This is more of a Facebook link than a blog post, but hats off to the BMJ as they have recently published some excellent articles in which neat truth appears to be very controversial (if you pedal b*ll*cks for a living).
Now they have published Dr Ravnskov's response to Ebrahim's pro statin for primary prevention paper. It's a nice reply and it's great to see a medical journal giving a voice to sanity. Of course, hats off to Dr R for being that voice.
You can read the letter here.
Peter
Uffe Ravnskov said
ReplyDelete"The reason why statin treatment may result in cancer is probably not an effect of the drug, but that low cholesterol predisposes to cancer."
Are there any studies which show that vegetarians/vegans have a higher incidence of cancer than the general population?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3261846/
ReplyDeleteLack of Effect of Lowering LDL Cholesterol on Cancer: Meta-Analysis of Individual Data from 175,000 People in 27 Randomised Trials of Statin Therapy
Conclusions
In 27 randomised trials, a median of five years of statin therapy had no effect on the incidence of, or mortality from, any type of cancer (or the aggregate of all cancer).
Type of statin
In the 22 trials that compared statin therapy versus control, rate ratios for cancer incidence and death from cancer were similar irrespective of type of statin (Figures S9 and S10). In particular, there was no evidence that rate ratios differed between statins that are hydrophilic (pravastatin and rosuvastatin: cancer incidence RR 1.02 [95% CI 0.96 to 1.08]; cancer mortality RR 0.99 [95% CI 0.89 to 1.09]) and statins that are mostly lipophilic (atorvastatin, fluvastatin, lovastatin, simvastatin: cancer incidence RR 0.98 [95% CI 0.92 to 1.05]; cancer mortality RR 1.01 [95% CI 0.91 to 1.13]).
The present report now demonstrates clearly that such reductions in LDL cholesterol do not increase the rate of cancer or cancer death, overall or at any particular site, during a treatment period of about 5 years (and more prolonged follow-up in some of the trials does not indicate any later excess) even among older individuals or those who have their cholesterol levels reduced to very low levels. These findings provide considerable reassurance about the safety of using more intensive statin regimens to lower LDL cholesterol levels substantially in patients who remain at high risk of major vascular events.
@Charles
ReplyDeletePlenty of sources to sift through here that might be relevant:
http://healthydietsandscience.blogspot.com/search?q=cancer
@Ash
ReplyDeleteCare to comment on my study and care to answer my question re cancer and vegetarians/vegans.
As to your studies - are we going to play the game of I show you a study and you show me your study
What will that prove
http://onlinelibrary.wiley.com/doi/10.1002/ijc.24668/full
ReplyDeleteSerum cholesterol levels in relation to the incidence of cancer: The JPHC study cohorts
We observed no association between cholesterol levels and the incidence of total cancer, and major-site cancers except for liver and stomach cancer which had a strong inverse association in the large population-based prospective cohort study of middle-aged Japanese men and women. The inverse association for stomach cancer diminished substantially after exclusion of the early 3-year incident cases and advanced cases, but that for liver cancer remained.
The strong and sustained inverse association for liver cancer, which was consistent with a previous finding of Japanese mortality study,33 needs other interpretations. First, since liver is the only organ to produce cholesterol, liver cancer, even when limited in this organ, is usually accompanied by liver cirrhosis, and may have lowered serum cholesterol levels34 before the “incidence” in clinical and epidemiological studies. Drinking habits, however, did not modify the association between cholesterol levels and risk of liver cancer in this study. Second, ∼80% cases of liver cancer were proceeded by the infection of hepatitis C virus,28 commonly genotype 1b virus, which lowered serum cholesterol levels substantially.29 However, the possibility that the inverse association was confounded by the hepatitis C virus infection may be small because we found a similar inverse association regardless of the infection. It is also possible that the infection of hepatitis C virus was enhanced by low serum cholesterol levels probably because the virus enter liver cells less competitively through low-density lipoprotein (LDL) receptor35 and/or oxidized LDL scavenger receptor.36
No association between total cholesterol levels and risk of colorectal cancer for either sex in general populations is noteworthy.
