the placebo effect e.g. Nothing acts faster than Anadin so use nothing!

Expert opinion. Even "experts" with lots of letters after their names get things wrong and have personal biases, hence the controversies over MMR, HIV/AIDS, Cholesterol etc.

Epidemiological studies. A being associated with B doesn't necessarily mean that A caused B, as the association may have been due to random chance or due to both being caused by C, D, E........Z etc.

Case studies. The number of subjects are usually quite small, or just 1.

Small/non-randomised/unblinded/non-placebo-controlled/non-crossover trials

Large randomised double-blinded placebo-controlled crossover trials.

Meta-studies of large randomised double-blinded placebo-controlled crossover trials.

Even the last 2 items aren't perfect. Study outcomes can be manipulated by tweaking the methodology (e.g. using pre-trial screening) so if a trial is funded by a large company, the methods used need to be examined very carefully. In addition, the abstract can mis-represent the full study. I have seen this on more than one occasion. Here's a classic example: Intensive lipid lowering with atorvastatin in patients with coronary heart disease and chronic kidney disease: the TNT (Treating to New Targets) study. The Conclusion reads: "Aggressive lipid lowering with atorvastatin 80 mg was both safe and effective in reducing the excess of cardiovascular events in a high-risk population with CKD and CHD." because there was a 15-32% reduction in major cardiovascular events. Wow, that's impressive! What the abstract failed to mention was the fact that there were 26 more deaths in the 80mg Atorvastatin group than in the 10mg group. What's more important - having a major cardiovascular event or dying?

In conclusion, when you read something on the internet, do some research of your own before taking it as fact. Use Google, Wikipedia and PubMed.

Why counting Calories and weighing yourself regularly can be a waste of time.

To lose weight, eat fewer Calories than you burn. Sounds fairly straightforward, doesn't it? Well, all sorts of things can mess up this simple maxim.

What is a Calorie?

One dietary Calorie (Cal) is 1000calories, or 1kcal for short. A calorie (cal) is the amount of energy required to heat 1g (1mL) of water by 1degree C. As 1cal is a tiny amount of energy, kcal is commonly used. I prefer to use kcal rather than Cal, as the first word in a sentence is always capitalised which could cause confusion.

The SI unit of energy is the Joule (J) and is the amount of energy required to lift a 1kg weight 1m into the air. As 1J is also a tiny amount of energy, kJ is commonly used. There are 4.186kJ in 1kcal.

Why counting kcals can be a waste of time.

1) When the label on a packet of food states that the food contains Xkcals or YkJ, the number could be in error. See Food Composition Analysis and its Implications for Dietary Planning.

2) Most people are utterly hopeless at judging portion sizes, even when using a measuring spoon! Watch the following video made by Leigh Peele called Fat Loss Tips! Shocking!

Why weighing yourself regularly can be a waste of time.

As mentioned previously, scales cannot distinguish between muscle, body-fat, glycogen+water, urine, faeces etc. Bodyweight can fluctuate considerably on a day-by-day basis. The following list details various occurrences and their effect on bodyweight.

Occurrence___________________Weight change (lb)
Glycogen supercompensation________~+10
Glycogen replenishment/depletion_+/-4 to 5
Pre-menstrual water retention_____~+5
Eating a high-sodium meal__________+2 to 3
Fluid retention on airplane flight +2 to 3
Going to the loo (No.2)____________-1 to 2
Going to the loo (No.1)___________~-0.5
Drinking a mug of tea_____________~+0.5

So step away from the scales. There's nothing to see here, folks!

And finally, a little light relief. If I just waffle on about Diet & Nutrition all the time, it can get boring. So here's a YouTube video of a really cool Ninja cat that must have watched the Doctor Who episode "Blink". You know, the one with the Weeping Angels. http://www.youtube.com/watch?v=muLIPWjks_M

How to lose body-fat healthily.

Previous Blog posts have been about Carbohydrates, Fats & Proteins. However, when you go to the shops, you buy food. So this blog post is also about food.

1) Eat 6 meals or 3 meals and 3 snacks per day to keep your blood glucose stable. I used to believe that it kept your metabolic rate high, but I now know this to be a myth. Skipping breakfast is not advisable as the low blood glucose that it can produce encourages overeating later.

2) All meals and snacks should contain proteins, fats and fibrous carbs i.e. all meals and snacks should be roughly "balanced".

3) Slow sugary/starchy carbs can be eaten in meals/snacks at breakfast and before/after workouts/exercise/intense activity. If/when you are sedentary, keep slow sugary/starchy carbs to a minimum. Keep fast sugary/starchy carbs to a minimum (except for the occasional treat or post-workout) as they can cause large fluctuations in blood glucose and insulin levels. The more intense exercise you do, the more slow sugary/starchy carbs you can eat.

4) Drink >1.5 litres of no-added-sugar watery drinks per day. If your urine is darker than straw, drink more. If you're weeing too often, drink less.

5) Balance your omega-6 and omega-3 essential fatty acids (EFAs) by eating about 100g of omega-3 rich oily fish (sild, sardines, pilchards, mackerel, herring, salmon, trout, fresh tuna etc) per day or supplement with fish oil capsules such that you get at least 2g of EPA+DHA per day. Please note that tinned tuna contains virtually zero omega-3 fat.
If you're vegetarian or vegan, eat 25g (women) or 50g ( men) of powdered linseeds (a.k.a. flaxseeds) per day with lots of fluids or supplement with flaxseed oil in bottles/capsules such that you get at least 10g (women) or 20g (men) of flaxseed oil per day.

6) Eat 2 to 3 portions of low-sugar fruits per day - preferably before meals/snacks. Minimise your consumption of high-sugar fruits.

Proteins are:- Meats, poultry, fish, eggs, cheese, Quorn, seeds, nuts, legumes (peas, beans & lentils).

Fibrous carbs are:- All vegetables that grow above ground level, bulbs (onions, leeks, garlic etc) and "vegetable" fruits (tomatoes, peppers, cucumbers/courgettes, aubergines, avocados, olives etc).

Slow sugary/starchy carbs are:- All-bran, no-added-sugar muesli, oats, sweet potatoes, lightly-boiled new potatoes eaten hot, cold or refrigerated, Basmati rice, non-overcooked legumes & root veggies, lumpy wholegrain rye breads, Burgen/Vogel's soya & linseed breads.

Fast sugary/starchy carbs are:- White wheat breads, wholemeal wheat breads, most breakfast cereals including Shredded Wheat, Weetabix, Cheerios, Grapenuts etc, sugar, sweets, chocolate, cakes, biscuits, cereal bars, sweetcorn, overcooked tubers e.g. jacket potatoes, overcooked root veggies, overcooked legumes e.g. baked beans.

High sugar fruits are:- Ripe & over-ripe bananas, grapes, pineapples, sweet apples, sweet pears, sultanas, raisins, currants and any dried fruits with added sugar.

Low sugar fruits are:- Berries, stone fruits, citrus, Granny Smith apples, Conference pears. Dried apple rings, apricots, pear halves, peach halves and prunes without added sugar are high in sugar but they release that sugar very slowly.

Fats are sats, monos and the EFAs mentioned above. Butter is high in sats and monos. Olive oil & spreads are high in monos. Sunflower/safflower/corn oils & spreads are very high in omega-6 EFAs - minimise your consumption of these. Don't fry or roast with high-EFA oils as they oxidise and convert into trans-fats too quickly. Meats contain sats, monos and some EFAs. Minimise your consumption of anything with the word "hydrogenated" in the ingredients list.

