Tuesday, October 23, 2012

Humane Slaughter?


Humane rape.

Humane murder.

Humane slavery.

Humane genocide.

Humane pedophilia.

This YouTube video carries the title "Local Flavor TV: From Grass to Grill - Part 2 - Certified Humane Slaughter."

If you have the guts, put yourself into the cow's place and ask:

If like this steer you had not committed any crime, yet someone tricked and prodded you into walking into a device that closed down on your neck to restrain you would you call their trick humane?

If that someone then shot a bolt into your cranium while you struggled to free yourself (as did this steer), would you call him or his process humane?

If the butcher then hung you up by your legs and cut your throat while your heart continued to beat, would you call him or the process humane?

Humane decapitation?

I don't think that humane slaughter can exist.  I think the phrase provides a euphemism intended to put you back to sleep. 




Charles Grashow said...


Latest blood test results


Total Cholesterol - 242 mg/dL
LDL-C (Direct Measure) - 118 mg/dL
HDL-C - 76 mg/dL
Triglycerides - 41 mg/dL
Apoliprotein B - 104 mg/dL

Charles Grashow said...


“Humane slaughter, like humane rape, does not exist. The phrase is a euphemism intended to put you back to sleep.”
Primal Wisdom, ex paleo blogger

It was interesting to hear how paleo didn’t work for him, but clearly extremism is very attractive to him. And I agree with many feminists that the use of comparisons like this by mostly male animal rights extremists is extremely insulting to rape victims. But honestly, it’s not very surprising given this blogger’s history of it’s all about me politics. His discussions defending conventional meat on “paleo libertarian” (with guest star Richard Nikoley!) are hilariously classic.

Source: donmatesz.blogspot.com

Charles Grashow said...


Peter said...


excellent and thought provoking input. Thanks a lot.


you have a quite prosperous serum cholesterol concentration there, very well above physiological levels. Did your doctor put you on lipitor?

1) William Roberts (American Journal of Cardiology, editor-in-chief)

"It is time to move on from a goal “to decrease risk” to a goal “to prevent plaques” (21). To do so requires much lower levels of LDL cholesterol than advocated by the guideline publications. My goal for all individuals worldwide is a serum LDL cholesterol at least <100 mg/dL and ideally <60 mg/dL. The beauty of the JUPITER trial is that it dramatically demonstrates what incredible reductions in events can be produced in a short period of time (<2 years) by reducing the LDL cholesterol by 50% even when starting from a level considered by many to be normal (<130 mg). The mean level (108 mg/dL) might be considered “good” or even “great” by many physicians, but lowering it to 55 mg/dL (by rosuvastatin 20 mg/dL) decreased all events by >40%, indeed nearly 50%, including a reduction in stroke by 48%! This trial beautifully shows that we can drastically reduce or even prevent atherosclerotic events and expensive procedures by taking a single pill every day and do it safely. Most Americans will not reach the JUPITER treatment levels (LDL cholesterol 55 mg/dL) by diet alone. The statin drugs have been ingested by humans now for nearly 30 years, and their safety and thus benefit/risk ratio may be the best of any proven useful medication. The toxicity resides mainly in atherosclerosis, not in the drug"

"....The lower the LDL cholesterol the better, and this principle has been established repeatedly despite the voices of the anticholesterol, antistatin fallacy mongers! It's the cholesterol, stupid!"


2) This great review discusses eloquently how unadjustment for regression dilution (systematic error) has failed to show the real association of serum cholesterol concentrations to coronary heart disease in many uniformly high-risk Western cohorts characterized by very high population-wide cholesterol concentrations.

3) High quality prospective cohorts which have corrected for regression dilution bias have firmly establish the independent, continuous, positive and log-linear nature of the associations between TC cholesterol and both CHD and Ischemic stoke even within population that have low serum cholesterol concentrations to begin with!

Cholesterol, coronary heart disease, and stroke in the Asia Pacific region

“Numerous other observational studies, particularly in men, have demonstrated a strong, continuous, graded, and independent association between cholesterol and the risk of CHD.1–,6 The current data clearly extend these findings to Asian populations with substantially lower average levels of cholesterol, and confirm that effects are similar in men and women”


4) Elevated total cholesterol: its prevalence and population attributable fraction for mortality from coronary heart disease and ischaemic stroke in the Asia-Pacific region.

“Conventional methods for estimating disease burden severely underestimate the effect of TC. Cholesterol-lowering strategies could have a tremendous effect in reducing cardiovascular deaths in this populous region”


Jozef Varhaník said...

Humane gardening.

The veggies must be horrified!
You are ripping them apart, leaves and rhizomes from stems!
And the grains?
You are stealing and grinding up their children!
Brutal and disgusting!

Also, kill all lions.

Charles Grashow said...


Cholesterol Lowering, Cardiovascular Diseases, and the Rosuvastatin-JUPITER Controversy
A Critical Reappraisal

Results The trial was flawed. It was discontinued (according to prespecified rules) after fewer than 2 years of follow-up, with no differences between the 2 groups on the most objective criteria. Clinical data showed a major discrepancy between significant reduction of nonfatal stroke and myocardial infarction but no effect on mortality from stroke and myocardial infarction. Cardiovascular mortality was surprisingly low compared with total mortality—between 5% and 18%—whereas the expected rate would have been close to 40%. Finally, there was a very low case-fatality rate of myocardial infarction, far from the expected number of close to 50%. The possibility that bias entered the trial is particularly concerning because of the strong commercial interest in the study.

The results of the trial do not support the use of statin treatment for primary prevention of cardiovascular diseases and raise troubling questions concerning the role of commercial sponsors.

In conclusion, the results of the JUPITER trial are clinically inconsistent and therefore should not change medical practice or clinical guidelines. The results of the JUPITER trial support concerns that commercially sponsored clinical trials are at risk of poor quality and bias. Documentation of the failure of the JUPITER trial to demonstrate a protective effect of rosuvastatin is all the more important as it occurred in the context of the failure of more than 12 other cholesterol-lowering trials published in recent years and in various clinical settings.1 - 9 ,45 - 48 None of these trials provided significant evidence of protection against CHD complications—especially fatal complications—by cholesterol lowering. Two other cholesterol-lowering studies were either not published49 or abruptly halted50 because of lack of effect. These failures strongly suggest that the presumed preventive effects of cholesterol-lowering drugs have been considerably exaggerated.

Clearly, the time has come for a critical reappraisal of cholesterol-lowering and statin treatments for the prevention of CHD complications. The emphasis on pharmaceuticals for the prevention of CHD diverts individual and public health attention away from the proven efficacy of adopting a healthy lifestyle, including regular physical activity, not smoking, and a Mediterranean-style diet.

Financial Disclosure: Dr Abramson has served as an expert for plaintiffs' attorneys in litigation involving the pharmaceutical industry (not involving rosuvastatin), as an unpaid consultant to the Federal Bureau of Investigation and the Department of Justice in investigations involving the pharmaceutical industry, and as a consultant to Wells Fargo Insurance Services.


SO - tell me again why I should take a statin drug??

Charles Grashow said...


To repurpose a handy metaphor, let's call two of the first Homo sapiens Adam and Eve. By the time they welcomed their firstborn, that rascal Cain, into the world, 2 million centuries of evolution had established how his infancy would play out. For the first few years of his life, he would take his nourishment from Eve's breast. Once he reached about 4 or 5 years old, his body would begin to slow its production of lactase, the enzyme that allows mammals to digest the lactose in milk. Thereafter, nursing or drinking another animal's milk would have given the little hell-raiser stomach cramps and potentially life-threatening diarrhea; in the absence of lactase, lactose simply rots in the guts. With Cain weaned, Abel could claim more of his mother's attention and all of her milk. This kept a lid on sibling rivalry—though it didn't quell the animus between these particular sibs—while allowing women to bear more young. The pattern was the same for all mammals: At the end of infancy, we became lactose-intolerant for life.

Two hundred thousand years later, around 10,000 B.C., this began to change. A genetic mutation appeared, somewhere near modern-day Turkey, that jammed the lactase-production gene permanently in the “on” position. The original mutant was probably a male who passed the gene on to his children. People carrying the mutation could drink milk their entire lives. Genomic analyses have shown that within a few thousand years, at a rate that evolutionary biologists had thought impossibly rapid, this mutation spread throughout Eurasia, to Great Britain, Scandinavia, the Mediterranean, India and all points in between, stopping only at the Himalayas. Independently, other mutations for lactose tolerance arose in Africa and the Middle East, though not in the Americas, Australia, or the Far East.

In an evolutionary eye-blink, 80 percent of Europeans became milk-drinkers; in some populations, the proportion is close to 100 percent. (Though globally, lactose intolerance is the norm; around two-thirds of humans cannot drink milk in adulthood.)