In summary, low total cholesterol levels were not associated with the incidence of total cancer, and major-site cancers except for liver and stomach cancers. After exclusion of the early incident cases and advanced cases, the inverse association diminished for stomach cancer, but remained for liver cancer for persons with or without hepatitis C virus antibody. These findings did not support that low serum total cholesterol levels increase the risk of total cancer, colorectal cancer or other major sites of cancers except for liver cancer. The robust inverse association between total cholesterol levels and risk of liver cancer, regardless of incident time, stage, virus infection and drinking habits remained to be examined in further studies.
@Ash
ReplyDeletehttp://healthydietsandscience.blogspot.com/2012/06/low-cholesterol-levels-increase-risk-of.html
http://www.ncbi.nlm.nih.gov/pubmed/7783302
Serum total cholesterol and mortality. Confounding factors and risk modification in Japanese-American men
In our study, TC level was not associated with increased cancer or all-cause mortality in the absence of smoking, high alcohol consumption, and hypertension.
BUT you said
The results of the study show that middle-aged men with low cholesterol are at greater risk of death from stroke, cancer and all-causes compared to men with higher cholesterol.
THAT IS NOT TRUE!! SO - You Lie
I saw many time information about the connection between low cholesterol and weaker immunity.I was interested in it because I was trying to find some explanations beyond anecdotal evidence and common sense to that phenomenon which many LCarbers reported improved resistance to infections . I could try to locate all that again if somebody is interested.
ReplyDeleteCharles, do you think that the information about the improvement in a general immunity would satisfy somehow your criteria?
I don't know why Dr Ravnskov choose to write mostly about a cancer as a possible complication from statines in the article, may be because he was reading about such research recently, and everybody knows about other statines complications already (muscle pain, neuromuscular problems,depression, memory problems,and the rest ). Possible complications are well known, but considered to be not very important somehow, while getting a statine complication may be way worse than developing some cardiovascular condition with age. My periodontist recently had to retire early because couple years ago he took a statine for several months, developed some leg weakness, stopped statines, but in while his hands began to shake, the biopsy was made, and it was found statines damaged his hand muscles. End of his working history, he is doing a paperwork to get a disability.
Yeah, Ash...or David or whatever your name is...stop lying, you lying liar.
ReplyDeleteUh, Charles - quit being a self-righteous (and completely wrong) dick.
ReplyDeleteYou asked if there's any studies - I posted a link to a SEARCH on a site that I know has HUNDREDS of studies listed all about cholesterol and such malarkey which I have zero affiliation with, and I suggested you check the source materials as you might find something relevant.
But I guess that's too difficult, you'd rather just accuse me of writing lies like a pompous trigger-happy ass who sounds like they're probably low in cholesterol.
Charles is on statine, he said so during his discussion with Dr.Eades,it is the reason he sounds like he is low in cholesterol.
ReplyDelete@Ash
ReplyDeleteWhat about this is a lie?
http://healthydietsandscience.blogspot.com/2012/06/low-cholesterol-levels-increase-risk-of.html
http://www.ncbi.nlm.nih.gov/pubmed/7783302
Serum total cholesterol and mortality. Confounding factors and risk modification in Japanese-American men
you said
The results of the study show that middle-aged men with low cholesterol are at greater risk of death from stroke, cancer and all-causes compared to men with higher cholesterol.
The study said
In our study, TC level was not associated with increased cancer or all-cause mortality in the absence of smoking, high alcohol consumption, and hypertension.
Do you really think I have the time to go thru EVERY link you post to see if there are any more lies?
Serova said...
ReplyDeleteCharles is on statine, he said so during his discussion with Dr.Eades,it is the reason he sounds like he is low in cholesterol.