Some foods fall in-between categories like yellow bananas which are medium speed sugary/starchy carbs. Green bananas are slow carbs and black bananas are fast carbs.

Depending on your insulin sensitivity, speed of metabolism and exercise levels, you may get away with eating fast sugary/starchy carbs - you'll just have to "suck it and see".

One final bijou tip-ette:- Avoid walking down "dodgy" supermarket aisles (confectionery, cereals, booze, fizzy drinks) as "What the eye don't see, the heart don't grieve over".

Happy New Year folks!

A blast from the past.

Look who's turned up on the BBC food boards after a 4-5 years absence. A big "Welcome back" to Zoë Harcombe, who has the site 'Why do you overeat? When all you want is to be slim' and The Harcombe Diet.

We agree on most things. The problem with counting Calories is that, if you reach your Calorie limit by 6pm, what do you do? Spend the rest of the evening hungry and go to bed with a rumbling tummy & hunger pangs? Or just have one teensy-weensy bite to eat, which turns into a "nom-a-thon"? I know what I would do, as I can resist anything.......except temptation!

What we don't agree on is that Calories don't count. I say that they do. So does Lyle McDonald and Anthony Colpo. For people who are restrained to a hospital bed, changing the relative proportions of carbohydrate & fat (keeping protein constant) in their diet makes no difference whatsoever to their long-term weight gain/loss (ignoring glycogen + water weight differences). What it does make a difference to is how much these restrained people would beg for food. On a high-carb diet, I was much hungrier than when I was on a low-carb diet. This is why I ate way too much on the former diet (& got fat) and ate much less on the latter diet (& got slim).

It's thought that Insulin is the only hormone responsible for body-fat storage. This isn't correct.

Insulin makes the body store glucose (from dietary carbohydrates) and amino acids (from dietary proteins) and stops the body from burning fats. Therefore, having chronically-high serum insulin levels (hyperinsulinaemia) is not desirable for people wishing to burn body-fat for fuel.

As we all know, dietary carbohydrate raises serum insulin levels by raising blood glucose. See http://www.mendosa.com/gilists.htm.

However, dietary protein also raises serum insulin levels. See http://www.mendosa.com/insulin_index.htm.

Eating most fats with carbohydrates raises serum insulin levels even higher still, although fats lower the glucose response. See http://jn.nutrition.org/cgi/reprint/133/8/2577.pdf. What do junk foods mostly consist of? High-GI carbohydrates + fats. However, omega-3 fats reduce the hyperinsulinaemia caused by the other fats. See http://diabetes.diabetesjournals.org/cgi/reprint/53/suppl_1/S166.pdf.

Eating fat on its own does not raise serum insulin levels. See http://intl.ajcn.org/cgi/reprint/75/3/505.pdf. However, it's still possible to gain body-fat by eating too many Calories of dietary fat. Acylation Stimulating Protein (ASP) makes the body store dietary fat as body-fat. See http://www.jlr.org/cgi/reprint/30/11/1727.pdf.

The amount of food that free-living people (i.e. people who are not restrained to a hospital bed) eat depends mostly on their appetites. This is affected by the food that they eat (the low blood glucose that follows hyperinsulinaemia causes severe hunger pangs) and also advertisements. Watch this Google video of Adam Curtis' BBC documentary The Century Of The Self - Part 1 of 4.

I hope that you all had a good Christmas.

Proteins: Dogs' Doodads.

"Mmmm! These Korean meatballs really are the dogs' b*llocks!" said Hugh Dennis on "Mock the Week" as "Things you don't hear on TV cookery programmes".

For an overview on Protein, see http://en.wikipedia.org/wiki/Protein.
For an overview on Protein in nutrition, see http://en.wikipedia.org/wiki/Protein_in_nutrition.

I'm not going to write any more about protein, as somebody else already has. So, I am referring you to Lyle McDonald's protein articles, as what Lyle doesn't know about protein fits on a postage stamp........a very small one!

I shall now take a break. Merry Christmas everyone!

Fats: Spawn of Satan or Dogs' Doodads?

Fats get a lot of bad press in the media. There are so many adverts with "X% fat-free" or "only 1g of fat per Jaffa Cake" as if that's going to stop you from getting fat when you "om nom nom" your way through a whole box of the things!

Saturated fats are usually described as "bad" and polyunsaturates are usually described as "good". This is simplistic. Everything is bad in excess, even polyunsaturates. The thing about fats is that there are four basic types (saturates, monounsaturates, omega-6 polyunsaturates and omega-3 polyunsaturates) and they need to be consumed in roughly the right proportions for optimum health. Suffice it to say, the majority of people in the West do not eat them in anywhere near the right proportions. So, what exactly are fats?

Fats

Fats are an ester of glycerol and three fatty acids and are also known as triglycerides or triacylglycerols.

1 molecule of glycerol + 3 molecules of fatty acid = 1 molecule of triglyceride + 3 molecules of water.

It's the fatty acids that determine whether a fat is sat, mono etc. The four different types of fatty acid all have a CH3 at one end and a COOH at the other. The difference is in the middle section.

Saturated fatty acids have a middle section consisting of all CH2's. Here's a diagram for Stearic acid (the predominant fatty acid in beef):-

__H H H H H H H H H H H H H H H H H O
H-C-C-C-C-C-C-C-C-C-C-C-C-C-C-C-C-C-C-O-H
__H H H H H H H H H H H H H H H H H

Monounsaturated fatty acids have one C=C bond in the middle, which is usually (but not always) 9 from the left-hand end resulting in monounsaturates usually being referred to as omega-9's, as omega is the letter at the end of the Greek alphabet. Here's a diagram for Oleic acid (the predominant fatty acid in olive oil):-

__H H H H H H H H_____H H H H H H H O
H-C-C-C-C-C-C-C-C-C=C-C-C-C-C-C-C-C-C-O-H
__H H H H H H H H H H H H H H H H H

Omega-6 polyunsaturated fatty acids have two or more C=C bonds in the middle with the last one always being 6 from the left-hand end. Here's a diagram for Linoleic acid (the predominant fatty acid in sunflower oil):-

__H H H H H_____H_____H H H H H H H O
H-C-C-C-C-C-C=C-C-C=C-C-C-C-C-C-C-C-C-O-H
__H H H H H H H H H H H H H H H H H

Omega-3 polyunsaturated fatty acids have three or more C=C bonds in the middle with the last one always being 3 from the left-hand end. Here's a diagram for Alpha-linolenic acid (the predominant fatty acid in flax-seed oil):-

__H H_____H_____H_____H H H H H H H O
H-C-C-C=C-C-C=C-C-C=C-C-C-C-C-C-C-C-C-O-H
__H H H H H H H H H H H H H H H H H

These diagrams are slightly misleading. Where there is a C=C bond, there are two H's on the "underside" only of the molecule. This asymmetry causes the H's to repel each other and bend the molecule into a V-shape at each C=C bond. C=C bonds with H's on the same side are known as "cis" bonds. The above molecule is really cis, cis, cis (c,c,c) Alpha-linolenic acid. The other type of C=C bond is known as "trans" and looks like the following diagram:-

__H H H___H H___H H___H H H H H H H O
H-C-C-C=C-C-C=C-C-C=C-C-C-C-C-C-C-C-C-O-H
__H H___H H___H H___H H H H H H H H

This is a diagram of trans, trans, trans (t,t,t) Alpha-linolenic acid. As the H's are on opposite sides of the molecule, they do not repel each other and the molecule is straight as shown above. Note that saturated fatty acid molecules are naturally straight. Therein lies the problem with trans-fatty acids. They're straight, like saturated fatty acids but have unsaturated bonds which are prone to oxidation. See http://www.cyberlipid.org/perox/oxid0002.htm WARNING! Heavy-duty organic chemistry!

