I can no longer see the name of Ronald Krauss without immediately thinking “small dense Krauss”.
Bad Peter! Hee Hee.
Actually his whole series of AGE RAGE and ALE posts starting July 2008 are well worth a read.
So is the rest of the blog if you like techy stuff.
Ronald Krauss came up in a couple of other contexts recently so I thought I’d dig up some of his material.
Much of the best stuff is subscription only, but there are several free access papers which I found on PubMed.
This makes his dilemma somewhat clearer: if he is less diffident about some of his results he might lose his reputation, if he’s not positive enough he may lose his funding. Such is the Politics Of Diet.
There’s an interview with him which clarifies his position. IMO nutrigenomics and pharmacogenomics are the way forward: too much medicine uses the wrong kind of statistics, assuming a population is uniform and follows a bell curve when it may well be several genetically distinct sub-populations with sigificantly differing responses to food or drugs.
He co-authors this paper
Pharmacogenomics: Challenges and Opportunities (the pdf is free)
The next step after discovering your specific genes is to discover ways to adjust your environment (diet, drugs, exercise) to control their expression – but I’m getting ahead of myself.
He’s spent much time and effort in deconstructing the “lipid hypothesis” and elucidating the complexity of the systems involved, which go far beyond “eating fat makes you fat/gives you cardiovascular disease”
are a selection of papers covering this subject.
Here’s an important passage from the latter
It has been demonstrated in offspring genetically predisposed to phenotype B that a very low fat, high carbohydrate diet can induce expression of this phenotype. Recently, both genetic and dietary factors have been reported to affect LDL size phenotypes in baboons. Thus, LDL subclass phenotypes may result from interaction of multiple genetic and environmental determinants, and the trait can be viewed as a marker for the mechanism underlying these effects.
is a fairly typical bunch of complacency: one wonders if carbohydrates would have been mentioned at all were it not for the presence of Ronald Krauss on the team.
The L-TAP survey revealed that lipid management was suboptimal for all patients with and without CHD. Although 95% of investigators indicated that they were aware of the NCEP guidelines and believed they followed them, only a small proportion achieved the recommended LDL goals. Lack of achievement is likely caused by failure to titrate medications, inappropriate drug choices, limited effectiveness of some medications, intolerance to some drugs, and failure to address patient noncompliance.
Er, no! Lipid management was suboptimal because the diet chosen did not differ significantly from the diet it replaced. How about them apples?
isn’t this exactly what everyone is told to do, and does – but IT DON’T WORK! Listen to Uncle Ron!
Here he is in a recent paper renovating the reputation of dairy fats and covering the often observed phenomenon that while increased saturated fat intake may (or may not) increase LDL, it also increases HDL and helps reduce triglycerides, thus replacing small dense and oxidisable LDL with decently fluffy particles. I had something of a “Duh!”moment when cheese was found to be more beneficial than milk – well milk is often used as a hypostop due to its carb content, you can’t do that with cheese (or butter)!
Clinical trials in which replacement of saturated fat occurs in the context of reduced total fat and increased carbohydrate have generally not been associated with improvements in CVD is something that passed the other authors of the above AHA paper by, and they didn’t even duck.
One factor he failed to mention was Vitamin K2. Now I go along with some of the Paleo folks in limiting milk (bizarrely I prefer skimmed, but only use it in my coffee) but I have reverted to butter and cheese, partly for this reason and partly because it has rebalanced my HDL and LDL quite nicely.
OK, one last one
He is somewhat diffident about the importance of his results. he’s a bit more gung ho here and the resulting editorial was interesting, but what he really needs is a cheerleader. Step up Jeff Volek (along with Richard Feinman, natch)
A few items I’ve picked up, some old and from other blogs, forums or elsewhere, one or two more recent.
One from Mark Hyman in the Huffington Post
This is quite a good breakdown of the “lipid hypothesis”, though I can’t say I was so impressed with his site which is an irritating mix of good sense and dogma (like most health sites, mine included hahaha)
Richard Feinman has a good go at low fat diets for diabetics
take a whack at some other current dietary myths
Finally the BBC has more bleating from our own UK eejits
I especially liked the line
In April this year, the government launched a programme of health checks for people aged between 40 and 79 who are not already diagnosed with heart disease, diabetes, kidney disease or have had a stroke.
Doesn’t this make it sound like they are looking for Infidels who are not already ill, in order to make them so? Or am I too cynical?
The aptly named Diabetes UK chief executive, Douglas Smallwood, said pre-diabetes was a “ticking timebomb”.
“It’s staggering that seven million people in the UK have pre-diabetes, which is often a precursor to type 2 diabetes, a serious condition which can lead to long-term complications such as heart disease, stroke, kidney failure, amputation and blindness.