I take 10mgs Atorvastatin/day due to the fact that I have some SNPS which predispose me to higher cholesterol
When I was doing LC/Paleo my lipid panel became a cause for concern
Blood draw 3/12
Lipids (VAP Test)
Total Cholesterol - 324
HDL Cholesterol - 84
LDL Cholesterol (Calculated) - 230
Iranian LDL Cholesterol Calculation - 186
Triglycerides - 54
Triglycerides/HDL ratio - .64
Pattern size - A - large and bouyant
Sub Class infomation
HDL-2 (Large, Bouyant; most protective) - 31 Ref range >10 mg/dL
HDL-3 (Small, dense; least protective) - 54 Ref range >30 mg/dL
Blood draw 10/12
LDL-P 1430
Small LDL-P 132
LDL-C (Calculated) 199
TC - 274
HDL-C 69
Triglycerides 31
Trig/HDH ratio - .45
http://www.lecturepad.org/dayspring/lipidaholics/pdf/LipidaholicsCase291.pdf
Let’s get rid of the nonsense seen all over the internet that atherosclerosis is an inflammatory disease, not a cholesterol disease. That is baloney-with the reality being that it is both. One cannot have atherosclerosis without sterols, predominantly cholesterol being in the artery wall: No cholesterol in arteries – no atherosclerosis. Plenty of folks have no systemic vascular inflammation and have atherosclerotic plaque. However clinicians have no test that measures cholesterol within the plaque – it is measured in the plasma. It is assumed, that if total or LDL-C or non-HDL-C levels are elevated the odds are good that some of that cholesterol will find its way into the arteries, and for sure there, are many studies correlating those measurements with CHD risk. Yet, we have lots of patients with very low TC and LDL-C who get horrific atherosclerosis. We now recognize that the cholesterol usually gains arterial entry as a passenger inside of an apoB-containing lipoprotein (the vast majority of which are LDLs) and the primary factor driving LDL entry into the artery is particle number (LDL-P), not particle cholesterol content (LDL-C). Because the core lipid content of each and every LDL differs (how many cholesterol molecules it traffics) it takes different numbers of LDLs to traffic a given number of cholesterol molecules: the more depleted an LDL is of cholesterol, the more particles (LDL-P) it will take to carry a given cholesterol mass (LDL-C). The usual causes of cholesterol depleted particles are that the particles are small or they are TG-rich and thus have less room to carry cholesterol molecules. Who has small LDLs or TG-rich LDL's? – insulin resistant patients! After particle number endothelial integrity is certainly related to atherogenic particle entry: inflamed endothelia have inter-cellular gaps and express receptors that facilitate apoB-particle entry. So the worse scenario is to have both high apoB and an inflamed dysfunctional endothelium. Is it better to have no inflammation in the endothelium – of course! But make no mistake the driving force of atherogenesis is entry of apoB particles and that force is driven primarily by particle number not arterial wall inflammation
http://circ.ahajournals.org/content/116/16/1832.full.pdf
SO - started low dose statin+ CoQ10+other supplements
blood test results - 10/18/13
TC 126
LDL 71
ApoB 64
HDL 48
TG 36
non-HDL 79
Vitamin D3 - 46 with normal 30-100
ya gotta tend to your gut garden:
ReplyDeletehttp://www.ncbi.nlm.nih.gov/pubmed/23656565
http://www.sciencedaily.com/releases/2012/01/120112193440.htm
Probably most relevant are the WHO mortality figures (164 countries, 2002 mortality figures).
ReplyDeleteOne place to find the graph (courtesy of Ricardo Carvalho) is here:
http://syontix.com/part-five-cholesterol-leaky-gut-endotoxemia-and-heart-disease/
It is very easy to see relationship of the curve for noncommunicable diseases, with increased mortality for low (below 190) and high (230+) TC.
It is less easy to read the line for II.A (malignant neoplasms), but it you squint carefull along the bottom of the chart, you will see that there is a significant and progressiveincrease in mortality when TC is below 190 and this time, there is no matching upward curve for high TC.
The whole chart is extremely interesting and should be compulsory reading for all doctors!
How reasonable is it to choose the chance of neiromascular damage over the chance to get an atherosclerosis? What is more detrimental to the quality of life? When an immediate illness is treated with a side-effect causing drug, it is easer to justify the treatment, than when we are talking about lowering the chances of some condition in a future.
ReplyDelete@Galina
ReplyDeleteName a drug that doesn't have side effects?
This comment has been removed by the author.
ReplyDeleteI can name a drug that has only side effects and no main effect, because even its meager "positive" effect doesn't come from the mechanism it is prescribed for (cholesterole lowering):
ReplyDeleteStatins.
Charles,
ReplyDeleteIt was my point - you choose to take a drag with know list of very undesirable side-effects.
After seeing Peter approving of the potato sack comment you'd think someone would get the hint.
ReplyDelete“Effect of different antilipidemic agents and diet on mortality: a systematic review.”