Our bodies take trans-fatty acids and incorporate them into cell membranes as if they were saturated fatty acids. This results in atherogenicity (artery-clogging), damage to the immune system and other health problems. Trans-fatty acids are found in partially-hydrogenated vegetable oils and so any processed foods or cooking/spreading fats which has the word "hydrogenated" high-up in the ingredients list should be avoided. These truly are bad fats. There are also naturally-occurring trans-fatty acids made by bacteria in the stomachs of ruminant animals, like Conjugated Linoleic Acid (CLA). This looks a bit like the diagram below:-

__H H H H H_____H___H H H H H H H H O
H-C-C-C-C-C-C=C-C=C-C-C-C-C-C-C-C-C-C-O-H
__H H H H H H H___H H H H H H H H H

This has one of the C=C bonds shifted to the left and also has one cis bond and one trans bond, so the molecule is always bent. CLA has possibly beneficial properties but medical studies show mixed results. It's certainly not artery-clogging, so don't let anyone put you off eating butter from grass-fed cows (e.g. New Zealand butter) by saying that it has trans-fats in it. CLA is a harmless trans-fat.

Anyway, back to diet. Saturated fat consumption should be about 10% of total calories. This is because, even though sat fats are not essential (our bodies can manufacture them), this guarantees adequate levels of sex hormones in the body. Total polyunsaturate consumption should be about 5% of total calories, with a ratio of omega-6 (O6) to omega-3 (O3) of between 1:2 and 4:1. As O3's are only found in greater quantities than O6's in flax-seeds (a.k.a. linseeds) and oily fish, and many people eat way too little or no oily fish (and who, other than body-builders and some vegetarians/vegans, eats flax-seeds?), the O6:O3 ratio in the West is about 20:1. This is due to the widespread consumption of meats, eggs & milk from grain-fed animals, grains, nuts and seeds. So, it’s not surprising that there are high rates of heart disease and other inflammatory diseases in the West, as O6's end up in series 1 & 2 prostaglandins and series 2 prostaglandins are pro-inflammatory. O3 fats end up in series 3 prostaglandins, which are anti-inflammatory.

So eat up yer oily fish if you're not vegetarian or vegan. Otherwise, eat up yer ground-up flax-seeds!

Monounsaturates can make up 15% to 35% of total calories, depending on activity levels. Remember from the histogram in the Blog post Everyone is Different, sedentary people on average burn twice as much energy from fats as from carbs. So, if energy from protein is 25% say, 25% of energy can come from carbs and 50% can come from fats i.e. a 2:1 ratio of fats:carbs. The cyclists at the left-hand end of the histogram in Chapter 1 would do best on 25% protein, 5% carbs, 70% fat when sedentary, whereas the cyclist at the right-hand end of the histogram would do best on 25% protein, 60% carbs, 15% fat when sedentary. When active, more carbs are needed by everyone.

Which fats contain which fatty acids? See http://www.manitobaharvest.com/nutrition/index.asp?itemID=183 for a Comparison of Dietary Fats chart. Click http://www.apag.org/oleo/fatsoils.pdf for tables of Properties & Composition of Vegetable & Special Oils and Properties & Composition of Animal & Marine Fats & Oils.

For high-temperature cooking, saturates are the least likely to oxidise (when they're on fire, they're oxidising!), followed by monos, then omega-6's with omega-3's being the least stable. An oil doesn't have to be smoking to be oxidising. Alpha-linolenic acid oxidises at room temperature, which is why linseed oil is used to varnish cricket bats and soften putty. The best non-animal fat for high-temperature cooking is Coconut Oil, followed by Palm Oil and then Olive Oil. Extra-Virgin Olive Oil (EVOO) has a lower smoking temperature than refined Olive Oil (due to higher levels of free fatty acids), but has higher levels of polyphenol antioxidants, which makes it pretty heart-healthy.

Oils high in polyunsaturates shouldn't be heated above 100 degC, as polyunsaturates can change from the cis configuration to the trans configuration at temperatures as low as 102 degC. See http://www.harricksci.com/accessories/Oil-Analysis-by-ATR.pdf

Carbohydrates: Dogs' Doodads or Spawn of Satan?

Depending on which side of the fence you're on, Carbohydrates are either the Dogs' Doodads or the Spawn of Satan. As I get older, I prefer to sit on the fence. Let's start with the basics.

What are Carbohydrates?

Carbohydrates are so named because they have the generic formula (CH2O)n. C is carbon and H2O is water hence Carbo-Hydrate. There are several different types.

1) Sugars. There are monosaccharides, the most common being Glucose (a.k.a. Dextrose), Fructose and Galactose. There are disaccharides, the most common being Sucrose, Lactose and Maltose. Disaccharides are 2 monosaccharides linked by a glycosidic bond formed by a condensation reaction (removal of a water molecule, usually by an enzyme). Disaccharides have to be hydrolysed (have a water molecule added back in, usually by an enzyme) into monosaccharides before they can be absorbed in the gut.
Sugars are simple carbohydrates.

2) Starches. These are chains of glucose molecules linked by glycosidic bonds. Starches have to be hydrolysed into glucose molecules before they can be absorbed. There are unbranched chains like amylose which is also known as resistant starch. There are branched chains like amylopectin and maltodextrin. Glycogen is a branched chain "animal starch" that is synthesised inside muscle and liver cells and which can be rapidly converted back into glucose inside cells.

3) Non-Starch Polysaccharides (NSPs). These are also known as fibre and there are 2 types: soluble (e.g. pectin, beta-glucan & cellulose) and insoluble (e.g. bran). These aren't absorbed, but gut bacteria can feed on soluble fibre.
Starches and NSPs are complex carbohydrates.

For more information, see http://en.wikipedia.org/wiki/Carbohydrate

The amount of carbohydrate that someone needs varies from person to person and increases with the intensity and volume of exercise done. See Everyone is Different. What are the best carbs to eat? "Complex" ones from "wholegrain" cereals? Not necessarily.

Simple vs Complex

TV ads for breakfast cereals bang on about the wholegrain goodness of complex carbohydrates releasing energy slowly. The terms "Simple" and "Complex" actually refer purely to the chemical structure of a carbohydrate and have nothing to do with how fast they turn into blood glucose in the body. The Glycaemic Index (GI) (or Glycemic Index if you're American) relates to how fast carbohydrates turn into blood glucose in the body. See http://www.mendosa.com/gilists.htm for a list of 750 foods and their GI & GL (GL = Glycaemic Load = GI/100 x carb content per serving). Here are a few extracts. Note: a GI of 55 is low; a GL of 10 is low.