Charles Grashow said...

ark Thomas, an evolutionary geneticist at University College London, points out that in modern-day Turkey, where the mutation seems to have arisen, the warm climate causes fresh milk to rapidly change its composition. “If you milk a cow in the morning,” he says, “by lunchtime it's yogurt.”
Yogurt has plenty of benefits to confer, among them large testicles, swagger, and glossy fur—at least if you're a mouse—but most salient to our ancestors was that the fermentation process that transforms milk into yogurt consumes lactose, which is a sugar. This is why many lactose-intolerant people can eat yogurt without difficulty. As milk ascends what Thomas calls the “fermentation ladder,” which begins with yogurt and culminates with virtually lactose-free hard cheeses, ever more lactose is fermented out. “If you're at a party and someone says, 'Oh, I can't eat that—I'm lactose intolerant,' ” he says, “you can tell them to shut up and eat the Parmigiano.”

Analysis of potsherds from Eurasia and parts of Africa have shown that humans were fermenting the lactose out of dairy for thousands of years before lactose tolerance was widespread. Here is the heart of the mystery: If we could consume dairy by simply letting it sit around for a few hours or days, it doesn't appear to make much sense for evolution to have propagated the lactose-tolerance mutation at all, much less as vigorously as it did. Culture had already found a way around our biology. Various ideas are being kicked around to explain why natural selection promoted milk-drinking, but evolutionary biologists are still puzzled.

Healthy Longevity said...

Cholesterol denialism is futile.

Recently published in the JACC

Effect of Long-Term Exposure to Lower Low-Density Lipoprotein Cholesterol Beginning Early in Life on the Risk of Coronary Heart Disease
A Mendelian Randomization Analysis

Results: All 9 polymorphisms were associated with a highly consistent reduction in the risk of CHD per unit lower LDL-C, with no evidence of heterogeneity of effect (I2 = 0.0%). In a meta-analysis combining nonoverlapping data from 312,321 participants, naturally random allocation to long-term exposure to lower LDL-C was associated with a 54.5% (95% confidence interval: 48.8% to 59.5%) reduction in the risk of CHD for each mmol/l (38.7 mg/dl) lower LDL-C. This represents a 3-fold greater reduction in the risk of CHD per unit lower LDL-C than that observed during treatment with a statin started later in life (p = 8.43 × 10−19).

Conclusions: Prolonged exposure to lower LDL-C beginning early in life is associated with a substantially greater reduction in the risk of CHD than the current practice of lowering LDL-C beginning later in life.

Importantly, we evaluated 9 polymorphisms located in 6 different genes, including polymorphisms in the genes that encode for the targets of both statins and monoclonal antibodies directed against PCSK9. Although each of these polymorphisms presumably affects circulating LDL-C levels by a different mechanism, and the per-allele effect of these SNPs on LDL-C levels varied by more than 6-fold; all 9 polymorphisms were associated with a highly consistent reduction in the risk of CHD when measured per unit lower LDL-C. This finding suggests that the effect of long-term exposure to lower LDL-C on the risk of CHD appears to be independent of the mechanism by which LDL-C is lowered. Therefore, the method of lowering LDL-C is likely to be less important than the magnitude and timing of LDL-C reduction. As a result, diet and exercise are probably as effective at reducing the risk of CHD as are statins or other treatments that lower LDL-C when started early in life (and when measured per unit lower LDL-C).


Association between change in high density lipoprotein cholesterol and cardiovascular disease morbidity and mortality: systematic review and meta-regression analysis

The meta-regression analysis included 108 randomised trials involving 299 310 participants at risk of cardiovascular events. All analyses that adjusted for changes in low density lipoprotein cholesterol showed no association between treatment induced change in high density lipoprotein cholesterol and risk ratios for coronary heart disease deaths, coronary heart disease events, or total deaths. With all trials included, change in high density lipoprotein cholesterol explained almost no variability (<1%) in any of the outcomes. The change in the quotient of low density lipoprotein cholesterol and high density lipoprotein cholesterol did not explain more of the variability in any of the outcomes than did the change in low density lipoprotein cholesterol alone. For a 10 mg/dl (0.26 mmol/l) reduction in low density lipoprotein cholesterol, the relative risk reduction was 7.2% (95% confidence interval 3.1% to 11%; P=0.001) for coronary heart disease deaths, 7.1% (4.5% to 9.8%; P<0.001) for coronary heart disease events, and 4.4% (1.6% to 7.2%; P=0.002) for total deaths, when adjusted for change in high density lipoprotein cholesterol and drug class.

To take into account non-lipid effects of specific drugs (such as potential pro-thrombotic effects of hormone therapy), we included a categorical variable of drug class in the meta-regression model and did a meta-regression analysis stratified by drug class. We used R2 to measure the proportion of the variability in the log risk ratio of an outcome explained by the statistical model.

Anonymous said...

"Everything is possibly wrong, let us see." THIS is the correct scientific attitude to have brought to us by Richard P. Feynman, one of the smartest people in human history and a man who KNEW what science is.

Both cholesterol hypothesis skeptics as well as cholesterol hypothesis proponents should keep this in mind.

Charles Grashow said...


Low-Density Lipoprotein Levels in Patients With Acute Heart Failure

"Our study demonstrates a higher all-cause mortality rate in patients with LDL values <71 mg/dL when compared with those >130 mg/dL. This difference was also significant when restricting analysis to only those patients taking statins, a subgroup analysis meant in part to exclude those who may have a physiologic decrease in circulating LDL levels, as discussed below."

"Several mechanisms for the apparent benefit of higher total serum cholesterol levels have been proposed. The three most popular theories are the endotoxin lipoprotein hypothesis, the coenzyme Q10 (ubiquinone) hypothesis, and the selenoprotein hypothesis. The endotoxin lipoprotein hypothesis, proposed by Rauchhaus and colleagues,27 states that patients with HF experience mesenteric venous and bowel wall edema, which, in turn, causes bacterial translocation and endotoxin release into the bloodstream. Lipoproteins are then needed to bind endoxtoxin and decrease the systemic release of proinflammatory cytokines. The ubiquinone hypothesis suggests that statin use decreases available levels of ubiquinone, which is needed for the production of ATP in order to meet the metabolic demands of cells. Lastly, the selenoprotein hypothesis reasons that statins interfere with the enzymatic isopentenylation of selenocysteine tRNA and prevent its maturation to a functional tRNA molecule. This results in a decrease in available selenoproteins, which are a necessary precursor to selenoprotein enzymes that serve a similar antioxidant role to ubiquinone."

"Our study calls to attention the important correlation between decreased levels of serum cholesterol and increased mortality in advanced HF. Moreover, extending that correlation it further indicates that low levels of LDL cholesterol are also associated with a poor prognosis in HF.

Disclosure:  There are no relationships with industry to disclose."

Charles Grashow said...


The LDL to HDL Cholesterol Ratio as a Valuable Tool to Evaluate Coronary Heart Disease Risk

"An LDL-C/HDL-C ratio point for initiating lipid-lowering therapy should be determined. The current NCEP guidelines recommend levels of LDL and HDL that represent a ratio of about 2.5. Current research suggests risk of death from cardiovascular disease begins to increase significantly around a ratio of 3.3–3.7."

My current LDL/HDL ratio is: 1.55

Charles Grashow said...

One Japanese investigator has suggested the target index for regression of atherosclerosis should be less than 2.0 for primary prevention and less than 1.5 for secondary prevention. Based on the ROC curves, the cut-off point was 2.3 in this study. The detailed analysis stratified by LDL-C/HDL-C quartiles (Figures 1(a) and 1(b)) may confirm this cut-off value.

Eileen Weintraub said...

Thank you for thought provoking sane analysis of a compassionate diet. As our world goes towards 9 billion people we can do no less. Anyone who argues otherwise is selfish and lacking empathy.

Charles Grashow said...


BTW - Eileen what is your current diet like?

The Humane Hominid said...


That's only the beginning of an investigation. It often doesn't stay that way after the evidence has been weighed. A person who remains in that mode of thought is profoundly UNscientific.

Preponderance of evidence matters. Some hypotheses are wrong (most are, in fact). But some are actually well-supported enough by evidence that "questioning" them becomes foolish and cynical.

Feynman understood that, too.

Peter said...


1) Your LDL-C is about 150% higher to what is physiologically normal.

2) Lowering LDL-C volume has a causal relationship to reduced cardiovascular end points, no matter what mechanism is used: diet, excersise, bile-acid sequestrant, bypass of the illeal (POSCH-trial), statin, etc. No such causal relationship has been established with HDL -cholesterol volume.

3) A consistent epidemiologic association point that high circulating HDL volume may protect against artery disease in uniformly high-risk Western societies. These same cohorts have established that favourable LDL to HDL ratio may be protective. These are association, they may be even powerfull associations! However, a leap of faith is required if believing that elevated HDL concentrations due to abundant consumption of SFA and dietary cholesterol will protect against diseases of affluence. Moreover, randomized controlled mendelian trials with hundred of thousands participants have found no relationship with elevated HDL (and thus favourable LDL to HDL ratio) and protection against cardiovascular disease.

