Thursday, 31 December 2009

The dirty, robbing bastards!

...said the characters Janice and Ray, on the Catherine Tate Show. Having whinged about Channel Five in the past, I will now whinge about the BBC.

I watched episode 1 of "The Day of the Triffids" on BBC iPlayer and very good it was, too. So far, so good. I then tried to watch episode 2. It was available in High Definition format only. I bought my lap-top in May 2003 and it isn't up to displaying High Definition programmes on Flash Player 10. I could listen to the programme for a while, but Firefox has a memory leak, which accelerates when trying to play High Definition programmes on Flash Player.

Once all of the memory has been used up, Firefox displays a dialog box, locks-up or just terminates. I disabled Virtual Memory on my lap-top as Hard Disk is ~500,000 times slower than RAM. I have 1GB of memory and that's it. My lap-top won't take more than 1GB of RAM.

So, Aunty Beeb. Why can't I watch programmes in either Low Definition or High Definition formats?

P.S. The BBC message-boards recently changed to the BBC iD system. I tried to migrate Nigeepoo (I've been using that username there since March 2003) to the BBC iD system to be informed "Your username appears to contain a profanity". You couldn't make this stuff up! They will be sorting it out at some point...

I'm temporarily posting there with the username Nigeep00.

P.P.S. I was so busy whingeing, that I completely forgot to wish all my readers a Happy New Year. So......


Look after your tyres.

Many years ago, I used to drive a Signal Yellow Ford Fiesta 1.1S (all 3 of my cars have been bright yellow - it's a very safe colour). In 1982, around Christmas time, I had a minor prang which dented the front offside just beside the headlamp. When I got home, I tried to get my hand up the front wheel arch to inspect the damage but the wheel was in the way so I applied full left lock. What I then saw sent a chill down my spine.

Both front tyres had perfect tread on the outside edges but were worn right down to the steel belts on the inside edges. This was due to tracking error (excessive toe-out) forcing the treads outward as the car moved forward. When I had the tyres replaced and the tracking corrected, the steering felt much lighter (I didn't have power steering).

Fast-forward to 30th December 2009....

I had a slow puncture in my rear nearside tyre (due to a nail) so I went to the garage to get it repaired. The garage informed me that both rear tyres were unserviceable due to a complete lack of tread between the inside & outside edges of the tyres. My car has wide tyres and apparently, this happens even when tyres are inflated to the correct pressure.

Last week, I was driving around on snow & ice on two semi-bald tyres that provide traction, as Mazda MX-5s have Rear Wheel Drive. I got lucky...twice!

Moral of the story:- Check your treads across the full width of the tyres.

Tuesday, 29 December 2009

I'm a secret lemonade drinker...

R. White's, R. White's! I'm a trying to give it up-a but it's one of those nights, R. White's, R. White's! R. White's lemona-a-ade. I'm a secret lemonade drinker...*fade to outtro*

Who remembers the above advert about a man in striped pyjamas creeping downstairs to raid the fridge for R. White's Lemonade and getting caught in the act? It reminds me of another advert currently running for Crunchy Nut Cornflakes where a man is caught eating someone else's Crunchy Nut Cornflakes in the middle of the night having been overheard on a baby monitor. Having had his bowl confiscated, the sound of sobbing is heard on the monitor, which is thrown into a drawer to muffle it. "The trouble is they taste too good!"

Do the above examples sound a bit like drug addicts trying/failing to get their fixes? As Dr John Briffa commented on Losing the taste for sweetness trumps using ‘healthy’ sweeteners, in my book, "Most animals, it turns out, chose saccharin over cocaine. Blimey."

Blimey, indeed! See Intense Sweetness Surpasses Cocaine Reward. Why is this? A possible explanation lies in Hypoglycemia & Neurosis.

