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covid-19, more on fructose, vitamin D, treatments and the vagaries of testing

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Canto: Ok, so note that in the graphic from the previous post, Australia is third highest in the group of 31 countries studied for caloric intake from sweeteners, but we don’t use HFCS much at all.

Jacinta: It might be a misleading graphic too. You might be forgiven for thinking that it somehow shows the USA as the most unhealthy, sweet-toothy country on the list, and Australia in third position, but since we’re more concerned here with links between fructose and covid-19 co-morbidities such as obesity, diabetes, cardiovascular problems and oxidative stress, the graphic doesn’t tell us much.

Canto: Yes so I found on this indexmundi site a list of 195 countries – and that’s all of them – showing prevalence of diabetes 1 and 2. That’s to say, the percentage of the adult population (from 20 to 79) that is diabetic. The USA ranks 43rd on that list, and Australia is down at 137th, level with Finland and Japan. But the site doesn’t name sources, and provides an end-note on the unreliability of much evidence: ‘National health authorities differ widely in capacity and willingness to collect or report information’. I should also add that though the USA is 43rd, the only other major nations above them are just about every Middle Eastern country, Pakistan, South Africa, Egypt, Sudan and Mexico. Make of that what you will.

Jacinta: Let’s avoid that rabbit hole, and return to medcram update 83, which briefly describes vitamin D3 (cholecalciferol) metabolism. This may involve a bit of repetition but that’s rarely a bad thing for us. So the D3 that we absorb or ingest goes to the liver and is hydroxylased at the 25th position (25-OH), but it doesn’t become activated until it’s again hydroxylased at the first position by the kidney (1,25-diOH, aka 1,25 dihydroxy vitamin D). And there’s another enzyme that can convert the vitamin to inactive forms. 

Canto: With that, Dr Seheult looks at another article from 2013 which describes a rat study that indicates that if fed on a high fructose diet, lactating rats suffered reduced rates of active intestinal calcium transport and active vitamin D. Or, more, accurately I think, they didn’t get the increased rates and levels that would be expected during lactation. So, because calcium is essential for skeletal growth, the study says ‘our discovery may explain findings that excessive consumption of sweeteners compromises bone integrity in children’.

Jacinta: Interesting, and I presume that means consumption by the mother during pregnancy. Anyway, in more detail, what they found was that increased fructose intake inhibited the enzyme that converted vitamin D into the active form in the kidney, and promoted the enzyme responsible for the inactive forms. Disturbing, as Seheult says, for the excessive fructose in American diets, which may consequently affect calcium and vitamin D levels, though that would surely require more research. 

Canto: Well, the same group released more research in 2014 which found that chronic high fructose intake in calcium-sufficient rodents (rats and mice) reduced their active vitamin D levels. And a 2015 study from Iran looked at something different but again having to do with effects on enzymes and metabolism. They looked at S-methyl cysteine (SMC), and this recalls the investigation of N-acetyl cysteine (NAC) a few updates ago. Found naturally in garlic and onions, SMC is described as a hydrophilic cysteine-containing compound, which they investigated for its putative effects against oxidative stress and inflammation. So they induced oxidative stress in rats via a high-fructose diet over 8 weeks and then dosed them with SMC. Results from the high fructose diet were – here goes – increased blood levels of glucose, insulin, malondialdehyde, and tumour necrosis factor-alpha.

Jacinta: Okay so the increased insulin is presumably a reaction to the increased glucose. Its role is to absorb excess blood glucose, and too much of it can result in hypoglycaemia, low serum glucose levels. Malondialdehyde (MDA) is described as a marker for oxidative stress, so it’s not good. Tumour necrosis factor (TNF or TNFα) is a ‘multifunctional cytokine’, and although cytokines (types of proteins) perform many vital functions, the cytokine storm that appears to be associated with oxidative stress and covid-19 is a bad thing. 

Canto: But there were also decreased levels of glutathione (GSH), glutathione peroxidase (GPx) and catalase as a result of this fructose diet, and Seheult talked about these enzymes and such as important in reducing oxidative stress. However, the SMC dosing improved antioxidant enzyme activities and reduced levels of glucose, insulin and TNFα. 