4) Studying pooulation with very low serum cholesterol concentration as a baseline, Campbell and Junshi (1994) reported that the chief correlate to all diseases of affluence was elavated TC cholesterol (p = 0.01), which in turn was associated with intake of meat & total fat and inversely associated with intake of legumes and certain fiber extractions

5) Population that show near absence of coronary heart disease have uniformly low HDL (as well as low LDL). HDL-cholesterol concentration in the range 20-30s md/dl have been frequently observed in rural Chinese as well as once among inhabitants of Okinawa island too. All trophical hunter gatherers have low HDL too.

6) As you pointed out by citing a study, epidemiologic data from uniformly high risk Western cohorts have also established associations with low-cholesterol concentrations to all-cause mortality (no such relationship exist among culture which have uniformly low-cholesterol concentrations as a baseline). Similar associations have been established with low-blood pressure and low BMI to all cause mortality. I am sure that by now you can identify many medical conditions which cause sickness and results in low serum cholesterol (and low-blood pressure and BMI) thus undermining the nature of these biomarkers.

"Undiagnosed disease may cause changes in the lipid profile, contributing to reverse causality".

Optimal low-density lipoprotein is 50 to 70 mg/dl: Lower is better and physiologically normal

"People with heterozygous hypobetalipoproteinemia have total cholesterol levels as low as 80 mg/dl and LDL cholesterol levels as low as 30 mg/dl (30). This condition is associated with longevity (31), presumably due to the absence of atherosclerosis, but the lack of other adverse effects that might have accompanied a low LDL level suggests that such low levels of LDL are safe".

Peter said...

"Cholesterol lowering, cardiovascular diseases, and the rosuvastatin-JUPITER controversy: a critical reappraisal"

The above article is written by de Lorgeril, a reknown denilist who operated under conviction and faith and is thus anti-science by default. His fringe ideas about serum cholesterol are basically thin-air to biomedical society at large. Why would you want to listen to him, especially when he has been caught up by making highly dubious fringe claims based on lies and half-truths? De Lorgeril reminds me of the architects ad engineers who advocate 9/11 conspiracy theory.

Charles, you should align yourself with sincerity, not with sabotage, fraud and denial.

Jane said...

I suspect the problem is that eating meat gives you iron overload in your brain, which damages it and prevents you from seeing that the animal is having a bad time.

I used to do literature research for the Oxford Project To Investigate Memory and Ageing. There seems to be no doubt that iron overload is at the root of degenerative brain disease. We now know that two important Alzheimer proteins, APP and tau, are involved in iron export from neurons. http://www.alzforum.org/new/detail.asp?id=3052

Iron export requires copper. A diet of meat and white bread, which has had much of its copper removed and iron added, is pretty much guaranteed to damage your brain. I think Big Pharma knows this. See 'Drug giants give up on Alzheimer's cure' in the Independent last month.

Peter said...

Anyways, I want to wish Charles a good luck with the circulative HDL-volume theory, may the force be with it.

1)The HDL hypothesis: does high-density lipoprotein protect from atherosclerosis?

2) 'Good' HDL Cholesterol Can Also Be 'Bad' (2012)

"the HDL amplified inflammatory reactions several times over and could explain the latent chronic inflammation that is associated with high cardiovascular risk,"

"Lowering the LDL level is therefore still even more important than raising the HDL level."


3) Doubt Cast on the ‘Good’ in ‘Good Cholesterol’ (May, 2012)

"I’d say the HDL hypothesis is on the ropes right now,” said Dr. James A. de Lemos, a professor at the University of Texas Southwestern Medical Center"


Anonymous said...

The HUman Hominoid

MUCH uncertainty exists with the causes of coronary artery disease. I acknowledge this considerable uncertainty and the VAST unknowns. The unknowns are far greater thasn ANY knowns in coronary heart disease.

There are many, many problems with the cholesterol hypothesis.

For example:

The Lipid research Clnics Coronary Primary Prevention Trial from 1984 Out of 3,806 patients:

CAD mortality treatment 30 vs controls 38

total mortality : treatment 68 vs controls 71

This is NOT a supportive trial.

My position is NOT unscientific AT ALL. In fact, it is VERY scientific.

All we can be in science is LESS WRONG. That's it. That's all Einstein was- LESS WRONG than the other theories iof gravity. the next breakthrough will be less wrong than Einstein.

The cholesterol hypothesis supporters are FAR TOO CERTAIN. IT IS FAR from well established.


I understand science far better than you.

Anonymous said...

The Theory of General Relativity has FAR more evidence behind it than does the cholesterol hypothesis. It's not even close.

it's withstood the test of time 100 years.

The cholesterol hypothesis has MOUNTAINS of contradictory data and is very FLIMSY

Peter said...

"MUCH uncertainty exists with the causes of coronary artery disease. I acknowledge this considerable uncertainty and the VAST unknowns. The unknowns are far greater thasn ANY knowns in coronary heart disease".

LOL. The above "much is still uncertain" -gimmick was in hefty use by both Tobacco and Asbestos industry. In regards to lipid-theory that is nothing but nonsense. The merchants of doubt army attempt to use it to sabotage the truth. For you, I advice not make far-fetched infantile conclusions about things you have no clue about. Just let the scientists do their work.

"There are many, many problems with the cholesterol hypothesis.

For example:

"The Lipid research Clnics Coronary Primary Prevention Trial from 1984 Out of 3,806 patients:

This is NOT a supportive trial".

LOL. That trial was based on cholestyramine (a bile-acid sequestrants). The intervention group was told to take pulverized powder for 5 times a day with water. The powder was very untasty and very few could follow the guidelines all the way. The side-effects included bloatedness among other effects. Those few who managed to take the powder 5 times day saw tremendous reductions in cardiovascular events. The benefits were directly proportional to the intake of that untasty powder. Most participants tolerated just few shots per day.

That study had nothing to do with tracking all-cause mortality. It involved too young participants with too low follow-up. It was designed to show difference on coronary heart disease, not an all-cause mortality, which it succesfully did. One of the participants in the intervention group died because a burglar shot him, his death was marked as a violent death in the study. Based on that, cholesterol skeptics of their time, most of who worked for beef industry, claimed that cholesterol reduction causes violence.

As I wrote:

Lowering LDL-C volume has a causal relationship to reduced cardiovascular end points, no matter what mechanism is used: diet, excersise, bile-acid sequestrant, bypass of the illeal (POSCH-trial), statin, etc.

Peter said...
This comment has been removed by the author.
Peter said...

Cholesterol theory is one of the few theories in medicine which is bullet-proof.

In fact it would not even require much evidence. LDL -cholesterol levels over 200% above to what is physiological normal is a norm in Western socities. By physiological levels is meant by those LDL- levels which are seen in healthy neonates, all wild mammalians who do not develope atherosclerosis and members in socities where chronic disease including atherosclerosis is near absent.

Normal, non-retarded humans are perfectly able to gather that blood-pressure or BMI above 200% of the physiological norm is harmfull. Normal non-retarded people are also able to conclude and deduce that LDL +200% above to what is physiological normal cannot be too good.

Peter said...

Healthy chimpanzees who do not develope atherosclerosis have LDL cholesterol in the range of 40 to 70 mg/dl. These levels match to the levels observed in other healthy wild mammalians and members in cultures where chronic disease is near absent (rural China, Guetemala, Central-Africa, etc).

Charles has his LDL cholesterol around 118mg/dl. That's quite abundant but unfortunately very normal in Western socities. A leap of good faith is required if maintainig that these levels cannot cause problems as such.

Anonymous said...

NOTHING in science is bullet proof. You reveal how litle you know. Even General Relativity is NOT bullet proof. It is only the curent BEST GUESS as to how Nature works at large scales.

I PROVIDED the numbers for LRC-CPPT. They do NOT support cholesterol lowering.

Most people on here know NOTHING about science.


Charles Grashow said...

Jane said...
I suspect the problem is that eating meat gives you iron overload in your brain, which damages it and prevents you from seeing that the animal is having a bad time.

Iron export requires copper. A diet of meat and white bread, which has had much of its copper removed and iron added, is pretty much guaranteed to damage your brain.

1) I don't eat grains

2) My last blood test - 10/5/12

Iron - 77 ug/dL Ref Range 45-170 ug/dL

Iron Binding Capacity - 377 ug/dL Ref Range 205-512 ug/dL

Iron Saturation 20.4%

Jane - what is your diet like on a daily basis? Have you had a recent blood test? If yes what is your HDL, LDL, Triglycerides?

Peter said...

"PROVIDED the numbers for LRC-CPPT. They do NOT support cholesterol lowering".

Ofcourse it does, that's why the biomedical community used the study in order to legitimize cholesterol reduction. All-cause mortality had nothing to do with these considerations and no one care about it. As said, the participants were too young and the follow-up too short. In order to show difference in all-cause mortality you need a huge sample and a long follow-up. This study wasn't designed to show difference in all-cause mortality. It was designed to show a difference in cardiovascular end points.