ReplyDeleteFish oil more effective in reducing cardiac events AND all cause mortality without the nasty side effects of statins.
Charles Grashow said:
ReplyDelete"However clinicians have no test that measures cholesterol within the plaque – it is measured in the plasma."
Clinicians may not have such a test… but pathologists have!
And the preponderant component of arterial plaque is not cholesterol of any sort, but polyunsaturated fatty acids, principally omega-6, as foisted on us because of their supposedly "healthy" properties.
See C.V. Felton PhD, D. Crook PhD, M.J. Davies MRCP, M.F. Oliver FRCP, “Dietary polyunsaturated fatty acids and composition of human aortic plaques”. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(94)90511-8/abstract
@Growup
ReplyDeleteAn abstract is useless
John Velden said...
“Effect of different antilipidemic agents and diet on mortality: a systematic review.”
http://www.ncbi.nlm.nih.gov/pubmed/15824290
CONCLUSIONS:
Statins and n-3 fatty acids are the most favorable lipid-lowering interventions with reduced risks of overall and cardiac mortality. Any potential reduction in cardiac mortality from fibrates is offset by an increased risk of death from noncardiovascular causes.
Fibrates prescribed commonly are:
Bezafibrate (e.g. Bezalip)
Ciprofibrate (e.g. Modalim)
Clofibrate (largely obsolete due to side-effect profile, e.g. gallstones)
Gemfibrozil (e.g. Lopid)
Fenofibrate (e.g. TriCor)
A fibrate is NOT a statin!!
Charles,
ReplyDeleteYou quoted Dayspring above. The same statement from Dayspring also includes this:
"Could the low carb crowd be outliers and in them we can ignore LDL-C and LDL-P? The advocates of
those diets say there is no study showing harm of elevated LDL-P and LDL-C in patients
who have eliminated or drastically reduced their insulin resistance and inflammatory
markers by low carbing. That is true but what they want to ignore is that there is no data
anywhere that shows they are an exception. Their belief is that by reducing all other
atherosclerotic risk factors and normalizing their arterial wall and endothelial biology
that, apoB-containing lipoproteins like LDL cannot enter the arterial wall. Although
LDL-C and LDL-P in plasma are high none of the cholesterol content of the apoB particles gains entry into the arterial wall. Is that plausible???? Sure! But is that also erroneo us or wishful thinking? Sure?"
Dayspring acknowledges the dilemma. There aren't enough low-carbers studied over a long-enough period of time to draw any clear conclusion about the risks of high LDL-C and -P, regardless of particle size, under low-carb conditions. Since LCHF dieting is actively discouraged by mainstream medicine, it's a little hard to see how we get to empirical evidence.
There is empirical evidence HbA1C is an independent (and better) predictor of heart disease risk than LDL levels. See http://high-fat-nutrition.blogspot.com/search/label/Cholesterol%20within%20nations%20studies.
Some of us throw our lot in with statins. Others with LCHF. Only time will tell which was the better decision.
-- Bob
@Charles Grashow
ReplyDeleteFrom the paper we have, omega 3 showing higher effectiveness for both cardiac mortality and overall mortality than statins.
I was not comparing to Fibrates which are worse than both statins and omega 3.
Statins do have common notable side effects, certainly less benign than omega 3 fatty acid consumption.
This comment has been removed by the author.
ReplyDelete@Charles
ReplyDeleteI have the full. The general take away is the following: The significant association between the content of 20:4omerga6 in plaques and the content in serum may reflect vessel-wall catabolism of 18:2omega6.
The conclusion: However, the findings in our small group support the hypothesis that dietary omega6 and omega3 polyunsaturated fatty acids significantly influence the composition of human aortic plaques, suggesting that the protective effect of increased intake of polyunsaturated acids towards coronary heart disease may have been overstated.
Some key points: all kinds of fats were found in plaque (cholesterol was not assessed). Surprisingly and not surprisingly, MUFAs were greatest (they are also the greatest in the diet), followed by omega 6 and saturated fat, with omega 3 lagging behind.
But, when you look at the ratio of what ends up in plaque compared to what's in serum, omega 6s (20:2o6 and 20:4o6) seem to preferentially be selected for.