The last three items in the list are all simple carbs. As you can see, some wholegrain complex carbs turn into blood sugar faster than simple carbs. This because the wholegrains have been ground into powder which is rapidly digested and absorbed, despite the presence of fibre.

As fructose has such a low GI, does this mean that we can eat as much of it as we like? No. When we eat fructose, it passes from the small intestine into the portal vein and goes straight to the liver. As liver cells contain an enzyme called fructokinase (which has a high affinity for fructose), all dietary fructose is absorbed by the liver where it tops-up liver glycogen. Liver glycogen is also topped-up by glucose (obtained from the digestion of starchy carbs). Once liver glycogen stores are full, any further fructose is converted into.......triglycerides. High serum triglycerides are heart-unhealthy. See Cholesterol And Coronary Heart Disease.

Why is GI important? When we eat carbohydrates, they raise blood glucose levels. Pancreatic beta cells secrete a hormone called insulin, which allows glucose to pass into cells (by moving Glu-T4 transporters inside the cells). As glucose enters cells, glucose levels in the blood fall. It's a negative feedback loop. For millions of years, we lived on a diet of natural, unrefined carbohydrates and so the secretion of insulin never had to change blood glucose levels very rapidly.

When unnatural, refined, high-GI carbs are eaten, blood glucose levels rise much faster. This results in over-secretion of insulin (hyperinsulinaemia). This then shuttles too much glucose into cells and results in.......low blood glucose. Rapidly-falling and low blood glucose levels cause feelings of severe hunger and cravings to eat more carbs. It's a vicious circle. Hyperinsulinaemia also has other bad effects on the body. See http://www.mercola.com/2001/jul/14/insulin.htm to learn about Insulin and its Metabolic Effects.

GI has a weakness because adding fats and some proteins to high-GI foods lowers the GI but can increase the insulin response. Saturated fats, monounsaturates and omega-6 polyunsaturates raise the insulin response to carbs. Omega-3 polyunsaturates lower the insulin secretion produced by carbs.

There is another index called the Insulin Index (II). See http://www.mendosa.com/insulin_index.htm.
The II contains a few surprises. Some proteins (e.g. the whey in milk & yoghurt) produce a large insulin response. As over-secretion of insulin can cause low blood glucose which causes severe hunger pangs, it's not something that someone who wants to lose body-fat really wants. Therefore,the consumption of foods with an II greater than 60 should be minimised for optimum fat loss. So take it easy with the baked beans ("my carbohydrates are exceedingly complex"). Overcooking foods raises their GI & II and baked beans are well-overcooked in a sugary sauce. On the other hand, refrigerating some foods lowers their GI & II by changing the starch in them into resistant starch, even if the food is subsequently re-heated. Rice & potatoes are two such foods.

As the terms "simple" and "complex" are meaningless in terms of carbohydrates' effects in the body, I prefer to use the terms "slow" and "fast". In a nutshell, slow carbs are good and fast carbs are bad. These terms can be applied to proteins, too. Egg is slow and whey is fast. Sticking to mostly slow foods keeps blood glucose and insulin levels stable, which results in better appetite control and better health, too.

It was soaring serum insulin levels that were sending me to sleep all those years ago. Hyperinsulinaemia results in amino acids being shuttled into cells, too. However, L-tryptophan isn't shuttled into cells, so the level of this amino acid rises relative to others in the blood. As L-tryptophan competes with other amino acids to cross the blood-brain barrier, now that the competition has been removed, a lot of L-tryptophan enters the brain. Here, it's converted into 5-hydroxytryptophan (5-HTP) and then serotonin. High serotonin levels in the brain cause sleepiness. As serotonin is also a "feel-good" substance, it's no wonder that carbs can be addictive.

So remember, "Right carbs, right amounts, right times."

Everyone is Different.

Updated text in bold green.
If there is one thing that I have learned over the years of research into Diet and Nutrition, it's this: Everyone is Different. When I first discovered Low-carb Diets (thanks to the late Dr Atkins), I thought that it was the One True Diet, and I became a bit of an "Atkins Diet" bore telling everyone how wonderful it was and suggesting that everyone should be on it.

I now know that what suits me doesn't necessarily suit someone else. So why do "Healthy Eating" guidelines assume that everyone is the same and tell everyone to get 15% of their total calories from proteins, 55% from carbohydrates and 30% from fats?

To illustrate just how different people are, here's Fig. 2 from Determinants of the variability in respiratory exchange ratio at rest and during exercise in trained athletes. Used with permission.

Respiratory Exchange Ratio (RER) is the ratio of carbon dioxide breathed out to oxygen breathed in. This ratio depends on the fuel that the body is burning for energy. For example, if the body is burning 100% fat, RER = 0.7. If the body is burning 100% carbohydrate aerobically, RER=1.0. If the body is burning 100% carbohydrate anaerobically (flat-out sprinting), RER > 1.0. RER goes up & down depending on intensity of exercise, food intake (eating protein & carbohydrate increases it and extended fasting reduces it). Increasing cardiovascular fitness reduces RER.

The top diagram is a histogram of fasted RER & % fat oxidation vs. number of subjects. At the left-hand end of the histogram, there are two cyclists with a fat oxidation of 93 - 100%. At the right-hand end of the histogram, there is one cyclist with a fat oxidation of 20 - 27%.

There's a helluva big difference between burning 93 - 100% fat at rest and burning 20 - 27% fat at rest. Interestingly, average fat oxidation is 66%, which means that average carb oxidation is 34%. So, on average, at rest, people burn twice as much energy from fat as from carbs. So why do current "Healthy Eating" guidelines recommend almost twice as much energy from carbs as from fats for everyone, including sedentary people?

As exercise intensity increases, the peak in the histogram shifts to the right as shown in the lower diagram. At 25% full work-load, mean fat oxidation is ~53%. At 50% full work-load, mean fat oxidation is ~37% and at 75% full work-load, mean fat oxidation is ~13%.

I suspect that at 100% full work-load, mean fat oxidation is 0% i.e. 100% of energy is being obtained from carbs when sprinting flat-out. Somebody on a very low carb diet like Atkins induction (~20g net carbs/day) could keel over with hypoglycaemia if they exercised for any length of time at this rate.

As there is so much variation from person to person, you must find out for yourself your own optimum proportions of proteins, fats and carbohydrates and these depend upon the intensity and volume of exercise you do. It all sounds a bit complicated but it isn't really.

Just apply the principle of "Eat, monitor and adjust accordingly" as Toxic Toffee (ex-Muscletalk member) always used to say. The eating bit I will advise on in future Blog posts. The monitoring bit does not involve the use of bathroom scales.

Hang on, isn't "dieting" all about losing excess weight? Not necessarily. Remember the old joke: Q. What's the best way to lose 5lbs of ugly flab? A. Cut your head off! As your body is made up of water, muscle, fat, bones, cartilage, tendons, organs, glycogen, skin etc and your scales can't tell the difference between them, losing weight the wrong way can make you less healthy. However, losing weight the right way will make you more healthy.

If you starve yourself or skip breakfast or go for a fast run before eating breakfast, as your body is lacking in glycogen and amino acids, a large amount of a corticosteroid hormone called cortisol is secreted which converts muscle into amino acids, then glucose. It also suppresses your immune system and weakens your skin & bones.