Besides, who the hell cares about this study when we have tons of statin studies. No one uses bile-acid sequestrants anymore. Multiple lines of evidence show the causal role of LDL reduction and plummeting cardiovascular end point. When the follow-up is long enough or the condition of the patients is more acute, we see also a difference in all-cause mortality, as many statin trials has showed.

Atherosclerosis can be induced in a great variety of animal species including vegetarian and carnivore species (e.g. insects, birds, cats, dogs, non-human primates etc.) by raising serum cholesterol high enough and maintaining it long enough. Atherosclerosis can also be reversed by lowering TC enough and maintaining it long enough. The lipid deposits and foam cells disappeared but some fibrous tissue remained. Some species, such as the dog and rat, do not get elevated TC from a diet high in saturated fat and cholesterol. But when a way was found to elevate their TC they also developed atherosclerosis. This is so consistent no matter which species is tested that it appears to be a scientific law that elevated LDL can cause atherosclerosis. ) This can't be explained away by stress, inflammation or some infectious agent. In clinical trials, Dr. Esselstyn's group did better than Dr. Ornish's group even though Dr. Ornish used stress reduction and Dr. Esselstyn didn't. However Dr. Esselstyn's patients had lower LDL. And although inflammatory factors like infection can speed up atherosclerosis, oxidized LDL, foam cells and cholesterol crystals inside the artery wall provide their own inflammation.

In animal models atherosclerosis can be turned on-and off by simple manipulating the genes that dictate the effectiveness of cholesterol metabolism. Moreover, atherosclerotic artery can be simply transplanted to healthy animal with low cholesterol where the artery heal in a rapid pace. Transplant the artery in a mice that has a high cholesterol and damaged artery gets even worse.

BTW, are you creationist?

Charles Grashow said...


If you are referring to me - I'm NOT a creationist

BUT - we keep on asking for your background and you do not provide it

What is your background education wise

Charles Grashow said...

Peter said...
Healthy chimpanzees who do not develope atherosclerosis have LDL cholesterol in the range of 40 to 70 mg/dl.


Charles Grashow said...

Peter said...
"Cholesterol lowering, cardiovascular diseases, and the rosuvastatin-JUPITER controversy: a critical reappraisal"

The above article is written by de Lorgeril, a reknown denilist who operated under conviction and faith and is thus anti-science by default. His fringe ideas about serum cholesterol are basically thin-air to biomedical society at large. Why would you want to listen to him, especially when he has been caught up by making highly dubious fringe claims based on lies and half-truths? De Lorgeril reminds me of the architects ad engineers who advocate 9/11 conspiracy theory

Michel de Lorgeril, MD, Laboratoire Cœur and Nutrition, Faculté de Médecine, TIMC-IMAG, Université Joseph Fourier and Centre National de la Recherche Scientifique, UMR 5525, Domaine de la Merci, 38706 La Tronche, France (michel.delorgeril@ujf-grenoble.fr).

Why not e-mail him and tell him what you really think?

Anonymous said...

Esselstyn did not use IVUS to detect coronary disease in the arteries. he used the OUTDATED coronary angiugram which MISSES A TON of plaque.

You can have NO stenosis ( narrowing of the arteries) BUT STILL HAVE A DIFFUSELY DISEASED artery, as Dr. Steve Nissen showed in his IVUS lecture on Youtube.

We will never know IF Dr. Esselstyn REALLY did reverse heart idease because he did NOT USE IVUS- whihc is ultra accurate. Esselstyn coudl nto because IVUS was not availabel yet.

Dr. Nissen says he did not reverse it
NO DIET can reverse heart diease. Dr. Nissen admitted this and said there is NO SOLID EVEIDENCE that these Esselstyn diets reverse coronary artery disease.

lastly CORONARY ARTERY DISEASE MORTALITY: treatment 30 deaths vs controls 38 deaths

These ARE the numbers- absolute numbers NOT shady manipulated relative risk

Our of 3,806 poeple this is NOT supportive of cholesterol lowering, Coronary mortality was not affected



Anonymous said...

Dr. Michae DeBakey, the world renowned , pioneeriong heart surgeon NEVER accepted the cholesterol hypothesis. He REJECTED that cholesterol drove this disease. he saw CONTRADICTORY EVIDENCE int he over 18,000 patients he operated on. This is WORTH NOTING.

Did you know that?

The cholesterol hypothesis has MAJOR problems. Patients have had SVERE DISEASE with cholesterol levels at 111 mg/dl SEVERE DISEASE.

Charles Grashow said...



"Humans have more brain neurons than any other primate—about 86 billion, on average, compared with about 33 billion neurons in gorillas and 28 billion in chimpanzees. While these extra neurons endow us with many benefits, they come at a price—our brains consume 20% of our body's energy when resting, compared with 9% in other primates. So a long-standing riddle has been where did our ancestors get that extra energy to expand their minds as they evolved from animals with brains and bodies the size of chimpanzees?

One answer came in the late 1990s when Harvard University primatologist Richard Wrangham proposed that the brain began to expand rapidly 1.6 million to 1.8 million years ago in our ancestor, Homo erectus, because this early human learned how to roast meat and tuberous root vegetables over a fire. Cooking, Wrangham argued, effectively predigested the food, making it easier and more efficient for our guts to absorb calories more rapidly. Since then, he and his colleagues have shown in lab studies of rodents and pythons that these animals grow up bigger and faster when they eat cooked meat instead of raw meat—and that it takes less energy to digest cooked meat than raw meat.

In a new test of this cooking hypothesis, Herculano-Houzel and her graduate student, Karina Fonseca-Azevedo, now a neuroscientist at the National Institute of Translational Neuroscience in São Paulo, Brazil, decided to see if a diet of raw food inherently put limits on how large a primate's brain or body could grow. First, they counted the number of neurons in the brains of 13 species of primates (and more than 30 species of mammals). The researchers found two things: One, that brain size is directly linked to the number of neurons in a brain; and two, that that the number of neurons is directly correlated to the amount of energy (or calories) needed to feed a brain."

"These numbers show that there is an upper limit on how much energy primates can get from an unprocessed raw diet, Herculano-Houzel says. An ape's diet in the wild differs from a modern "raw food diet," in which humans get sufficient calories from processing raw food in blenders and adding protein and other nutrients. In the wild, other apes can't evolve bigger brains unless they reduce their body sizes because they can't get past the limit of how many calories they can consume in 7 hours to 8 hours of feeding per day. But humans, she says, got around that limit by cooking. "The reason we have more neurons than any other animal alive is that cooking allowed this qualitative change—this step increase in brain size," she says. "By cooking, we managed to circumvent the limitation of how much we can eat in a day."

This study shows "that an ape could not achieve a brain as big as in recent humans while maintaining a typical ape diet," Wrangham says."


Metabolic constraint imposes tradeoff between body size and number of brain neurons in human evolution


The remarkable, yet not extraordinary, human brain as a scaled-up primate brain and its associated cost

Anonymous said...

STATIN drugs have AT LEAST 12 effects we know of.


dietary cholesterol lowering trials were complete FAILURES to lower CAD mortality


NON stain cholesterol lowering drugs were COMPLETE FAILURES

It is extremely likely it is the 12 OTHER PLEOTROPIC EFFECTS OF STAINS NOT colesterol reduction, which is REPONISBLE for lowering CAD incidents and mortality in those WITH CAD- WITH CAD.

Statins cause HUGE problems They come with risk and their benefit is DRAMATICALLY overstated.

They help moderately IN THOSE WITH CAD. Cholesterol reduction is not likely to be part of it

Charles Grashow said...

@R A Z Z


Effect of Two Intensive Statin Regimens on Progression of Coronary Disease

Stephen J. Nicholls, M.B., B.S., Ph.D., Christie M. Ballantyne, M.D., Philip J. Barter, M.B., B.S., Ph.D., M. John Chapman, Ph.D., D.Sc., Raimund M. Erbel, M.D., Peter Libby, M.D., Joel S. Raichlen, M.D., Kiyoko Uno, M.D., Marilyn Borgman, R.N., Kathy Wolski, M.P.H., and Steven E. Nissen, M.D.

Maximal doses of rosuvastatin and atorvastatin resulted in significant regression of coronary atherosclerosis. Despite the lower level of LDL cholesterol and the higher level of HDL cholesterol achieved with rosuvastatin, a similar degree of regression of PAV
was observed in the two treatment groups. (Funded by AstraZeneca Pharmaceuticals;
ClinicalTrials.gov number, NCT000620542.)

Rosuvastatin did show a significant benefit with respect to disease regression as assessed according
to TAV, a secondary intravascular ultrasonographic end point, but the difference between the two regimens was relatively modest. These data show that the two regimens are similar in their ability to limit progression or induce regression of coronary disease, although a small difference in efficacy cannot be ruled out on the basis of the significant differences observed for the change in TAV. Our study shows that in appropriately selected patients, either regimen can be used to reduce the atheroma burden for the purpose of secondary


Effect of Intensive Compared With Moderate Lipid-Lowering Therapy on Progression of Coronary Atherosclerosis

A Randomized Controlled Trial

Steven E. Nissen, MD; E. Murat Tuzcu, MD; Paul Schoenhagen, MD; B. Greg Brown, MD; Peter Ganz, MD; Robert A. Vogel, MD; Tim Crowe, BS; Gail Howard, MS; Christopher J. Cooper, MD; Bruce Brodie, MD; Cindy L. Grines, MD; Anthony N. DeMaria, MD.