The article surmises that it is the susceptibility of these fractions to oxidation that may be responsible for their atherogenicity (via LDL oxidation).
My takeaway: as early as 1994 folks knew that the government’s heart healthy omega 6 campaign was bullshit.
@Michael, look on the bright side. Where else would you find a statin-taking-vegan trying to save the world one LC blog at a time? I couldn’t make stuff up as funny as Charles.
ReplyDeletePeter
@ Charles, if you only look at the abstracts on David Evan's links at Healthy Diets and Science, you might think they contradict his precis.
ReplyDeleteBut if you read the full-text articles you can see his summaries are accurate. He may be cherry-picking results that suit the "good cholesterol" hypothesis, but if the "bad cholesterol" hypothesis were true he would not be able to find hundreds of studies to pick cherries from, would he?
How many studies are there that seem to show cigarettes prevent cancer? Not many, if any. Once a true hypothesis is defined reasonably correctly it becomes hard to cherry-pick evidence to the contrary. Certainly not to the tune of hundreds of studies.
I think it is totally bizarre to compare side-effects of a drag which disrupts how a human body works in order to try to micro-manage a complex body system in attempt to change just a marker of metabolic health, and the chance of getting atherosclerosis even while living a healthy life-style. It is the fundamentally flawed approach toward health management. How many trails failed when prefect health markers like blood sugar and blood pressure were managed pharmacologically?
ReplyDeleteCharles:
ReplyDeleteYou are so strident and combative about your health choices. What about the effects of emotions and personal interactions on heart disease and health in general? Being pissed-off at people who have chosen a different diet or approach to health seems like such a waste of your time. Do you think you are going to change anyone's perspective here? Get outdoors with like-minded souls and enjoy yourself! Or, write a book about your experience.
Hi Peter,
ReplyDeleteTaken from Chris Kresser's article downplaying the harmfulness of fructose (http://chriskresser.com/ask-chris-is-fructose-really-that-bad):
"The bulk of the evidence suggests that lactate is an important intermediary in numerous metabolic processes, a particularly mobile fuel for aerobic metabolism, and perhaps a mediator of redox state among various compartments both within and between cells… Lactate can no longer be considered the usual suspect for metabolic ‘crimes’, but is instead a central player in cellular, regional and whole body metabolism."
What say you?
I ask because I was reading Stephanie Seneff's paper (http://people.csail.mit.edu/seneff/AMS.pdf) which argues that fructose (in humans) converts substantially to fat - Kresser argues the opposite with isotope studies in humans.
Lactate can open the door to heaven or hell depending upon the cells redox state. That is controlled by the charge separation of water into negative -OH groups and protons. Al the studies that Kresser talks about never control for this.....making his beliefs based upon faulty experiments. He is right to point out that what we all were taught about lactate is wrong. It is tied to the cellular terroir.
ReplyDeleteraphi,
ReplyDeleteAs far as I can see the role of fructose is the generation of glycogen in the liver. Penetration past the liver to the systemic circulation obviously happens if the uptake from the gut exceeds the liver’s ability to convert it to glycogen, and in excess, to fat.
This is the liver’s job. A giant orange juice will overwhelm the liver and we then have systemic fructose which can enter energy replete cells without the break of limited GLUT4s. The fructose specific GLUT5s are not acutely controlled by insulin so allow caloric overload. Insulin resistance increases to limit glucose derived calories to compensate for the mass of fructose.
Interstingly uric acid is essential to this process, I have a paper somewhere showing allopurinol blocks metabolic syndrome by stopping the formation of uric acid. Uric acid is a powerful antioxidant and you would expect it to wipe out the nano molar pulse of superoxide/H2O2 which triggers insulin signalling.
Of course uric acid is another devil incarnate which, from the above, is utterly essential. Oddly enough it is associated with metabolic syndrome AND longevity. It’s a coping mechanism. Getting rid of it does not strike me as a Good Idea.
People with metabolic syndrome will automatically generate a systemic lactate spike after bulk liquid fructose as you would expect.
I agree lactate is central to may crucial processes. Neurons appear to run on lactate, generated by glial cells. Glial cells take all the metabolic hits from glycolysis and feed “clean” lactate to neurons for which it is a one step conversion to pyruvate and the TCA. No glycerol 3 phosphate, no reverse electron flow, no superoxide so long as glucose never goes above some arbitrary but low number. Of course the lactate here is under strict control and comes from glucose.