“Identifying and educating people with pre-diabetes is vital as it’s not too late for many to make healthy lifestyle changes, reverse the condition completely and reduce their risk of developing type 2 diabetes.”
Now this is completely true, and as thousands of anecdotes and not a few research papers make plain it is also possible to reverse many of the symptoms of Type 2 diabetes itself BUT not by following current dietary policy as listed by DUK, the FSA. etc. etc. which is one of the causal factors in the ongoing “epidemics” of disease.
Recently my PCT has introduced a new restriction: HbA1c tests are now FORBIDDEN to all but registered diabetics. Since they also refuse to prescribe test strips this means prediabetics are deliberately refused the ability to monitor their condition, until they become full-fledged diabetics.
What’s wrong with this picture?
And as if by magic. there’s more today about the obesity “epidemic”
Head, meet desk, recursively
Jimmy Moore just listed my blog, along with a whole bunch of other ones, only some of which I previously knew. There looks to be some excellent resources on there.
I’m already spending so much time reading that I haven’t been doing any writing for a while. Just goes to show how much valuable information is there to be found.
Time to get my ass in gear. I have a few posts I was sitting on until I’ve finished reading some papers. I’ll see if I can finish at least one of them. Well, after I’ve walked to the shops and back and stocked up on meat, fish and veggies.
Today I was supposed to be taking mother to the hospital. The letter cancelling her appointment arrived just before we were due to set off. If the postman had been half an hour later we’d have driven for an hour, wasted our money in the hospital car park and driven back home again for nothing. Plus she may have pooped herself in the car. To say I am annoyed is typical British understatement. Particularly since until recently we have had an excellent relationship with our current doctors ( for a pleasant change from some of the previous incumbents). They have been doing the best they can under circumstances dictated by accountants: I spot yet another manipulation of waiting lists without any patient care actually being provided. Now I have to see if I can keep her alive for another month.
Seen in Pulse Today
“A CQC spokesperson said: ‘We expect providers always to comply with NICE guidelines and other national guidance unless they can show a good reason to vary from them.’
“‘The steps we can take range from a formal warning notice to prosecution and imposition of restrictions, or even closure of a service,’ said the spokesperson.”
The comments from actual doctors, who actually know a bit about medicine, are worth a read.
I saw something like this several years back: my mother, who was then with one of the few remaining NHS dentists in the area, was dragged off to spend half a day sitting in a Portakabin in a car park waiting to have her teeth examined.
My highly competent dentist had been determined to keep NHS provision as long as possible, and at one stage had so many extra patients he took on a new partner just to cope with the workload. However even he had to admit defeat following further changes in the NHS regime.
His opinion on what happened to mother (and obviously many other patients since this appeared to be a big ongoing operation) was that all NHS patients were being checked to ensure their NHS dentists were only complying with NHS treatments – by then mostly restricted to amalgam fillings and extractions – and NOT providing improved levels of treatment such as non-amalgam fillings, which may be initially more expensive but last a lot longer so are much more cost effective in the long term.
This “money saving” exercise would have cost for the ongoing rental of the Portakabin, rental for the land on which it stood, and salary of a dentist who was not actually providing ANY treatment at all, merely looking for faults with the treatment of real dentists.
I suspect with doctors they can do without some of these expenses merely by data mining: that could be done by a non-medically-trained clerk or three.
“You have diabetics with an A1c below 6? You will be sent for regrooving!”
“Your patients aren’t having enough heart attacks, clearly you are guilty of prescribing a low carb diet!”
etc. etc . . .
Here’s yet another nail in the coffin (literally) of good diabetic control
Michael Eades has a new book out.
Personally I’m putting it on my “might buy later” list. On the one hand I don’t tend to gain weight easily. On the other hand, when I do it always goes on around the middle. Last year I ploughed virtuously through the holiday season without putting on a pound – then suddenly gained some weight around January/February, and dropped it about as fast as I’d put it on.
If you’re more prone to doing this it might prove to be a good read.
Meanwhile he was interviewed on Tim Ferriss’ blog
which led to a fair bit of conflict
The best thing that came out of that thread IMO was a link to the transcript of an old BBC Horizon programme about the Atkins diet
Here you can see the epiphany of Eric Westman, one of the current leading researchers in nutrition and metabolism, and Gary Foster. Mary Vernon also makes an appearance.
As the transcript reveals, both Westman and Foster were initially cynical but had the cojones to actually run trials AND believe their results. The result, as they say, is history: Duke University is one of the leading centres for 21st Century dietary research.
I wonder if the BBC would be permitted to make such a controversial programme today?
To close down a blog near to you.