For patients with coronary heart disease, intensive lipid-lowering treatment with atorvastatin reduced progression of coronary atherosclerosis compared with pravastatin. Compared with baseline values, patients treated with atorvastatin had no change in atheroma burden, whereas patients treated with pravastatin showed progression of coronary atherosclerosis. These differences may be related to the greater reduction in atherogenic lipoproteins and C- reactive protein in patients treated with atorvastatin.

Charles Grashow said...

@ R A Z Z


Also in 2005, Nissen published the results of the REVERSAL trial, a headto-head comparison of the statins atorvastatin (Lipitor) and pravastatin (Pravachol). IVUS images showed that Lipitor had effectively halted the progression of plaque buildup, but coronary disease progressed considerably in those given Pravachol. The study suggested that treatments should aim to lower LDL, or “bad” cholesterol levels as much as possible.

In 2006, Dr. Nissen and his co-investigators reported on The ASTEROID trial (A Study to Evaluate the Effect of Rosuvastatin On Intravascular Ultrasound-Derived Coronary Atheroma Burden). The study concluded that intensive use of statins resulting in a decreased LDL and increased HDL can reverse the build-up of plaque in coronary arteries, as measured by IVUS.


Halting the progression of atherosclerosis with intensive lipid lowering: results from the Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) trial.
Nissen SE.
Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Cleveland, Ohio, USA. nissens@ccf.org
Intravascular ultrasonography is a catheter-based technique used to provide 3-dimensional views of the vessel lumen as well as the size and distribution of atherosclerotic plaques. This imaging technique was used in the Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) study, an 18-month, randomized, controlled, multicenter trial comparing the effects of intensive versus moderate lipid-lowering therapy on plaque progression in patients requiring coronary angiography. A total of 253 patients were randomized to atorvastatin 80 mg/day (intensive lipid lowering) and 249 patients were randomized to pravastatin 40 mg/day (moderate lipid lowering). Low-density lipoprotein (LDL) cholesterol levels decreased from a baseline mean of 150 mg/dL (3.9 mmol/L) in both groups to 79 mg/dL (2.0 mmol/L) in the atorvastatin group and 110 mg/dL (2.9 mmol/L) in the pravastatin group. High-sensitivity C-reactive protein (hs-CRP) levels decreased by 36.4% in the atorvastatin group versus 5.2% in the pravastatin group (P <0.001). For the primary end point of percent change in total atheroma volume, a significantly lower rate of progression from baseline was observed with atorvastatin (-0.4%) than with pravastatin (2.7%) (P = 0.02). Linear regression analysis showed an inverse relation between lipid reduction and plaque progression for both groups; however, at any given level of LDL cholesterol, the progression rate was lower with atorvastatin compared with pravastatin. Both regimens were well tolerated. The results show that intensive lipid lowering with atorvastatin 80 mg/day for 18 months halted the progression of coronary atherosclerosis, whereas more moderate lipid lowering with pravastatin 40 mg/day was associated with progression. The differences in the progression rate are likely to be a result of greater reduction in atherogenic lipoproteins and hs-CRP with intensive therapy


Effect of Very High-Intensity Statin Therapy on Regression of Coronary Atherosclerosis


Very high-intensity statin therapy using rosuvastatin 40 mg/d achieved an average LDL-C of 60.8 mg/dL and increased HDL-C by 14.7%, resulting in significant regression of atherosclerosis for all 3 prespecified IVUS measures of disease burden. Treatment to LDL-C levels below currently accepted guidelines, when accompanied by significant HDL-C increases, can regress atherosclerosis in coronary disease patients. Further studies are needed to determine the effect of the observed changes on clinical outcome."


Charles Grashow said...

Huge problems with the Nissen study


Table 2 - Final Laboratory Results (N=502)

Intensive - 80 mgs Atorvastatin

Final Total Cholesterol - 151.3 mg/dL

Final LDL-C 78.9
Final HDL-C 43.1
Final Triglycerides 148.4

The problem is that the LDL-c is a CALCULATED number using the Friedewald Formula which is TC-HDC-Trig/5 OR 151.3-43.1-29.7 = 78.5 (Close enough to the 78.9 listed)

HOWEVER if you use the direct measure of LDL or the Iranian calculation the true LDL for the final LDL-C is really 128.1!!

Here's a site for the calculation

SO - if the triglycerides are high then the LDL calculation is messed up

The final result is that the people who took 80 mgs of Lipitor a day still had LDL-C of 188 mg/dL AFTER using the statin

Peter said...


all wild mammalians, whether they have big brains or not, have very low serum cholesterol.



No, It wasn't. This is just your crank nonsense. You are operating under a religious conviction. The trial established a principle, which is demonstrated as correct over and over again. The lower the LDL, the better. You can read a detailed decription about the trial in Daniel Steinbergs book Cholesterol wars. What some crank once said has no relevance to the discussion at hand.

2) "It is extremely likely it is the 12 OTHER PLEOTROPIC EFFECTS OF STAINS NOT colesterol reduction, which is REPONISBLE for lowering CAD incidents and mortality in those WITH CAD- WITH CAD".

This is extremely unlikely. First, the reducting in coronary events is directly proportional with lowered LDL in statin trials with mean age at the randomization of 63. A reduction of 15% in LDL results in 15% drop in events, a reduction of 45% results in 45% reduction in clinical end-points, and so on.

Second, people with inherited LDL-lowering mutant in the statin targeted gene HMG-CoA that result in life-long exposure to low LDL show near 60% less risk for cardiovascular disease per every 1mmol/l (39mg/dl)drop in LDL. Third, no matter what mechanism is used, statins, surgical operation that result in lowered LDL (POSCH -trial), bile-acid sequestrant, statin, diet, etc lowered LDL results in lower risk for heart disease.

3) "The cholesterol hypothesis has MAJOR problems. Patients have had SVERE DISEASE with cholesterol levels at 111 mg/dl SEVERE DISEASE".

Let me guess. This is the same nonsense that Colpo uses. The guy with a 111mg/dl heart disease and plaque-laden arteries was dead. First, serum cholesterol levels decrease automatically post mortem. Second, what the cholesterol levels are at the age of the lifespan has very little effect on whether you get atherosclerosis or not. What matters is what the levels have been and how they have been maintained throughout the life. Magnitude and timing. Atherosclerosis starts initiating generally at 20's. Third, serum cholesterol levels start to plummet on elderly people as result of general decline in body functions. The cholesterol synthesis and absorption gets weaker resulting in terminal decline in serum cholesterol concentrations.

Peter said...

Person with a several decades of atherosclerotic burden at the backs, manifested in life-long exposure to elevated cholesterol can end up with atherosclerosis despite the showing relatively low cholesterol levels at the time of the measurement at the end of the lifespan. Moreover, despite modern drugs lower LDL very effectively, the plaques do not dissapear immeadiately and can still be rupture-prone. As I said, the benefits of LDL reduction depend on both magnitude and timing.

Ironically, the nonsense about the alleged peleitrophic effects of statins which you propagate has its origin in the propaganda aired by manufacturers of b-class statins.

Low-density lipoprotein cholesterol reduction and prevention of cardiovascular disease

"There was little question after the first major statin trials that the reduction in CVD was related to lipid lowering and was totally consistent and supportive of the lipid hypothesis. However, stimulated by funding from the pharmaceutical industry, in which competition was fierce for market share and was driven mainly by the efficacy of lowering LDL-C levels, manufacturers of less-effective agents for lowering LDL-C levels helped propagate “beyond LDL-C” theories; these theories were that statins reduced CVD events by means other than lipid reduction, often termed pleotropic effects, usually shown in in vitro laboratory studies or small, poorly standardized surrogate marker trials. This belief culminated in an RCT by a pharmaceutical company that was designed to show that more LDL-C reduction with a competitor's statin achieved no greater benefit.13 However, the results of that study clearly and convincingly showed otherwise, with additional reduction in CVD events with the drug that lowered LDL-C levels more. Even with this evidence, and perhaps with an even more powerful statin about to be approved, the investigators suggested that the reduced events were due to pleotropic effects of the more efficacious statin. However, the trial was soon followed up with results from another head-to-head RCT, with the same drug at different LDL-C lowering doses,14 which eliminated the pleotropic potential and rein-forced that lower is better"


Anonymous said...

I was getting sloppy. I meant to say no DIET alone can reverse heart disease.

There is no CURE for heart disease. However, statin drugs can halt or even reduce the plaque somewhat.

Plaque reduction does not neccesarily lead to lower strokes and heart attacks though. Plaque reduction and stroke and heart attack reduction are TWO SEPARATE THINGS.