Unless you have a lot of muscle to spare, it's body-fat that you should be losing, and to monitor this, either use a tape-measure around your waist, or check how loose/tight your clothes are, or strip-off and jump up and down in front of a full-length mirror. As Big Les (Muscletalk Moderator) says, "If it jiggles, it's fat!".

So, what happens if you eat too many carbs but your body doesn't burn them fast enough? Initially, carbohydrate intake tops-up liver and muscle glycogen stores, which increases carb-burning to compensate. The liver can store about 70g of glycogen and muscles can store about 400g of glycogen. If, despite increased carb-burning, more carbohydrate is consumed than is burned, glycogen stores continue to fill. When glycogen stores become full, RER increases to 1.0 and 100% of energy is derived from carbohydrate. Getting 100% of energy from carbohydrate means that zero fat is burned, so filling glycogen stores by eating loads of carbohydrate is not a good idea if you want to burn body-fat. Once glycogen stores are full, any additional intake of carbohydrate beyond that which is burned passes through the lipogenesis pathway - this basically means that carbs are turned into fat - which you end up wearing as body-fat. But there's even worse news. On the way to being worn as body-fat, fat is in the blood as triglycerides. This is bad for the cholesterol particles in your blood. See the Blog on Cholesterol and Coronary Heart Disease. What happens if you eat too few carbs? As stated above, a "carb-burner" taking in insufficient carbs could get hypoglycaemia.

How many grams of carbohydrate per day does it take to promote lipogenesis? Someone at rest burns ~1kcal/minute. If this is derived 100% from carbohydrate, this is equivalent to 0.25g of carbohydrate /minute, or 15g of carbohydrate /hour, or 360g of carbohydrate /day. Therefore, sedentary people who consistently eat more than 360g of carbohydrate /day will produce significant triglycerides. People who have The Metabolic Syndrome/Syndrome-X (a high proportion of people who have excess belly fat) have increased lipogenesis & higher serum triglycerides than healthy people.

Just discussing weight again for a moment, it's often said that all diets are the same, as weight loss is all about calories. This is true. See Is a Calorie a Calorie? However, body composition is determined by a combination of macro-nutrient proportions (i.e. the relative amounts of protein, carbohydrates and fat that you eat) and the intensity and volume of exercise.

So, if all you're interested in is weight loss, just count calories. If however, you wish to lose body-fat without losing muscle, you need to know how to determine what proportions of proteins, carbs and fats to eat (it's not that critical, but many people get it totally wrong). You need to know the difference between good carbs & bad carbs and good fats & bad fats. You need to know the best times to eat proteins, carbs and fats (it's also not that critical, but many people get that totally wrong as well). You need to know the difference between good exercise and bad exercise. That's it for now.

It's all about ME, baby!

In case you're wondering "Who is this Nigeepoo geezer and why is he wittering-on about Cholesterol, Diabetes & Vitamin D?", here's why......

The story starts in 1997. I'd just come through an acrimonious divorce and I was tired, bloated, 17st 7lb and depressed. Then a pamphlet dropped through my letterbox. It was from Agora Lifestyles, promoting a book by a Dr. Robert C. Atkins (never heard of him!). I didn't buy his book, but I read the pamphlet from cover to cover, and it described sleepiness after eating meals high in carbohydrate. Since childhood, I would feel very sleepy after eating starchy meals but I never knew why. So, despite my disbelief that Atkins' diet could work, I cut out bread, pasta, potatoes, rice, cereals etc - all of the things that we are constantly told are good for us because they are "low-fat".

Within days, I felt like a new man (oo-er, missus!) The sleepiness was gone, my weight slowly decreased and the heartburn I used to get was also gone. I was a total convert. By nature I'm very curious (which is why I became an Engineer), so I wondered how Atkins' diet worked. In 1999, I got Internet access at work and was delighted to see that there were people out there (some of them doctors) other than Atkins who were saying much the same thing.

In 2001, I got a shock when the company that I worked for lost a "must win" contract and I was put on the redundancy list. My health began to deteriorate and I was referred to an endocrinologist. It turned out that my pituitary gland was failing for no apparent reason and it was no longer stimulating my thyroid gland to secrete thyroxine. I was therefore prescribed levothyroxine. The upside to all this is that I am now exempt from all prescription charges. In addition, I get regular blood tests, so I can see the result of any dietary changes on my bloodwork.

As well as having a dodgy pituitary, I also had "the Metabolic Syndrome" (a.k.a. "Syndrome-X" in the US). This is a fancy name for pre type 2 diabetes. This meant that my fasting serum glucose, triglycerides, total cholesterol, LDL & uric acid were higher than they should have been and my HDL was lower than it should have been. It just so happens that a diet low in sugary & starchy carbohydrates is ideal for people with this condition.

I still didn't understand how Atkins' diet worked, so I studied some biochemistry web-sites to get a better understanding of human metabolism. In November 2002, I joined the Muscletalk forum after e-mailing the owner James criticising an article on ketogenic diets that he had written. Username "Nigeepoo" was born. Why Nigeepoo? I have a rather puerile sense of humour and think that putting "poo" on the end of a word is hilarious. It also suits my warm & fluffy nature!

This was the beginning of a new phase in my learning. From there, I found a US & then a Canadian (now closed) bodybuilding forum which allowed me to learn even more about nutrition. In January 2003, the BBC series "Diet Trials" studied the Atkins diet amongst others. At the end of the series, viewers were referred to a BBC Nutrition & Fitness board (now closed) and a Healthy eating board where I posted. As a result of various recommendations, I bought some books on running, diet & nutrition, metabolism and biochemistry. I also surfed PubMed and various journals, looking for studies on ketogenic diets and the effects of different proteins, fats and carbohydrates on subjects.

In 2004, my pituitary stopped secreting sufficient LH & FSH and in 2005 it stopped secreting sufficient GH, so I decided to take early retirement and take things a bit easier as I was having trouble with my memory & concentration. I decided to dump my nutritional knowledge to hard-copy before I forgot it, so I wrote an e-book, "Nigee's Guide to Losing Body-fat Healthily". That's not the only reason why I wrote it....you'll have to read it to find out the other one. Was that hint subtle enough?

Discovering Vitamin D3 at the beginning of 2007 was a major breakthrough, in terms of memory, concentration, mood and the Metabolic Syndrome. My endocrinologist was so pleased with my last set of blood and urine tests (all normal except for slightly raised cholesterol) that I don't need to see him anymore. I'll still have annual blood tests, to monitor my condition.

Right, that's enough about me, baby! Tomorrow, it's back to nutritional stuff again.

Cheers, Nige.

Cholesterol And Coronary Heart Disease

Cholesterol & coronary heart disease are mentioned in the media quite a lot. Unfortunately, most of what you see & hear is either wrong or oversimplified to the point where it misses out what's actually happening.

Fat and/or cholesterol doesn't stick to the insides of artery walls like grease on the inside of a drainpipe. This article sets about explaining what cholesterol is and what really happens to artery walls, and also tells you how to minimise your risk of having a heart attack or 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 and protein (water-soluble) at the other end and 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 limo'. Inside the limo', there are apo(lipo)proteins which are like the driver, as they determine where the particles go. The passengers are cholesterol, cholesteryl esters, phospholipids and triglycerides. These limo's come in different variants, like chylomicrons, VLDL, LDL, IDL and HDL, the difference being the type and amount of apoprotein and the relative proportions of cholesterol and other passengers, and there are also sub-groups of each type.