As if this wasn’t disconcerting enough
now comes this
Colour me cynical about “psychiatric” explanations for eating disorders, and many other disorders. I have (or perhaps I should say “had” because knowledge has advanced hugely) a degree in Psychology. In my day everything was “nurture” rather than “nature”, so I guess many people who have reached the top of the profession were similarly trained. This appeared to make little sense even then, I saw not a few babies pop out with many behavioural characteristics seemingly hardwired in, and things like twin studies where the twins were separated at birth and brought up differently have shown some purely freaky patterns.
So I incline to the belief that there may well be physiological reasons for some (probably not all) “eating disorders” which need to be looked into first. The metabolic pathway from food to ATP at the mitochondria is hugely complex and there are plenty of steps where things can go pear shaped.
The current standard dietary advice seems to be making more than a few of these metabolic steps go pear shaped in a large proportion of the population. “Eating disorders” seem to be increasing in parallel to many of the other “diseases of civilisation”.
From a purely psychiatric point of view, NOT following conventional advice becomes a “disorder” in itself, despite that it is worsening health in general: having beliefs or behaviours that differ from those of your social contemporaries can be seen as a personality disorder (completely ignoring the fact that they may be perfectly conventional views in a different society elsewhere in the world, or may actually genuinely be better than those of Conventional Wisdom).
I’d like to see a psychiatric explanation for giving diabetics a diet guaranteed to worsen their condition. Same for the obese, cardiovascular patients, etc. etc.
I like synchronicity: having just read that BBC story I then read Stephan’s blog
I previously had a theory that the dogmatic and often aggressive approach of high carbers in imposing their dietary choices on others and disrupting discussion of alternatives was a function of the high carb load in itself. Now I wonder if it’s the Omega 6 consumption that sets them off. The following series of posts on Omega 6 and Omega 3 are fascinating, rebalancing the ratio and adding more Omega 3s to a level which we (probably) evolved to handle rather than the totally unbalanced quantities of the Heart Healthy Diet has positive effects on not a few “mental” illneses along with the “physical” ones.
Next time your dietician tries to kill you, smile and offer her some fish.
You think she’s NOT trying to kill you? These were my original lipids
HDL 0.63 (24.6) LDL 4.22 (165) trigs 4.29 (380)
This what was happened when I followed a high carb low fat diet
HDL 0.66 (25) LDL 5.16 (201) trigs 3.70 (328)
Here they are after doing the opposite of what I was told
HDL 1.40 (55) LDL 2.40 (94) trigs 0.70 (62)
If you recalculate that LDL according to the Iranian Formula it drops to 1.97 (76) which brings me perilously close to William Davis’ 60 – 60 – 60.
Admittedly I am taking 10mg Simvastatin to achieve that.
Stephan posted his own numbers which are quite astonishing – but the pattern of improvement is not at all uncommon.
I learned how to do this from people on newsgroups, forums and blogs, which is why I’m here passing on what I’ve learned and links to the original sources.
Make the most of it before such blogs also fall prey to the Food Police and Conventional Wisdom and we are no longer permitted access to other than Official Sources.
My sort-of long term theory is that we carry a lot of genes which evolved to be used in emergencies, when they are adaptive. However environmental conditions now exist which switch on these genes and leave them chronically active. Not everyone in the population carries the same gene set, so the same environmental insult may have different effects on different individuals. The fact that certain families have lines and clusters of some but not other diseases is not uncommon.
Most of the evidence relates to insulin resistance, and leptin/resistance, which are connected to Metabolic Syndrome and Type 2.
Jenny just came up with something linking wheat to Type 1.
Until now my theory has been that wheat itself has been bred to be more toxic, maybe as a result of increasing disease resistance.
Her point on Soy is well made. I will assume the same process has occurred and that soy has also been bred to be more disease-resistant as it has become a major western crop (in the US not the UK, also in South America). As far as I know most current soy is GM, and one of its major markets apart from human food is animal fodder, so it’s very plausible that even if you avoid soy you will be hit by its lectins in the tissue of intensively fed animals. It’s imported into the UK in quantity.
Some research shows that there may be synergystic effects between environmental contaminants, like pesticides, which have only been tested singly and found to be “safe”. This makes me wonder whether there may be similar synergystic effects between soy lectins and wheat lectins.
The connection to Type 1 (and possibly other autoimmune diseases) is interesting: while Type 2 is far more prevalent than Type 1 (and even more so if you start to count “diabetes” from when glucose control starts to go downhill rather than waiting until pancreatic destruction has reached the point of no return), the actual rate of increase of Type 1 is faster.
Some authorities have tried to suggest that the two diseases are in fact one, but this doesn’t really fly. As far as I remember (I’d need to dig out the papers) while some of the inflammatory cytokines which carry off the beta cells are common, like TNF-alpha and Interleukin-6, which are both factors in most types of inflammation, other cytokines differ significantly.