The only things that matter are did it reduced actual heart attacks and strokes?
Most heart attacks happen from plaque BREAKING OFF- not the actual amount.

Statins seem to get rid of the lipid content of the plaque and leave behind the fibrous materail part of the plaque- a "STABLE SCAR" that won't rupture. There is nothing left to cause mortality and morbidity.

I have gotten away from heart disease research in favor of obesity, so I was a bit rusty.

Healthy Longevity said...


You said: "The only things that matter are did it reduced actual heart attacks and strokes?"

This is exactly what Dr. Esselstyn's study that you ridicule did, not to mention his newer decade long study of over 200 patients.

As I already pointed out, a meta-analysis of 108 randomized controlled trials of various medical and dietary based lipid modifying interventions found that lowering LDL cholesterol significantly decreased the risk of coronary heart disease and all-cause mortality, independent of pleotropic effects of specific drugs and changes to HDL cholesterol and triglycerides.

Peter said...

William C Roberts, the editor in chief of American Journal of Cardiology, author of over 1300 scientific papers, cardiovascular pathologist by training discusses whether atherosclerosis can be reversed.


Peter said...

"SO - if the triglycerides are high then the LDL calculation is messed up

The final result is that the people who took 80 mgs of Lipitor a day still had LDL-C of 188 mg/dL AFTER using the statin"

I wonder are you ever capable of posting something that would not be fully nonsense. Triglycerides of 150mg/dl do not make "too high" levels

"Another important limitation: At a triglyceride level of about 250 or higher, the Friedewald equation becomes less reliable because dividing triglycerides by a factor of 5 provides a less accurate estimate of VLDL".

Iranian study was made with people with elevated cholesterol

The Framingham study showed that that in 84% to 86% of the subjects, estimated LDL-C values were within 10% of the ultracentrifugally measured LDL-C when plasma triglyceride concentrations were under 200mg/dl

I am sure the Nissen et al. study utilized very nice laboratory for accurate estimates.

Jane said...

Hi Charles
Your iron numbers look pretty good to me, but I have no first-hand knowledge of these things. I never go to the doctor, and I've never had tests of any kind.

I eat a Hunza-style diet, adopted 30 years ago when I read about McCarrison's work. Whole grains, whole dairy, fruit and nuts and vegetables. Two meals a day and no snacks, wholemeal bread (with LOTS of butter) instead of meat.

Does it sound awful? I feel wonderful, I'm healthy beyond anything I could have imagined, I love my food but I'm never hungry. I know all about food cravings, that's what I used to get 30 years ago together with yo-yo weight and constant dieting. I know now my liver and pancreas weren't working properly and couldn't keep my blood sugar stable. That's what a diet of meat and refined carbs will do.

Anonymous said...

Dr. Esselstyn is a GREAT man. He is very dedicated and sets the standard for patient care. I cannot say anything bad about him.

Dr. Nissen, however, acknowledges that the Novel winning Goldstein was dead wrong that heart disease would be "gone with the century" because of LDL lowering statin drugs and arrogantly PREDICTED we would have "no heart attacks by the year 2000' . That is completely untrue.CAD is FAR more complicated.

Winning a Nobel Prize did not save them from being COMPLETEL;Y WRONG in Nissen's own words.

There is much more to heart disease than cholesterol - FAR more. 25% to 30 % of people who drop dead of coronary artery disease had NO TRADITIONAL RISK FACTORS WHATSOEVER- including Nissen's partner whom he mentioned.

We are MISSING A TON. Hopefully science will figure it out in the coming years.

Anonymous said...

"Even if statin drugs were in the water supply, we STILL would have CAD as the number one cause of death in developed nations"

- Dr. Steve Nissen

That is a true statement. CAD is hellishly complex. The cholesterol hypothesis is INCOMPLETE. It is far more than that.

Anonymous said...



30 CAD deaths

vs 38 CAD deaths (controls)

out of 3,806 people in the Lipid Research Clinics Coronary Primary Prevention Trial

is supportive of cholesterol lowering?

THOSE ARE the actual numbers of CAD deaths


Colpo and Steinberg are BOTH biased.

Dr. NISSEN is a better scientist and less biased than Steinberg and MORE HONEST.

Healthy Longevity said...


Cholesterol intervention starting very early life (ie. statins in the water supply) would result in a three-fold greater decreased risk of coronary heart disease compared to intervention started later in life. This would potentially make heart disease no longer the number one killer in developed nations. In prevention it is the timing and magnitude of lowering LDL that determines risk of CAD.

Your claim that it is impossible to reverse atherosclerosis suggests you are either ignorant of dozens of experiments on non-human primates that showed that cholesterol lowering dietary changes reverses the atherosclerosis process, which has been proven at autopsy, or have strong evidence demonstrating that these findings are not applicable to man.

You are incapable of even take into consideration the limitations of the Lipid Research Clinic Coronary Trial that Peter mentioned, and ignore the combined results from over 100 trials. I therefore refer you to the below paper.

Denialism: what is it and how should scientists respond?
Whatever the motivation, it is important to recognize denialism when confronted with it. The normal academic response to an opposing argument is to engage with it, testing the strengths and weaknesses of the differing views, in the expectations that the truth will emerge through a process of debate. However, this requires that both parties obey certain ground rules, such as a willingness to look at the evidence as a whole, to reject deliberate distortions and to accept principles of logic. A meaningful discourse is impossible when one party rejects these rules.


Anonymous said...

YOU are the only person in DENIAL.

You have NOT read ANY of my points I made TODAY. WE ARE MISSING A TON with regard to coronary heart disease.

I ALREADY addressed the reversal comment. I meant to say CURE.

EVEN NISSEN admits statins in the water supply would NOT do that much. CAD would still be the number one killer or near it.

CAD is FAR more complicated than YOU will ever admit.




Anonymous said...

Einstein and Feynman were scientific HEAVYWEIGHTS.

They took a completely NEW LOOK at a problem- completely new.

They acknowledged uncertainty and doubt and unknowns.

ALL we can be in SCIENCE is "LESS WRONG."

The BEST scientific theories we have ( evolution, General Relativity) are APPROXIMATIONS OF THE TRUTH at very best. That is it.

The lipid hypothesis is NOWHERE near as suported as General Relativity.

General relativity is not "corect", it is ONLY currently the very best guess as to how Nature works at large scales.

Both Einstein and Feynman admitted how little they knew and they were far smarter than guys like Steinberg . At least Nissen is HONEST and the least biased.

Healthy Longevity said...


Please cite peer-reviewed papers and take into consideration the studies we have cited when making claims.

So the 30% of people who die of CAD apparently have no documented risk factors, meaning that they maintain an LDL of <70 mg/dl throughout their entire lives?

Here is an interesting paper that notes the absence of coronary heart disease in traditional Asian populations that ate almost entirely plant based diets:

Anonymous said...

Talk with Dr. Nissen. Do some digging.

The number could be anywhere from 20% to 30 % . I believe 25 % is the figue I saw.

A significnt number of the population has NO TRADITIONAL RISK FACTORS- ALL OF THEM that are knwon AND STILL DROP DEAD.


There is muhc more to heart disease than cholesterol. Dr. DeBakey OPERATED onm diseased arteries. He DOUBTED the cholesterol hypothesis because the WEIGHT of the evidence contradicted it.

He saw WEIGHTY contradictory evidence. it is NOT the DRIVER. yes it is involved and can complicate things ( 600 mg/dl cholesterol level in an already damaged artery probably complicates things)BUT IT IS NOT THE DRIVER.

NO traditional risk factors TELL YOU WHAT YOU NEED TO KNOW. Only VISUALIZING the artery will tell you waht yuou need to know.

Dr. Naghavi tells WebMD.

W-E-I-G-H-T of the evidence is what matters in science NOT "amount." Issac Newton himself saod this.

Did you know Newton's laws are not, in fact , EVER strictly true? In most cases they are ONLY very good approximations.

Anonymous said...

Coronary artery disease is FAR from solved. The unknowns would fill the Pacific ocean. The knowns would fill an Olympic swimming pool.

MUCH uncertainty exists. There are MANY factors involved in coronary heart disease THAT HAVE NOTHING AT ALL to do with diet.

Viral infections, microbial infections, bacterial infections infectious diseases, toxins, poor sleep, depression, extreme lonliness etc.

Diet IS a factor in coronary artery disease specifically BUT ONE among many- many still unknwon.

Most diseases have NOTHING to do with diet.

Charles Grashow said...

Jane said...

"I eat a Hunza-style diet, adopted 30 years ago when I read about McCarrison's work. Whole grains, whole dairy, fruit and nuts and vegetables. Two meals a day and no snacks, wholemeal bread (with LOTS of butter) instead of meat."

Sounds like a very good diet to me although the vegans here will complain about the dairy.

Question - is the dairy raw, unpasturized?

Charles Grashow said...