"Who is drawn to such "peculiar" diets? The answer, it seems, is those who crave relief from repressed pain and stress in their lives. Sugar somehow elicits the secretion of the body's "feel-good" endorphins, so much so that the pain threshold of baby rats almost doubles. The blood of newborn human babies is routinely sampled by heel prick, a painful procedure that usually causes crying. However, after sugar is given, the tears are brief. Beta-endorphin levels increase in binge-eaters (Blass 1987-1995, Fullerton 1985), which may be why they over-eat.

However, endorphins eventually fall in chronically sugar-fed rats, and their pain thresholds fall with them (Roane 1990). In other words, you need more and more sugar to get the same relief, until you're in Betty Crocker country and your diet has become "peculiar." This kind of "habituation" is found in all opiate-mediated addictions, including chronic alcoholism (Genazzani 1982), in which opiate-like isoquinolones are formed from a breakdown product of alcohol and the neurotransmitter dopamine.

Endorphins, our self-made opiates, have receptors in brain structures mediating emotional feelings as well as those dealing with physical sensations of pain and stress. The sense of urgency we experience with a full bladder is caused by low endorphins. Babies who are breast-fed often appear ecstatic, and this state coincides with high levels of endorphins. In adults, there are high levels of endorphins during and after orgasm. Thus, endorphins motivate as well as providing comfort and gating pain. And they are among the most addictive substances on the face of the planet. So perhaps it's not so surprising that "20 percent [of hypoglycemics] give a history of intense, insatiable and irresistible craving for sweets and carbohydrates" (Buehler 1955), while the rest are strongly attached to their "peculiar" diets. Hypoglycemics are unwittingly trying to self-medicate their profound subconscious malaise with food.

A Canadian who was diagnosed hypoglycemic years ago told me that he was left to cry for the first eight months of his life, until his mother found that sweetened condensed milk comforted him. From then on, he had vast quantities of sugar. In therapy, he realized sugar comforted the buried desolation imprinted in him by his early deprivation, and that eating too little food was a symbolic recreation of this trauma."

As for me, when I was little, I remember eating Rusks, which were very sweet. I also recall getting a regular supply of French fancies and Corona lemonade, which were also very sweet. As we were quite poor, mum used to spend hours on a typewriter doing secretarial stuff to raise extra money. I found comfort in sweet foods. I now have a "sweet tooth" and get great pleasure from eating. Coincidence?

Modern baby formulas are crammed with sugar.

Another Quality Street, anyone? Or how about a wafer-thin mint?

Thursday, 24 December 2009

Look after your brain, Part 3.

Funnily enough, on the Mean Forum that I mentioned in my previous post and in the very same discussion, someone suggested two supplements of which I was unaware that can improve mental function.

1) SAMe (S-adenosyl-methionine). See S-adenosyl methionine: a natural therapeutic agent effective against multiple hallmarks and risk factors associated with Alzheimer's Disease and Polyunsaturated fatty acid and S-adenosylmethionine supplementation in predementia syndromes and Alzheimer's Disease: a review.

2) Methylcobalamin, sublingual. See From mild cognitive impairment to Alzheimer's Disease - influence of homocysteine, vitamin B12 and folate on cognition over time: results from one-year follow-up and Cumulative incidence of vitamin B12 deficiency in patients with Alzheimer's Disease.

Vitamin B12 should be taken sub-lingually (or nasally), as old people's stomachs secrete less Intrinsic Factor (required for B12 absorption in the gut) than young people's. Old people who take a Proton Pump Inhibitor (***prazole) for acid reflux secrete even less Intrinsic Factor still.

I will give these a try.

Continued on Look after your brain, Part 4.

Sunday, 20 December 2009

How many working brain cells do drug company lackeys have?

In Elvis lives!, I referred to the study Intensive lipid lowering with atorvastatin in patients with coronary heart disease and chronic kidney disease: the TNT (Treating to New Targets) study*, which came to the conclusion:

"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."