It would be insanity to allow Fanta to control lactate production.
Fruit seems ok if you must, extracted juice is bottled diabetes. Stan has that great ref to fruit juice and associated diabetes. Causation seems likely to me.
BTW, LC high saturated fat is a starvation mimetic. I’m circumspect about fruit. Some seems OK for recreational purposes, very occasionally. On a mixed paleo diet it’s probably OK, but I don’t go there.
Peter
Hey Peter,
ReplyDeleteWhat you said here: “People with metabolic syndrome will automatically generate a systemic lactate spike after bulk liquid fructose as you would expect.”
Made me think of Stephanie Seneff’s hypothesis (http://www.ncbi.nlm.nih.gov/pubmed/21402242) regarding the possible role of ABeta plaques in Alzheimer’s Disease not necessarily as causative agents initially, but more like stop-gap, ‘alternative buffer’ type measures —>
“An interesting theory regarding lactate proposes that astrocytes
shuttle lactate to neurons during periods of intense activity, to supply an alternative fuel source to glucose [8]. Indeed, lactate is inter- changeable with glucose to support oxidative metabolism in cortical neurons [76]. Under this hypothesis, astrocytes convert pyruvate to lactate (utilizing lactate dehydrogenase) and shuttle the lactate to neurons, which could generate ATP from it, thus further reducing their dependency on glucose metabolism in the mitochondria. This would result in reduced exposure to glucose in the neuron, thus decreasing susceptibility to glycation damage. Lactate supply directly from the blood serum is not an option for neurons due to the BBB.”
The seemingly contradictory correlations acting as coping mechanisms you mentioned here: “Oddly enough [uric acid] is associated with metabolic syndrome AND longevity. It’s a coping mechanism” —> seem conceptually similar to the role of ABeta plaques she proposes.
I’m getting through all her papers and whether or not she ends up vindicated (as to the fundamental cause of Mets) to any meaningful extent, her ideas are quite beautiful nonetheless [IMHO].
@Jack Kruse
ReplyDeleteHow should they control for this in your opinion?
raphi, this is probably close to what happens. I look at glucose as being benign at 4.3mmol/l. At 20mmol/l it will generate insulin resistance through mtG3Pdh on the mitochondrial surface. While it is possible to convert lactate to G3P I very much doubt that neurons will do this (not sure anyone has checked). This (hyperglycaemia) will induce the insulin resistance of caloric overload and, if extreme, will trash complex I initially and probably the mtDNA for critical complex I subunits for more long term damage.
ReplyDeleteTo me, hyperglycaemia is probably all you need. Some degree of insulin resistance (sucrose) and a rapid access refined source of bulk glucose (flour) would fit the bill.
Outside the brain you can limit the extent of hyperglycaemia from glucose using PUFA as your fat to limit ETFdh based FADH2, so limit reverse electron flow through complex I. If this limits post prandial hyperglycaemia the brain will last longer. The cost is, of course, maintained peripheral sensitivity to insulin in the face of hyperinsulinaemia. Both adipocyte hypertrophy and adipose tissue hyperplasia should follow. With unrestricted caloric entrance to cells they will accumulate triglyceride and/or divide. So you could hypothesis that bulk PUFA (to all peripheral tissues) should give obesity and cancer with some improved insulin sensitivity… No surprises there then.
The situation under conditions of very, very low fat intake are interesting too. It’s hard to induce insulin resistance in lab rats using sucrose, provided fat is held close to zero… But no one in their right mind would try this on a human IRL. Fat elimination from your diet is a neurobehavioral illness per se.
I keep thinking that the two transportable food commodities before refrigeration where sugar and flour… All human diets carry some fat, you don’t need to add that…
Peter
Yes indeed, sugar and flour. White sugar and white flour. They will trash your beta cells so you get hyperglycaemia, and your brain so you get Alzheimer's. I suspect the drug companies know this. They aren't looking for an Alzheimer cure any more, having produced various drugs at vast expense which either didn't work or made the patients worse.