Sir Robert McCarrison, in a paper entitled "Problems of Food, with Special Reference to India," which appeared in the Jan. 2, 1925, issue of the Journal of the Royal Society of Arts, said,

"Both man and animals derive their supply of vitamins directly or indirectly from the vegetable kingdom: from those sources to which reference is made in the first chapter of Genesis: 'from herbs bearing seed and from every tree in which is the fruit of a tree yielding seed . . . and from every green herb.' Certain animals are able to obtain from these sources alone all the materials--proteins, fats, carbohydrates, mineral elements and vitamins --requisite for their perfect nutrition. To enable them to do so they must eat these vegetable foods in very large quantities, and nature has endowed them with gastro-intestinal tracts capacious enough for the purpose. But man, whose gastro-intestinal tract is less capacious than that of herbivore, cannot obtain from vegetable sources alone all the food essentials for his energy requirements, nor for the attainment of the highest degree of physical efficiency. He can obtain a sufficiency of certain essentials, such as carbohydrates, mineral elements and vitamins from vegetable sources, but it is necessary for him to supplement the diet of seeds, tubers, roots, vegetables and fruit with a certain amount of animal food. Carnivora, again, do not make use of vegetable foods, from which vitamins are derived; they are thus dependent for their supply of these substances on the tissues of animals that do, and in which they are present in quantities which vary with the particular tissue."

Peter said...


"A significnt number of the population has NO TRADITIONAL RISK FACTORS- ALL OF THEM that are knwon AND STILL DROP DEAD".

You are emotionally unstable to handle the data and face the reality. It's unfortunate that you even refuse to look at the data before jumping to your infantile conclusion. As if we would not have heard the same message from cholesterol skeptics ever since the 1950's.

Those signficant number of Western people who drop dead "without no traditional risk factor" have LDL -cholesterol around +200% above what is physiologically normal. That's a norm among people "without no known traditional risk factors" in Western socities. You confuse normal to equal healthy. This is not always the case.

Anyone with a rudimental knowledge in global cardiovascular epidemiology knows how ridiculous your postulations are.

As an example: in rural Central-Africa TC cholesterol levels range from 110-135mg/dl which are the same levels that are maintained throughout the life. Cardiovascular mortality has been traditionally around zero in this part of the world, which is by no means exceptionall. Only extremely small amount of artery disease occur, mostly due birth defects.

1) ATP-3, expert panel:

"Only populations that maintain very low levels of serum cholesterol, eg. total cholesterol below 150mg/dl throughout the life do we see a near-absence of clinical CHD".

"Since LDL-cholesterol levels <100 mg/dL throughout life are associated with a very low risk for CHD in populations, they can be called optimal. Even when LDL-cholesterol concentrations are near optimal (100–129 mg/dL), atherogenesis occurs; hence, such levels must also be called above optimal. At levels that are borderline high (130–159 mg/dL), atherogenesis proceeds at a significant rate, whereas at levels that are high (160–189 mg/dL) and very high (≥190 mg/dL) it is markedly accelerated. These relationships are confirmed by the log-linear relationship between serum cholesterol levels and CHD risk observed in many populations.23"


2) Diagnostic Criteria for Dyslipidemia

“Low-density lipoprotein cholesterol (LDL-C) is identified in the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) report as the most abundant and clearly causal atherogenic lipoprotein on the basis of many observational and experimental studies over several decades.1 Guidelines from the American Association of Clinical Endocrinologists (AACE) are in agreement with NCEP ATP III that LDL-C is central in the diagnosis of dyslipidemia. Any LDL-C level above 100 mg/dL appears to promote atherogenesis”


Peter said...

Dietary pattern in much of rural Central-Africa is plant-based & low in fat. Staple foods are sorghum, maize, cassava, rice & beans which provide the bulk of calories.

1) "As to the risk factors in predominantly rural African populations in southern Africa, the principal dietary sources of energy were in the past and still are to an extent cereals (maize and kaffir corn or sorghum) and their products, wild spinaches, and a variety of legumes (cowpeas, sugar beans, Jugo beans), along with relatively low intakes of most vegetables and fruits and infrequent consumption of small quantities of milk and meat".

"Serum cholesterol levels of rural Africans in the past ranged from about 3.0 to 3.5 mmol/l and remain low"

Nutrition and Heart Disease Causation and Prevention Edited by Ronald Ross Watson and Victor R . Preedy

2) The epidemiology of coronary heart disease in South Africa

"Numerous reviews, past and present, have emphasised the rarity of coronary heart disease (CHD) in Africa. In 1960 in Uganda, CHD was considered to be 'extremely rare'. In 1977, black Africans were described as being 'virtually free of hypertension and CHD'.' In the same year, at Enugu, Nigeria, over a 4-year period, not one patient out of 348 with cardiac disorders had the disease. In 1983, in the UK, a leading article entitled 'British and African hearts' underlined the tremendous contrast between the experience of CHD in the two population groups: From 1988 to 1993 in Zimbabwe, at Parirenyatwa Hospital, the main referral centre for the country, there was an annual average of 6 black patients with acute myocardial infarction.' Even at present, as concluded in a comprehensive review compiled in Nigeria,'CHD is still rare ... despite its increased incidence in recent years.' This rarity applies particularly to rural dwellers, as recently noted in Tanzania.'"

".....Soweto (which now has a population of 3 - 4 million), according to records of the Department of Cardiology at Baragwanath Hospital (3 200 beds), 35 blacks were diagnosed with CHD in 1992,51 in 1993, and 62 in 1994. However, of the latter number only 36 were Sowetans; the rest lived elsewhere.Clearly CHD remains very uncommon in urban blacks in South Africa. To afford perspective, it could be asked how uncommon CHD is in urban blacks, compared with its occurrence in Western populations? Of the population of Soweto, almost all attend Baragwanath Hospital when serious illness occurs. If it is assumed that all the 36 patients with CHD mentioned ultimately died from the disease, CHD would be responsible for only about 0.2% of the roughly 20000 deaths occurring annually in Soweto, an extremely low proportion even allowing for uncertainties. In Europe, in the Seven Countries Study, for those in the Mediterranean countries and inland the age-standardised 25-year CHD mortality percentages were 4.7% and 7.7%, respectively. The proportions reported for countries in Northern Europe and for the USA were far higher, namely 16.0% and 20.3%, respectively. These comparisons with Western populations underline the very low occurrence of CHD in urban blacks"


Peter said...

A nice overall look to our present, detailed understanding of the various process involved in atherosclerosis is provided in this great video by PrimitiveNutrition.

Primitive Nutrition 45: Anything but LDL, Part III

The above video covers among other sources this very illustrative paper about the detailed process in mechanical level that occur in atherosclerosis:

Inflammation in Atherosclerosis: From Pathophysiology to Practice

Primitivenutrion has also excellent video that illustrates cardiovascular disease epidemiology. People with healthy physiological cholesterol levels do not drop dead because of CHD:

The Futility of Cholesterol Denialism, Part 2: Cholesterol in Populations

Anonymous said...

You're whacked out, Peter. You make no sense. Try a THOUGHT EXPERIMENT- you know what EINSTEIN used to do.

THINK a little.THINK. The cholesterol hypothesis has WEIGHTY contradictory evidence. WEIGHT is what matters.

Epidemiological evidence is the LOWEST form of evidence there is.

There is MUCH to learn about the pathogenesis of cornary artery disease. It is in NO WAY figured out yet.

Jane said...

Yes RAZZ, it is figured out. Here's what Leslie Klevay says about heart disease and copper.

'...the Western diet is frequently low in copper. Copper deficiency is the only nutritional insult that elevates cholesterol (7), blood pressure (8), and uric acid; has adverse effects on electrocardiograms (7, 9); impairs glucose tolerance (10)... and which promotes thrombosis and oxidative damage. More than 75 anatomic, chemical, and physiologic similarities between animals deficient in copper and people with ischemic heart disease have been identified. ...'

If you look up 'statins magnesium' you will find statins only work because they do what magnesium should be doing. It could not be clearer that heart disease is caused by a diet of meat and refined carbs.

Jane said...

Great McCarrison quote.
No, the dairy I eat is normal supermarket stuff, although the milk is organic. I made a decision 30 years ago only to eat things that were easy to obtain and inexpensive, because I wanted to know whether everybody could be healthy like the Hunza.

Anonymous said...

No ,Jane. YOU are a CRANK. NO genuine scientists points to a hunk of meat and says it is the "cause" of herat disease.

You have A LOT of learning to do about what genuine science is.

Stephan Guyenet ( a man who knows what science is) is on MY side for your information.

There are SO MANY FACTORS COMPLETELY UNRELATED TO DIET involved in coronary artery disease.

Watch some Richard Feynman videos and LEARN how science works.

Charles Grashow said...


without blood work how do you know how "healthy" you are

Are you not curious to know what your LDL-C, HDL-C, Triglycerides and Total Cholesterol are?

Jane said...

Hi Charles
Why should I want to know my numbers? If they're all wrong, what could I do about it? I cannot change my diet because it would destroy my experiment. My health is still improving, and I need to know how far a Hunza diet can take me. I still need glasses for reading, and the foot deformity I used to have is not completely corrected.