The different variants are affected by how much triglycerides there are circulating in the blood. High serum triglycerides (caused by a chronic over-consumption of sugary & starchy carbohydrates for one's activity level) result in cholesterol-depleted, triglyceride-rich particles and low serum triglycerides result in cholesterol-rich, triglyceride-depleted particles. Therein lies the problem. As cholesterol is a powerful anti-oxidant, small, dense (Type B) cholesterol-depleted particles are more prone to oxidation than large, buoyant (Type A) cholesterol-rich ones.

LDL that becomes oxidised is bad LDL and is swallowed-up by scavenger macrophages. These then swell-up into foam cells which embed themselves into the intima of artery walls. Other processes also occur which cause cholesterol and calcium to build-up as a plaque in the media of artery walls. To see a cross-section through a typical artery wall, click here and scroll down to the bottom of the page. Unoxidised LDL is not bad and is not swallowed-up by scavenger macrophages.

This plaque build-up pushes the inner artery wall inwards making the artery narrower in cross-section, impeding the flow of blood through it. This can cause angina pectoris (pain in the chest) as the heart muscle is starved of oxygen. Eventually, especially if there are low levels of anti-inflammatories in the blood, the plaque can rupture, causing chunks of plaque to circulate and block-up narrow coronary arteries causing a heart attack, or narrow cerebral arteries causing a stroke.

It's possible to reduce serum triglycerides quite drastically by eating long-chain omega-3 fats from oily fish. These inhibit the conversion of glucose into triglycerides, but beware. Inhibiting the conversion of glucose into triglycerides can result in increased blood glucose levels (which is also not good - see below) if sugary/starchy carb intake is too high. Solution? Reduce your sugary/starchy carb intake to suit your 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 anti-oxidants.
Chronically-high blood pro-oxidants.
Chronically-low blood anti-inflammatories.
New! Chronically-low Vitamin K2 (causing calcium to build up in the media of artery walls).

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.

2) Have blood glucose (BG) tested regularly. If you're lucky, you may be able to request 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 is the No.1 best way to damage your arteries and get them clogged-up.

4) Take a good B-complex tablet each day containing B6, B12 & Folic acid, which lowers homocysteine levels.

5) Ensure that your diet is high in natural anti-oxidants from coloured veggies (beta-carotene), fruits (Vitamin C + bioflavonoids), tomatoes (lycopene), sesame seeds (gamma-tocopherol), Brazil nuts (selenium), alcohol and/or red wine in moderation, green tea in moderation, extra-bitter chocolate in moderation, onions/garlic etc.

6) In men and non-menstruating women, excess iron in the blood is pro-oxidant, so don't supplement with iron. Menstruating women have the opposite problem, so they should supplement with iron.

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.

8) New! Eat a diet high in Vitamin K2. For food sources of vitamin K2, see here.

What about Benecol & Flora Pro-Activ?

These yoghurts & spreads contain plant sterols or stanols, which reduce total serum cholesterol by up to 15%. However, as explained above, it's LDL quality that counts, not quantity, and there is no evidence to show that these foods save any lives.

What about statins?

Statins (HydroxyMethylGlutarate Coenzyme-A Reductase inhibitors) reduce total serum cholesterol. They also have anti-inflammatory and anti-clotting effects by reducing levels of the non-sterol derivative mevalonate and its subsequent products. Click here to see the cholesterol synthesis pathway. Statins do save lives in people who have already had a heart attack and also in men between the ages of 30 and 60. However, younger or older men and all women do not get reduced number of deaths, though heart-attack deaths may be lower. I would strongly recommend anyone who is taking statins to supplement with at least 100mg/day of Coenzyme-Q10, as the synthesis of this vital substance is suppressed by them. Note that fish oils also have anti-inflammatory and anti-clotting effects as well as anti-arrhythmia effects and they don't suppress the production of Co-Q10.

What about eating cholesterol?

When cholesterol is eaten, the liver secretes less to compensate. An average egg contains about 250mg of cholesterol and the vast majority of people (who don't have any genes for familial hypercholesterolaemia) can eat two eggs a day without significantly affecting their serum cholesterol level. Click here.

A big shout out to to the guys & gals from forums.ebay.co.uk

I don't know how you found this Blog as I get the message "Error: you do not have permission to view the requested forum or category." when I click on the link from whence you came. So, how did you find me?

EDIT: Now I know how you found me and why. If you want to lose some flab or stop falling asleep after lunch, read Nigee's Guide to Losing Body-Fat Healthily. If your get up and go has got up and left, see the Vitamin D article.

Blood Glucose, Insulin & Diabetes

How does the body regulate blood glucose?

At any given moment, there is about 4.5g of glucose circulating in your blood (5mmol/L x 180g x 5L). As the brain alone uses about 6g of glucose per hour in the absence of ketones, blood glucose (BG) level could fall to zero within an hour if we ate no sugary/starchy carbs. If we ate a mere 5g of glucose, BG level could double. As very low BGs are fatal and very high BGs damage proteins by a process called glycation (a bit like caramelisation), the body keeps BG levels within fairly tight limits by the use of a negative feedback (NFB) control system.

How does a negative feedback control system work?

NFB systems consist of a non-inverting (more in → more out) part, which in this case are the islet cells of Langerhans (a.k.a. pancreatic beta cells), as increasing BG level results in increasing insulin secretion. It's actually a bit more sophisticated than that. Beta cells can store insulin and dump it into the blood if there is a sudden increase in BG level. This is analogous to the accelerator pump in a carburettor, which dumps petrol into the engine if you slam your foot on the accelerator pedal, i.e. it produces a rapid response. The dumping of insulin from beta cell storage is known as the Phase 1 insulin response. If this (or the accelerator pump) fails, there is a lag in the response; this will become significant below.

Increasing BG level results in increasing insulin secretion from beta cells and is known as the Phase 2 insulin response

The other part of a NFB system is the inverting (more in → less out) feedback part, which in this case is split into three parts, all working in parallel. They are:

1. Liver - increasing insulin level results in decreasing Hepatic Glucose Production.
2. Muscle cells - increasing insulin level shifts GLU-T4 transporters which shuttle glucose from the blood into cells, decreasing BG level.
3. Fat cells - increasing insulin level shifts GLU-T4 transporters which shuttle glucose from the blood into cells, decreasing BG level.

What can go wrong?

There are three main types of diabetes:

1) Type 2 diabetes. This is by far the most common (about 95% of all cases) and is usually caused by abdominal obesity. Type 2 diabetes has two main mechanisms going on. The first is a progressive insulin resistance of target tissues (firstly liver, then muscles and then fat cells in that order) possibly caused by increased levels of saturated fatty acids being fed to the liver from abdominal fat stores, and chronically-high BG and insulin levels caused by chronically over-consuming high glycaemic load carbohydrates, possibly accompanied by large amounts of saturated fat and/or large amounts of omega-6 fat. A sedentary lifestyle lowers the sensitivity of muscle cells to insulin. Insulin resistance also has a hereditary link. It may also be linked to a Vitamin D deficiency, see here.

Insulin resistance weakens the feedback in the NFB system, resulting in further increased BG and insulin levels (hyperinsulinaemia). Increased BG level causes increased damage to beta cells by glycosylation. Increased insulin level causes further insulin resistance as target tissues become increasingly insensitive (a bit like louder and louder music making you progressively deafer and deafer). Eventually, beta cells become too damaged to secrete sufficient insulin and insulin levels begin to fall. This results in a massive rise in BG level and this is now full-blown Type 2 diabetes.