ReplyDeletehttp://www.independent.co.uk/life-style/health-and-families/health-news/drug-giants-give-up-on-alzheimers-cure-8153606.html
It looks like plaques are harmless as raphi suggests, and tangles are the problem. Tangles block intracellular transport. Autophagy fails because damaged stuff can't get to lysosomes for breakdown. The brain people are getting very excited about this.
There shouldn't be any tangles if an enzyme called phosphatase-2A is working properly. It's a manganese enzyme. Hahaha. White flour has very little manganese and white sugar has none at all. I wonder when the drug companies will be telling us about this.
@Jane
ReplyDelete"Yes indeed, sugar and flour. White sugar and white flour"
Your being cheeky: the implication behind what you're saying here (and in the posts above) is that the manganese in those non-white sugars & flours negates the other harmful effects.
Why not get manganese from other things than sugar or flour? Can you really build a convincing argument for such a dietary approach? (don't waste your time, you'd be chasing rainbows)
[Karl Popper] “the method of science as the method of bold conjectures and ingenious and severe attempts to refute them.” ---> you're not even attempting this (as far as I can tell from what you're saying in the comments)
Hi raphi
ReplyDeleteYou think I'm cheeky? Well Peter is quite cheeky too so I don't expect he minds. Especially since I did exactly the same thing to his arch enemy.
Yes of course I think the minerals and other things in whole grains negate the harmful effects. Minerals are there for a reason. When the grain germinates they activate enzymes of carbohydrate metabolism. Eat the carbohydrate without them and it becomes toxic.
And of course you don't need to get your manganese from sugar or flour. Paleolithic people ate legumes! Legumes have lots of manganese and lots of phytic acid to inhibit iron absorption. There's really nothing better to eat with your red meat. Chili con carne, yum.
Mousterian vegetal food in Kebara Cave, Mt Carmel
http://www.sciencedirect.com/science/article/pii/S0305440304001694#
'This paper reconstructs the vegetal diet of the Middle Paleolithic humans in Kebara cave (Mt. Carmel, Israel) on the basis of a large collection of charred seeds and other vegetal food remains uncovered during the excavations. ... almost all plant remains (3313 seeds, 78.8% of total charred remains) belong to the legume family ... we assume that the main source of energy in the diet of the Kebara inhabitants was the legumes ...'
@Jane
ReplyDeleteYour first remarks are too irrelvant and silly to address.
You realise phytic acid inhibits other nutrients than iron, right?
Also, I doubt HGs purposely spent energy gathering foods just so their constituent nutrients/minerals could NOT be utilized...
We found legume remains in a cave many thousands of years ago, ergo ---> eat legumes?
Hhhmmm, a very flimsy & superficial argument.
I'm out. Enjoy your time on the interwebz. Careful, the tubes are windy!
We could also wash down glazed donuts with tea or coffee which are rich in Mn (I am actually joking if it is not clear enough).
ReplyDeleteraphi the control is the redox potential of the cells or tissues in question.
ReplyDeleteJane says:
ReplyDelete... we assume that the main source of energy in the diet of the Kebara inhabitants was the legumes ...'
The full quote: "We believe that acorns were eaten and provided an important source of energy. But since we have only scant scientific evidence we assume that the main source of energy in the diet of the Kebara inhabitants was the legumes, as their seeds form the vast majority of plant remains found in the cave."
Key words: scant evidence.
Words for Jane to look up: qualitative versus quantitative.
Interesting quote from the article: "The danger of excess consumption of legumes is contracting lathyrism; this medical condition causes its victims to walk on the balls of their feet with the pelvis tilted. On the Indian subcontinent, the stage of lathyrism is crudely but usefully classified on a four point scale of increasing physical impairment: no-stick cases (mildly affected), one stick cases, two-stick cases (severe impairment), and crawler-stage cases, when victims are unable to move the legs and the hands are used to move the body on the rump."
Legumes anyone?
@Stipetic
ReplyDelete'Scant evidence' refers to the acorns, not the legumes. Please read the paper again. While you're at it, notice how much of the legumes you have to eat to get lathyrism.
@raphi
Until recently it was thought that ancient humans lived on meat, which explained their large brains. Nowadays it's generally accepted that vegetarians have large brains too.
