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.

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.

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!

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.

"Summary

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.

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:-

1) LDL CHOLESTEROL (LDL-C) DOES NOT CLOG YOUR ARTERIES. LDL-C IS NOT BAD CHOLESTEROL.

2) OXIDISED LDL-C (OX-LDL-C) DOES CLOG YOUR ARTERIES. OX-LDL-C IS BAD CHOLESTEROL.

3) LARGE, FLUFFY (PHENOTYPE A) LDL-C OXIDISES SLOWLY.

4) SMALL, DENSE (PHENOTYPE B) LDL-C OXIDISES RAPIDLY.

5) AS THE PERCENTAGE OF CALORIES FROM FAT DECREASES, YOU GET LESS PHENOTYPE A AND MORE PHENOTYPE B.

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.

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.

Look after your brain, Part 2.

Mum used to use a transdermal Natural Progesterone Cream (to reverse hair loss) but she stopped using it some time before she became mentally impaired. I found a half-full pot of the stuff in mum's house and have instructed the nursing staff to rub a blob of cream on mum's skin each day to see if it makes any improvement to her Lewy Body Dementia. See Regeneration in a degenerating brain: potential of allopregnanolone as a neuroregenerative agent , Regenerative potential of allopregnanolone and Progesterone receptors: form and function in brain.

Getting mum to eat more smoked salmon has definitely perked her up. I've also managed to re-introduce turmeric into her diet (she was spitting out the turmeric pills as they were large & unchewable) by getting the nursing staff to stir a teaspoonful of turmeric powder into her orange juice (I & she can't taste it) once every few days. Luckily, she never had any problems taking the Vitamin D3 & K2 capsules/gelcaps.

Finally, I'm trying to get mum on low dose Aspirin, as Aspirin inhibits the aggregation of proteins (synuclein, beta amyloid) on charged polymers in amyloid diseases, such as Parkinson’s disease, Alzheimer’s disease, etc., according to Dr Art Ayers. As mum has a hiatus hernia, which causes acid reflux, her GP may not allow her to do this even though mum is taking a Proton Pump Inhibitor and Gaviscon. See The role of anti-inflammatory drugs in the prevention and treatment of Alzheimer's disease and Non-steroidal anti-inflammatory drugs (NSAIDs) and other anti-inflammatory agents in the treatment of neurodegenerative disease.

Continued on Look after your brain, Part 3.

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 (and magnesium) to function correctly.

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.