There are five main treatments for Type 2 diabetes:

1. Lifestyle interventions - reduced intake of high glycaemic load carbohydrates and/or increased intake of omega-3 fats and/or increased intake of Vitamin D3 and/or increased intense exercise and/or loss of abdominal fat.
2. Sulphonylureas - drugs which stimulate beta cells to secrete even more insulin. Unfortunately, that's a bit like flogging a dying horse as it doesn't address the problems caused by weakened feedback and eventual beta cell failure is inevitable, resulting in the need for insulin injections.
3. Biguanide drugs such as Metformin - increase insulin sensitivity in target tissues. This strengthens the feedback in the NFB system, which results in reduced BG and insulin levels. This combined with lifestyle interventions can return the NFB system to normal operation.
4. Thiazolidinediones - also increase insulin sensitivity in target tissues, e.g. muscle and fat, as well as possibly improving the secretory function of beta cells.
5. Insulin injections take the strain off beta cells, but may worsen insulin resistance of muscle tissues resulting in increasing obesity.

2) Type 1 diabetes. This is much less common (about 5% of all cases) and is caused by an autoimmune disease. One possible mechanism is as follows: Due to an increase in Zonulin (see here ), the gut becomes more permeable than it should (a.k.a. Leaky Gut Syndrome) and allows protein fragments to pass into the blood. These are destroyed by antibodies. However, if a protein fragment happens to have the same sequence of amino acids as a protein in our own body, the antibodies then set about destroying parts of our own body. Examples of this are gluten (proteins found in wheat, rye, barley and oats) producing antibodies in the blood that can destroy the gut causing Coeliac Disease or skin cells causing Dermatitis Herpetiformis or mucous membranes causing Sjogren's Syndrome or brain cells causing Cerebellar Ataxia. As there is an association between the consumption of cows' milk and the incidence of type 1 diabetes (see here ), it is quite possible that, in susceptible individuals, fragments of casein protein enter the blood in this way resulting in antibodies that destroy pancreatic beta cells.

Another possible mechanism is autoimmune attack after a viral infection.

Once all of the beta cells are destroyed, no insulin is secreted and insulin injections are required. If some beta cells survive, there is a possibility that normal BG level can be maintained if sugary/starchy carbohydrate intake is much reduced.

3) Latent Autoimmune Diabetes of Adulthood (LADA). The percentage of cases with this is unknown as it is often misdiagnosed as type 2 diabetes. This is a slow developing diabetes that is more like type 1 in origin (autoimmune with antibodies) but is often misdiagnosed as type 2 because of the age at diagnosis and the relatively slow progression of the disease (slow compared to type 1 but fast compared to type 2). See here. It is believed that Sir Steven Redgrave has this type of diabetes. Whether his autoimmune disease was triggered by a huge intake of milk (to build those Olympic-winning muscles) we will never know.

What else can go wrong?

As stated earlier, loss of the Phase 1 insulin response can occur. This usually happens when beta cells are chronically over-secreting insulin due to a chronically-high intake of sugary/starchy carbs and are unable to store any. This results in a lag in insulin response. This isn't a problem if low glycaemic load carbs are eaten and BG levels change only a little or very slowly. However, if high glycaemic load carbs are eaten, this produces a large and rapid rise in BG level. If a NFB loop with a lag in it is presented with a sudden change in input level, its output overshoots. This results in too much insulin being secreted, which eventually results in low BG levels! This is known as rebound hypoglycaemia. The solution? Stick to low glycaemic load carbs.

Where does blood glucose come from if I haven't eaten?

When no sugary/starchy carbs are being digested, BG starts to fall. Adrenaline and noradrenaline (catecholamine hormones) are secreted by the adrenal medulla into the blood and also by sympathetic neurons. Like glucagon (see below), they stimulate the mobilisation of glycogen and triacylglycerols (stored fats) by triggering the production of cyclic AMP (adenosine monophosphate). Adrenaline and noradrenaline differ from glucagon in that their glucose-producing effect is greater in muscle glycogen than in liver. They also inhibit the uptake of glucose by muscle. Instead, fatty acids released from adipose tissue are used as fuel. Adrenaline also stimulates the secretion of glucagon and inhibits the secretion of insulin. Thus, catecholamines such as adrenaline and noradrenaline increase the amount of glucose released into the blood by the liver and decrease the utilization of glucose by muscle.

Pancreatic alpha cells secrete glucagon. This hormone mobilises the conversion of liver glycogen into glucose. The liver only stores about 70g of glycogen, but when combined with water, a larger mass of glucose can be generated. Eventually, liver glycogen stores become depleted and BG level falls again. Glucagon also stimulates gluconeogenesis in the liver, which is the production of glucose from non-carbohydrate precursors, like the conversion of glucogenic amino acids, such as glutamine, into glucose. This causes slow muscle wastage unless there is sufficient protein intake to provide the necessary amino acids. When BG falls to about 3.3mmol/L, the pituitary gland kicks-in and secretes ACTH (adrenocorticotropic hormone) which stimulates the release of cortisol from the adrenal cortex. Cortisol further stimulates gluconeogenesis in the liver. When BG level falls to about 2mmol/L, the pituitary secretes GH (Growth Hormone) which has an anti-insulin effect.

What else does insulin do?

Insulin has many metabolic effects in the body apart from lowering BG level. It's a very anabolic hormone and an insulin spike is usually desired post workout to maximise the uptake of glucose and amino acids by muscle cells. There's nothing wrong with the occasional short-term insulin spike. It's chronically-high insulin levels that cause long-term health problems like high blood pressure & clogging of arteries.

Vitamin D

Vitamin D is known as the "Sunshine Vitamin" and it was once thought that a deficiency in it was rare and that it was only involved in calcium homeostasis in bones, and that a lack of it only caused Rickets/Osteomalacia. Recent research however has shown that not only is Vitamin D involved in a whole host of bodily processes but that a deficiency in it is actually very common, leading to a whole host of degenerative diseases.

What is Vitamin D?

A good overview on Vitamin D can be found here. An informative 1 hour presentation called "Vitamin D deficiency: The Cause of Everything?" can be found here. Another 1 hour presentation called "Vitamin D and Prevention of Chronic Diseases" can be found here. In addition, read this article.

How common is Vitamin D deficiency?

According to Hyppönen & Power, in a large sample of the white British population born in 1958, 60.9% of subjects had serum 25(OH)D (the active metabolite of Vitamin D) of less than 75nmol/L in Summer & Autumn, and 87.1% had serum 25(OH)D of less than 75nmol/L in Winter & Spring.

Here's my experience of Vitamin D3. For many years, I was struggling to cope with my job and I eventually took early retirement on the grounds of ill-health. In mid-2006 I was given a serum 25(OH)D test and the result was 73nmol/L. As the Reference Range for serum 25(OH)D is 33-200 nmol/L, I was technically not deficient in Vitamin D. Subsequent events suggested otherwise.