However it makes sense that there may be a common factor behind the increases of autoimmune conditions, allergic conditions including asthma, and other diseases where inflammatory attack is part of the process, since all of these “diseases of civilisation” show recent increases in incidence.
It probably makes even more sense that there are a bunch of common factors interracting.
No I’m not going to let the wheat off the hook, in fact I may charge it and the soy with conspiracy.
There’s a theory that Type 2 is a two-strike disease, and an argument as to which comes first, the insulin resistance or the loss of pancreatic insulin output, both of which appear to be necessary. (Although breakdowns in the control circuit may have a similar effect to loss of beta cells in certain forms where the insulin could be produced but isn’t, or where insulin is produced but fails to shut down the glucagon output from the pancreatic alpha cells.) There are a whole bunch of feedback and feedforward loops involved, such that the worsening of one side of the equation worsens the other.
The classic view of Type 2 put forward by most of the meeja and all too many Medical Professionals and even some Type 1s is that it is a disease of fat lazy old people caused by the obesity.
That doesn’t even come close.
There’s a strong genetic predisposition, which has led to the theory of the Thrifty Gene: this makes evolutionary sense in that people with a predisposition to turn a temporary excess of food rapidly into fat can then live off it through the ensuing famine and outsurvive “normies”, whereas this becomes maladaptive in a world of continous feasts.
This has been parallelled with hibernatory species who feed themselves up, go torpid and live off the stored fat until food once more becomes available. Seasonal Affective Disorder, anyone?
It follows that the ability to switch insulin resistance on and then off again when required may well be what evolved originally.
Now one thing that switches insulin resistance off in humans is exercise. Growing more muscle increases glucose disposition simply because more muscle contains more GLUT-4 receptors. Actually using the muscle translocates these glucose transporters to the cell surfaces ready to grab glucose when necessary.
I have a paper by Colin Bibby on Sedge Warbler Migration but annoyingly only the first page now seems to be available FOC.
Sedge Warblers are sparrow-sized birds that breed in the UK and Northern Europe, then migrate across the Sahara to winter in subsaharan Africa.
In order to make this journey they double their body weight. They are insectivorous. Many birds which are adapted to seed eating feed their young on insects – the high protein high fat low carb diet grows the nestlings more rapidly.
Now what’s interesting about these warblers is that they stuff their faces with insects to put on all the fat they use as fuel for the migration – BUT they eat high carb insects – Plum Reed Aphids which are little bags of concentrated plant sap full of sugars. Some other insectivorous birds will eat berries prior to migration probably for the same reason – they need to put on body fat quickly and carbs are the fastest way.
Here’s my belief: they can switch on insulin resistance at will which enables them to rapidly stash carbs as body fat, driven by the ensuing high insulin levels, exactly as happens with humans. Then when they start their journey they are able to switch the IR off again and use the fat as fuel, in exactly the same way that many endurance athletes have discovered.
Next time researchers start their tinkering with genetically modified mice or rats, maybe they should consider Sedge Warblers instead?
Mark Sisson (whose blog I have been missing out on while I read other stuff, quite inexcusable really, but he and his contributors are so damn prolific) had a whinge about Conventional Wisdom not once but twice.
Dead on cue, when I logged in earlier I had a notification of a couple of blog posts that might be related.
Pretty damn good stuff! (And look at the dates)
Mary Vernon’s blog no longer seems to be there but here she is interviewed by Jimmy Moore.
The first of these two items contains a very valuable shortlist of relevant papers, the second is yet another boring old success story similar to all those thousands of boring old success stories I’ve been reading for years on many different diabetes (and other) forums and blogs.
JUST ONCE I’d like to read a story where someone cut their carbs and all (or even one) of the dire predictions their Health Care Professionals made actually came true.
If you’re not totally bored yet here’s a thread from the ADA Forum which is the sort of “not evidence” you might expect the world’s leading diabetes charity to want to study forthwith
(taps fingers impatiently)
Anyway, gotta go, I now have a couple more blogs and a few more papers to plough through . . .
The internet is full of scams (you noticed huh???) all too often you see some link to a Revolutionary Diabetes (or insert favourite disease) cure. Usually you are exhorted to send money for either a poorly written book containing information cut and pasted from some allegedly “official” site, or a poorly spelled rewrite of same, or some miracle cure pills which may well contain crap but may equally well contain genuinely useful supplements (that’s if your diet is deficient in them) which could however be purchased much more cheaply as generics elsewhere.
Try this for example (hint: you need to click on any of the links to get the point)
OK, this one might just work though.
 look at current farm gate prices
 check the number of adverts for xxx low fat product on TV
 buy shares
 take the profit and spend it in your local greengrocer, butcher, fish shop or farmers’ market
 eat the results