I then pointed out the following teensy-weensy flaw in the conclusion:

"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 worse? Having a major cardiovascular event or being dead?"

On a Mean Forum far away, I pointed out this teensy-weensy flaw in the conclusion and was told "are you really that retarded?" Funnily enough, I never got an answer from that person as to how the conclusion in red was justified by the data in green. I helpfully suggested that it might have something to do with the fact that Atorvastatin 80mg is a 700% increase in sales compared to Atorvastatin 10mg.

I then received an e-mail from Pfizer ® Customer Service with a spoofed sending address (it was fairly obvious that it was spoofed as it was my e-mail address!). There was the usual helpful Outlook Express "Some pictures have been blocked to help prevent the sender from identifying your computer. Click here to download pictures" message. I didn't click. Well, would you? I deleted the e-mail. I've now enabled comment moderation just in case this 'tard feels like spamming my Blog.

Pfizer manufactures Atorvastatin. Ho-hum!

*Funding for the study was provided by Pfizer Inc., New York, New York. Dr. Shepherd has received consulting fees from AstraZeneca, GlaxoSmithKline, Merck, Oxford Biosensors, Pfizer Inc., and Schering-Plough, and lecture fees from AstraZeneca, Merck, and Schering-Plough. Dr. Kastelein has received consulting fees and lecture fees from Pfizer Inc., AstraZeneca, Merck, and Schering-Plough, and grant support from Pfizer Inc. and AstraZeneca. Dr. Bittner has received consulting fees from CV Therapeutics, Novartis, Pfizer Inc., Abbott, and Reliant, and grant support from Pfizer Inc., Atherogenics, Merck, Kos Pharmaceuticals, Abbott, CV Therapeutics, and the National Institutes of Health. Dr. Deedwania has received consulting fees and lecture fees from Pfizer Inc. and AstraZeneca. Dr. Breazna, Dr. Wilson, and Dr. Zuckerman are all employees of Pfizer Inc. Mr. Dobson is an employee of Envision Pharma Ltd., which was a paid consultant to Pfizer Inc. in connection with the development of the manuscript. Dr. Wenger has received consulting fees from CV Therapeutics, Sanofi-Aventis, Schering-Plough, AstraZeneca, Abbott, Merck, and Pfizer Inc., and grant support from Pfizer Inc., Merck, and the National Heart, Lung, and Blood Institute.

Saturday, 12 December 2009

How many working brain cells do researchers have?

Apparently (according to a Japanese study referred to in Am I Missing Something??? ), eating/drinking lots of sugary & starchy carbohydrate causes postprandial hyperglycemia (high blood glucose after meals) in people with type 2 Diabetes. No sh*t, Sherlock! Postprandial hyperglycemia "causes damage to blood vessels, inflammation and oxidation and these cause clogged vessels and heart attacks." I think we're all in agreement that postprandial hyperglycemia is BAD. So, how to tackle this thorny problem? By pharmacological approaches i.e. drug therapies. Like, Duh!
And what is Diabetes-UK's (& the ADA's) dietary advice to people with type 2 Diabetes?
The actual amount of carbohydrate that the body needs varies depending on your age, weight and activity levels, but it should make up about half of what you eat and drink." & under Ten steps to eating well:
"At each meal include starchy carbohydrate foods
Examples include bread, pasta, chapatis, potatoes, yam, noodles, rice and cereals. The amount of carbohydrate you eat is important to control your blood glucose levels." Like, Duh!

I've been doing a bit of research on methylglyoxal (MG) as a result of reading Methylglyoxal on Atkins... Uh oh! Apparently it's very toxic, therefore ketogenic diets are BAD, mmm-kay? MG causes Insulin Resistance and Advanced Glycation End-products which are both deemed to be undesirable.