In January 2007, after reading the above study and a study by Vieth, Kimball, Hu & Walfish, I began to supplement with 2,000iu/day of Vitamin D3 and also used a UVB+IR lamp for 3 minutes each night. At first, nothing happened and I was pretty sceptical about getting any improvement. However, after about 8 weeks, I began to notice an awakening in my brain. This continued, and by March 2007, I was feeling quite perky. Friends commented on the fact that I had become very chatty and I was also waking early in the morning raring to go, totally unlike my former self. In May 2007, I had another serum 25(OH)D test and the result was 115nmol/L. Another interesting result was my serum triglycerides, something that's usually always higher than desirable. My TGs were 1.4mmol/L (RR less than 1.8mmol/L). This was the lowest result since tests began in 2002.

I began to get bored with standing around stark naked in front of a UV lamp for 3 minutes each night and I stopped doing this. Slowly, my brain began to go back to sleep. I couldn't understand why as I thought that 2,000iu/day of Vitamin D3 (10 x RDA) was more than enough. In November 2007, I had another serum 25(OH)D test. When I saw my endocrinologist in December 2007, I was quite shocked to see that the result was now 70nmol/L. I immediately increased my Vitamin D3 intake to 5,000iu/day (25 x RDA) and within 2 weeks, my brain started to wake up again. In May 2008, serum 25(OH)D was 173nmol/L and in September 2008 it was 163nmol/L.

See also The urgent need to recommend an intake of vitamin D that is effective.

What foods contain it?

For a list of the top 432 foods highest in Vitamin D, see here. Beware of foods that have been supplemented, as Vitamin D2 may have been used. This is much less effective than Vitamin D3 according to Armas, Hollis and Heaney. Vegetarians & vegans may not want to eat foods containing Vitamin D3 as this is sourced from animals (e.g. the lanolin from a sheep's coat). Eating the Standard English Diet, it is difficult to obtain 5,000iu/day of Vitamin D. The cheapest way to get a lot of it is by going out in the sun in a swimsuit for 20 or so minutes in the middle of the day in Summer & Autumn, which costs absolutely nothing! As Vitamin D is fat-soluble, the body can build up stores to keep it supplied during Winter & Spring.

Vitamin D deficiency, Insulin Resistance and The Metabolic Syndrome/Type 2 Diabetes

According to Hyppönen and Power, there is a strong association between decreasing 25(OH)D, increasing BMI (Body Mass Index) and increasing HbA1c (glycosylated haemoglobin). Increasing HbA1c is associated with increasing Relative Risk of mortality, according to Khaw, Wareham, Bingham, Luben, Welch and Day, summarised here.

According to Chiu, Chu, Go and Saad, there is a positive correlation of 25(OH)D concentration with insulin sensitivity and a negative effect of hypovitaminosis D on ß cell function. Subjects with hypovitaminosis D are at higher Relative Risk of Insulin Resistance and The Metabolic Syndrome.

An Oral Glucose Tolerance Test in September 2008 showed that I had absolutely normal Glucose Tolerance (2 hours post-glucose load serum glucose = 3.7mmol/L) whereas in 2003 I had moderately impaired Glucose Tolerance (2 hours post-glucose load serum glucose = 8.7mmol/L). Now that's what I call a result!

Vitamin D deficiency and Cancer

According to Lappe, Travers-Gustafson, Davies, Recker and Heaney, subjects receiving 1400-1500mg/day supplemental calcium and 1100iu/day supplemental Vitamin D3 have a Relative Risk of getting any type of cancer of 0.402 which is equivalent to a 60% reduction in the risk of getting cancer compared to the non-supplementing group. If the first 12 months results are discarded (to exclude any subjects who already had cancer when they started the study), the RR is 0.232 which is equivalent to a 77% reduction in the risk of getting cancer. One wonders what the results would have been if 5,000iu/day of Vitamin D3 had been used. See also Diaz, Paraskeva, Thomas, Binderup and Hague.

Vitamin D deficiency and Mental function

According to Vieth, Kimball, Hu & Walfish as mentioned above, supplementing with 4,000iu/day of Vitamin D3 produces a large reduction in the "Miserableness Factor" without affecting serum Calcium levels. According to Wilkins, Sheline, Roe, Birge and Morris, Vitamin D deficiency is associated with low mood and worse cognitive performance in older adults. According to Gloth, Alam and Hollis, Improvement in 25(OH) D is significantly associated with improvement in depression scale scores in a group of 15 subjects with SAD.

NEW! According to Cherniack, Troen, Florez, Roos & Levis S , Hypovitaminosis D is prevalent among older adults, and several studies suggest an association between hypovitaminosis D and basic and executive cognitive functions, depression, bipolar disorder, and schizophrenia.

Vitamin D deficiency and High Blood Pressure

According to Forman, Giovannucci, Holmes, Bischoff-Ferrari, Tworoger, Willett and Curhan, plasma 25(OH)D levels are inversely associated with the risk of incident hypertension.

Vitamin D deficiency and the Immune System

According to Cannell, Vieth, Umhau, Holick, Grant, Madronich, Garland and Giovannucci, Vitamin D deficiency predisposes children to respiratory infections. According to Ginanjar, Sumariyono, Setiati and Setiyohadi, The active form of vitamin D produces and maintains self immunologic tolerance.

Vitamin D Deficiency and Falls

According to Dharmarajan, Akula, Kuppachi and Norkus, in the pilot study of older adults with gait imbalance and falls, vitamin D deficiency was observed in 54% of patients tested and previously unrecognized.

Vitamin D Deficiency and Chronic Pain

According to Plotnikoff and Quigley, all patients with persistent, non-specific musculoskeletal pain are at high risk for the consequences of unrecognized and untreated severe hypovitaminosis D. According to Al Faraj and Al Mutairi, Vitamin D deficiency is a major contributor to chronic low back pain in areas where vitamin D deficiency is endemic. According to Gloth, Lindsay, Zelesnick and Greenough, there may be a pain syndrome associated with vitamin D depletion that appears as hyperaesthesia worsened by light, superficial pressure or even small increments of movement.

But doesn't the sun damage the skin and cause skin cancer?

Inappropriate sun exposure can certainly damage the skin. Chronic overexposure to the sun (e.g. farmers and other outdoor workers) causes wrinkly, leathery skin and skin cancers such as Basal Cell Carcinoma & Squamous Cell Carcinoma. These are benign skin cancers which are easily removed and rarely fatal. Acute overexposure to the sun (e.g. people getting severe sunburn on foreign holidays) causes the much more serious Malignant Melanoma. This condition, if not caught early enough, has a very high risk of mortality. However, sensible sun exposure has more benefits than hazards. See Does solar exposure, as indicated by the non-melanoma skin cancers, protect from solid cancers: vitamin D as a possible explanation.

Is it possible to get too much Vitamin D?

It is possible to overdose with Vitamin D by supplementation. According to Vieth, published cases of vitamin D toxicity with hypercalcemia, for which the 25(OH)D concentration and vitamin D dose are known, all involve intakes of >40,000iu/day. People suffering from Sarcoidosis, Hyperparathyroidism, a history of Calcium Kidney Stones and Milk-Alkali Syndrome need to consult their GP before supplementing with Vitamin D. People prescribed Warfarin also need to be careful, as Warfarin is a Vitamin K antagonist, which can result in calcification of tissues.

It isn't possible to overdose by sun exposure as the metabolic processes down-regulate when ~10,000iu has been produced. To find out when the sun is strong enough to produce Vitamin D in your skin, see the Vitamin D Synthesis in Human Skin Calculator.