@ Jane
ReplyDeleteThe two are linked. Because the evidence on acorns was scant, they shifted their guess to legumes. It doesn't mean legumes are the main soure of food, it just means--the word THEY use is "assume"--that legumes are a main source based on the scant evidene of acorns, which makes their assumption carry the same amount of scantness as the acorms.
I don't need to re-read the paper to reassess whether you deliberatedly attempted to misrepresent the findings of the study--I posted the full quote. I have the full and know, as well as the authors do, that this is all conjecture. And that legumes were, on top of being toxic, only available for 4 months during the year. There's actually no evidence from the paper that these were actually ingested. I'm sure some were (qualitative versus quantitative) but this paper does not address this.
"Nowadays it's generally accepted that vegetarians have large brains too."
Again with misrepresenting the science behind the theory. Sad, really.
@Stipetic
ReplyDeleteI've been looking at the paper again, and I think you are right to question the statement 'the main source of energy in the diet of the Kebara inhabitants was the legumes'. This implies that over half their food was legumes, which it can't have been. I think they must have meant, legumes were the principal energy-rich plant food in the diet.
@Stipetic
ReplyDeleteSorry, didn't see your latesst comment before I wrote mine.
Stipetic, 'nowadays it's generally accepted that vegetarians have large brains too' was a joke. My apologies again.
ReplyDeleteAt the start of the comments Charles asked "Are there any studies which show that vegetarians/vegans have a higher incidence of cancer than the general population?" with regard to low LDL-C.
ReplyDeleteOne way to answer that is that there are studies to show that replacing more-saturated animal fats with less-saturated vegetable oils a) lowers LDL-C and b) increases the rate of cancer.
For example, the Israeli Paradox papers, various animal experiments, and even some Heart-Healthy Diet RCTs.
Now that's not about vegetarians vs meat eaters, but it is about closely equivalent animal and vegetable foods, and the vege equivalent doesn't come off best.
1/3 of young women on raw food vegan diets stop menstruating. That's a result that I find a little more meaningful than small percentage differences in the incidence of more-or-less inevitable illnesses of ageing.
Peter, since statistics is so often the subject of your posts, that these findings can often be quibbled over, I think this is worth a read. It seems to tie back to your objections over the years to data that appear to have been massaged. A bit off the specific topic here, but worth a read. Brad
ReplyDeletehttp://www.nature.com/news/scientific-method-statistical-errors-1.14700
This is nice: the most common probable cause of the acquired Complex 1 inhibition postulated here.
ReplyDeleteCholine deficiency alters the composition of mitochondrial membranes; cardiolipin in these membranes is oxidized, and membrane concentrations of phosphatidylethanolamine and phosphatidylcholine are decreased [43, 44]. These membrane changes result in mitochondrial decreased membrane potential [14, 45] and in reduced activity of complex I of the respiratory chain [44, 46].
Choline is found in a variety of foods, but it is particularly abundant in egg yolks and animal sources of protein (see www.ars.usda.gov/SP2UserFiles/Place/12354500/Data/Choline/Choln02.pdf). Many of these high-choline foods are high in fats or cholesterol (e.g. eggs) and are being avoided by many people who then do not achieve the recommended dietary Adequate Intake for choline [22, 23]. For example, several recent epidemiologic studies reported that 25% of Americans ate diets very low in choline (<203 mg/d in the Framingham Heart Study [24], <217 mg/d in the Atherosclerosis Risk In Communities study [25, 26] and <293 mg/d in the Nurse’s Health Study [27]; the Adequate Intake is 450–550 mg/day [22]).
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3601486/
Jane, you were right about complex 1 and methylation.
http://carcin.oxfordjournals.org/content/21/5/983.long
ReplyDeleteDietary choline restriction causes complex I dysfunction and increased H2O2 generation in liver mitochondria
Now bear in mind that this is happening in a milieu where both burning and export of FFAs has been decreased - so there is no benefit from IR. The liver may be hungry for sugars and this leads to sweet tooth and storage in adipocytes which are not so IR.
It may also promote hepatic gluconeogenesis.
Which fits in with what Paul Jaminet is saying here.
http://perfecthealthdiet.com/2010/11/dangers-of-a-zero-carb-diet-ii-micronutrient-deficiencies/
And maybe when the PHD claims DM2 results that compete with VLC, it's because the PHD is very high in choline, while some VLC regimes are choline deficient.