Consider this:
MG is a glycolysis (conversion of glucose to pyruvate) inhibitor. As MG inhibits glycolysis in cells, uptake of Blood Glucose by cells decreases. Oh, look. Cells have become Insulin Resistant! As uptake of Blood Glucose by cells decreases, Blood Glucose rises. Oh, look. Increased Advanced Glycation End-products! It's bleedin' obvious (to anyone with a sufficient number of working brain cells) that, on a high-carb diet, MG is toxic. It's a no-brainer that MG's toxicity disappears on a low-carb/keto diet, when you actually want cells to burn fatty acids/ketones rather than glucose. Like, Duh!

In fact, strangulating the glucose pathway in cells may have benefits. See Cancer.

Here's another one. According to Progressive bone mineral content loss in children with intractable epilepsy treated with the ketogenic diet (KD), "The KD resulted in progressive loss of BMC." And yet, just above, "Growth and bone health status were suboptimal as were serum 25-OHD concentrations and dietary intake of calcium and vitamin D." Like, Duh!

Thursday, 10 December 2009

Why Most Published Research Findings Are False.

Following on from The future: I just saw it, I thought you might find this 2005 study by John P. A. Ioannidis of interest.


There is increasing concern that most current published research findings are false. The probability that a research claim is true may depend on study power and bias, the number of other studies on the same question, and, importantly, the ratio of true to no relationships among the relationships probed in each scientific field. In this framework, a research finding is less likely to be true when the studies conducted in a field are smaller; when effect sizes are smaller; when there is a greater number and lesser preselection of tested relationships; where there is greater flexibility in designs, definitions, outcomes, and analytical modes; when there is greater financial and other interest and prejudice; and when more teams are involved in a scientific field in chase of statistical significance. Simulations show that for most study designs and settings, it is more likely for a research claim to be false than true. Moreover, for many current scientific fields, claimed research findings may often be simply accurate measures of the prevailing bias. In this essay, I discuss the implications of these problems for the conduct and interpretation of research."

For more on this, see Who pays the piper and Who pays the piper part 2.

Thursday, 3 December 2009

Some more nails for the coffin of the "healthy low-fat" diet.

Every time someone writes "I'm eating a healthy low-fat diet", I cringe. It's presumptuous to assume that, because the fat content is low, the diet is automatically healthy. The media tell us it's healthy. The government tells us it's healthy. "Experts" tell us it's healthy. It must be healthy, right? Um...

See After-eating effects: Carbohydrates vs. fats and Reduced oxidation of dietary fat after a short term high-carbohydrate diet.

The low-fat diet was white bread, potatoes, tuna, chicken, carrots, canned fruit, fruit juices, cola, jam, marmalade, sweets, and sugar cubes.

The higher-fat diet was less of the above, plus a fat spread, which consisted of a mixture of lard, palm oil, olive oil, and corn oil (the ratio of polyunsaturated to saturated fat was 0.5:1).

Please excuse the following "shouting", but some facts need to be shouted from the rooftops:-






If you don't believe me (and why should you?), see A very-low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins, with particular reference to the following figure:-

At 50% fat intake, ~15% of the subjects have phenotype B. At 20% fat intake, ~50% of the subjects have phenotype B. At 10% fat intake, over 60% of the subjects have phenotype B. The subjects were all men, but women are no different in this respect.

Warning: The above study and similar studies by Dreon & Krauss have had the methodology tweaked to achieve a desired result. See The Conflation Game.

And now we have Dietary fat intake and subsequent weight change in adults: results from the European Prospective Investigation into Cancer and Nutrition cohorts.

"Results:...The difference in mean annual weight change was 0.90 g/y (95% CI: –0.54, 2.34 g/y) for men and –1.30g/y (95% CI: –3.70, 1.11 g/y) for women per 1 g/d energy-adjusted fat intake (residual method).

Conclusions: We found no significant association between the amount or type of dietary fat and subsequent weight change in this large prospective study. These findings do not support the use of low-fat diets to prevent weight gain."

Note: -1.30g/y means that as dietary fat intake increased, weight decreased.