Jacinta: So this SNC seems another promising antioxidant treatment. Meanwhile, watch your sugar intake, especially with fructose. More studies required of course, but I suppose there are ethical issues involved in fattening up and inducing oxidative stress on human subjects with a high fructose diet. Okay updates 84 and 85 deal with questions that hospitalised covid-19 patients might want answered, so we’re going to skip those or we’ll never catch up on these updates. With update 86 they’re into the second half of June and noticing a resurgence of the virus. So at the Johns Hopkins site they’ve ‘working to fill the void of publicly accessible covid-19 testing data’, because without testing you obviously can’t work out the numbers.

Canto: But more than testing itself, the turnaround of results is a problem. A young woman was just on the tube saying it took three weeks to get her test results, which renders the test useless. And another person on the tube reported that she’d tested positive, felt generally okay or asymptomatic, then tested negative, after which she came down with a heavy case replete with many of the covid-19 symptoms, and then tested positive again. How can this happen?

Jacinta: It’s still a mysterious virus, but to return to the update and Johns Hopkins, they’re generally looking at US data, but I’m interested in understanding the testing process and how well it maps the prevalence of this virus. The website has a graphic which shows the fairly rapid rise in daily testing from March through to June (with a drop-off from mid-June, when perhaps they thought it was more under control), and the number of positive daily tests, which hasn’t of course risen so much, so that the percentage of positive test results has gradually fallen. The WHO recommends that the percentage of positive tests, the positive percentage rate (PPR), in nations or states where there’s widespread testing, should be under 5% for at least fourteen days before those states can start ‘relaxing’, but I’ve read different, more flexible recommendations elsewhere from health authorities, so it seems still a matter of educated guesswork with an unpredictable pandemic. 

Canto: For the different US states, looking at the figures now in mid-August, the figures are weird. Washington has a PPR of 100% (?!) and are testing 1 in every 10,000, so it seems they’re only testing those they know are positive? That’s top of the list and bottom is North Carolina with a PPR of -13.1, and yes that’s a minus, and they’re testing -.09 in every thousand, and I’ve no idea what that means.

Jacinta: But most states’ figures are clear enough. New York is at 0.8% PPR with over 4 tests per 1000, which is good, but Nevada, Idaho and Florida are at over 16% PPR, each with around 1.5 tests per 1000, and that’s obviously a problem. An indication of the lack of centralised control of the situation – it’s hard to compare data from state to state. Anyway, the key, some say, is to scale the testing to the size of the epidemic in that nation/state, not to the state’s population – but how can you do that when you’re using the testing to determine the size of the epidemic?

Canto: Well presumably if nobody is reporting unusual, covid-like symptoms, as is the case here in South Australia, you don’t need to spend so much time, money and energy on testing. Not the case in the USA. Anyway, in this update, Dr Seheult noted, as we have been, that the case numbers for covid-19 are increasing, but the death rate is decreasing slightly, or at least levelling off. Possibly a result of more testing combined with better treatment. They may also be catching weaker levels of the virus due to measures put in place. But there’s no evidence as yet that the virus itself has become less potent, and this seems unlikely. 

Jacinta: And speaking of treatments, the steroid dexamethasone is apparently reducing mortality by as much as 35% for covid-19 patients on ventilation, according to a WHO preliminary report of work done at Oxford. It’s only good for those with severe hypoxia and associated problems though, but its a cheap, off-patent medication which can be added to the box of tricks for ICUs, once the data is confirmed. 

Canto: Okay, next time….

References

Coronavirus Pandemic Update 83: High Fructose, Vitamin D, & Oxidative Stress in COVID-19

Coronavirus Pandemic Update 86: COVID-19 Testing & Cases Increasing but Daily Deaths Decreasing

https://www.indexmundi.com/facts/indicators/SH.STA.DIAB.ZS/rankings

https://coronavirus.jhu.edu/testing

 

Written by stewart henderson

August 19, 2020 at 1:50 pm

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