Jane said...

If Stephan Guyenet is 'on your side', why did you stop commenting on his blog? I comment there all the time as you know, and I thought he must have kicked you out.

Charles Grashow said...

Jane said...

"Hi Charles

Why should I want to know my numbers? If they're all wrong, what could I do about it? I cannot change my diet because it would destroy my experiment."

This is an incredibly STUPID statement.

Peter said...
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Peter said...

This article provides an elaborated and detailed account on the mechanics of atherosclerosis. The catalysator is elevated LDL cholesterol which is needed together with inflamation, something which elevated serum cholesterol levels are capable to produce on their own.

Brown & Goldstein provide a help for those who are curious and keen to avoid atherosclerosis

"Several lines of evidence suggest that plasma levels of LDL-cholesterol in the range of 25-60 mg/dl (total plasma cholesterol of 110 to 150 mg/dl) might indeed be physiologic for human beings. First, in other mammalian species that do not develop atherosclerosis, the plasma LDL-cholesterol level is generally less than 80 mg/dl. In these animals the affinity of the LDL receptor for their own LDL is roughly the same as the affinity of the human LDL receptor for human LDL, implying that these species are designed by evolution to have similar plasma LDL levels. Second, the LDL level in newborn humans is approximately 30 mg/dl, well within the range that seems to be appropriate for receptor binding. Third, when humans are raised on a low fat diet, the plasma LDL-cholesterol tends to stay in the range of 50 to 80 mg/dl. It only reaches levels above 100 mg/dl in individuals who consume a diet rich in saturated animal fats and cholesterol that is customarily ingested in Western societies".

Jane said...

Why is it a stupid statement? Did you misunderstand me?

I don't know why people have their blood lipids measured unless it's to prove what a healthy diet they eat. I don't need to prove that. I also think these numbers can be misleading. Gary Taubes has good numbers but he eats a diet that may be damaging his brain.

Anonymous said...

Scientific laws are not absolute.

A scientific law could be changed tomorrow with new evidence, gained perspectives, or realization of past mistakes. Scientific laws and scientific theories are completely different animals that serve different roles. There is NO heirarchy whatsoever. A scientific law can be changed just as easily as a scientific theory.

Goldstein et al are outright wrong. Winning a Nobel Proze does not in any way make you infallible.

Their prediction was WAAAAY off base completely that with statins we would have no more heart attacks from coronary artery disease by 2000.

CAD is FAR more complex than the whole HDL /LDL fiasco.

I have no idea what some peopel on here havbe such an emotional attachment to the cholesterol hypothesis. People in the biomedical research wold are moving in a DIFFERENT direction

CAD is inflammatory. This is why people with Rheumatoid Arthritis are at at last a 4 fold increase in risk to get CAD compared to the normal population.

CAD is FAR, FAR, FAR from being figured out.

Healthy Longevity said...

R A Z Z said: CAD is inflammatory. This is why people with Rheumatoid Arthritis are at at last a 4 fold increase in risk to get CAD compared to the normal population.

Risk of cardiovascular mortality in patients with rheumatoid arthritis: a meta-analysis of observational studies.
CONCLUSION: Published data indicate that CVD mortality is increased by approximately 50% in RA patients compared with the general population. However, we found that study characteristics may influence the estimate.

A second factor is the introduction and propagation of the thesis that atherosclerosis is an inflammatory disease (15). Yes, a few mononuclear cells are regularly seen in experimentally produced atherosclerotic plaques but not commonly in plaques of patients with fatal coronary disease or in plaques excised by endarterectomy (16, 17). And, yes, some blood inflammatory markers are commonly elevated in persons with atherosclerotic events. But, many patients have atherosclerotic events when the high-sensitivity (hs) C-reactive protein (CRP) is normal (<1 mg/dL), and patients with the highest levels of hs-CRP (e.g., rheumatoid arthritis, systemic lupus erythematosus) have only a slightly higher frequency of atherosclerotic events than do others of similar age and sex with normal or near-normal hs-CRP levels. The same principle, however, does not apply to cholesterol. The patients with the highest serum levels of total and LDL cholesterol, namely those patients with homozygous familial hypercholesterolemia, have an incredibly high frequency of atherosclerotic events, and they have them at very young ages—teenage years (18). And patients with the next highest serum LDL cholesterol levels, namely those with heterozygous familial hypercholesterolemia, have atherosclerotic events often in their 30s and 40s.

R A Z Z said: Epidemiological evidence is the LOWEST form of evidence there is.

Denialism: what is it and how should scientists respond?
Stanton Glantz, professor of medicine at the University of California, San Francisco and who has made a great contribution to exposing tobacco industry tactics, is a frequent target for tobacco denialists. He is described on the Forces website as ‘infamous for being the boldest of liars in “tobacco control” that most ethically challenged gang of con artists’, adding that ‘he cynically implies his research into smoking is science, banking on the sad fact that politicians, let alone the media, have no idea that epidemiology is not real science and that his studies define the term junk science’.

Stop spamming and start producing evidence. Do you attack people on other websites because they suggest that tobacco is a cause of CAD and cancer simply because there are still unanswered questions and has not been proven in large clinical trials? Or do you just like to attack people who provide evidence from over 100 clinical trials showing that LDL increases the risk of CAD just because you refuse to comprehend that your diet raises LDL and therefore may put you at a higher risk of CAD?

Christoph said...

It started with posts about potatoes, and led to utt.er insanity

George Henderson said...

Wow, cholesterol of 242, so supraphysiological that it's in the range associated with lowest all-cause mortality.

Is death from natural causes, then, like consensual sex?

Is cruelty therefore irrelevant?

high LDL on a diet of refined carbohydrates, with all their associated toxins (both natural and added), is BAD whether you eat meat or not.
high LDL on a diet free from refined carbs, grains and toxins is meaningless with regard to CVD risk and protective against cancer and sepsis.

You are mistaking two different things which give the same sign.

A knock on the door from the Gestapo is not the same as a knock on the door from the Jehovah's Witnesses.

Peter said...
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Peter said...
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Peter said...

THE CAUSE OF ATHEROSCLEROSIS (William Roberts, American Journal of Cardiology, editor-in-chief)

"In contrast to feeding cholesterol and/or saturated fat, it is not possible to produce atherosclerotic plaques in herbivores by raising the blood pressure chronically, by blowing cigarette smoke in their faces for their entire lifetimes, or by somehow raising the blood glucose levels without simultaneously feeding them an atherogenenic diet. Presently, it is commonly stated that “atherosclerosis is an inflammatory disease.” Inflammatory cells, however, are infrequent in plaques of coronary arteries studied at necropsy or in endarterectomy specimens. When present, the few mononuclear cells—even giant cells—appear to be present due to a reaction to the deposits of lipid (pultaceous debris) present in the plaque.“ Inflammation” appears to be a surrogate for elevation of serum C-reactive protein or various cytokines (interleukins 1 and 6, tumor necrosis factor, etc), not for inflammatory cells in plaques. Thus, it is a definition situation, and the morphologic definition of inflammation is not applicable."


@George Henderson

cross-sectional information where the lipid-status was measured once at the last years of age span at elderly, uniformly high risk Western patients hardly tells very much. As the general health status of chronically sick Western old people crumble, so does the cholesterol absorprtion and synthesis resulting in terminal decline in serum cholesterol levels. Following the same line of logic, low-blood pressure & Low BMI are both associated with increased risk for all-cause mortality as many studies show. What are the chances that the health authorities are going to tell us high blood pressure is good and low BMI dangerous? Go figure.

Low cholesterol, mortality, and quality of life in old age during a 39-year follow-up

"More dispute has arisen regarding the association of low cholesterol and mortality in elderly persons. For example, in the Honolulu Heart Program low cholesterol was associated with greater mortality risk. Obvious explanations for the association are intervening factors that both increase mortality risk and decrease the cholesterol level. In the nine-year follow-up of the Helsinki Aging Study, mortality risk was associated with both lowered cholesterol synthesis and lowered cholesterol absorption, which reflect terminal decline and lead to lower serum cholesterol levels. These associations are not identified, and the relationship between cholesterol and mortality becomes distorted unless the follow-up is long enough"


Correct the regression dilution bias with follow-up measurements, conduct a long follow-up, control the co-founders and the crazy associations will dissapear.

1) Relationship of baseline serum cholesterol levels in 3 large cohorts of younger men to long-term coronary, cardiovascular, and all-cause mortality and to longevity.

"These results demonstrate a continuous, graded relationship of serum cholesterol level to long-term risk of CHD, CVD, and all-cause mortality, substantial absolute risk and absolute excess risk of CHD and CVD death for younger men with elevated serum cholesterol levels, and longer estimated life expectancy for younger men with favorable serum cholesterol levels"


2) Cholesterol, coronary heart disease, and stroke in the Asia Pacific region

"Numerous other observational studies, particularly in men, have demonstrated a strong, continuous, graded, and independent association between cholesterol and the risk of CHD.1–,6 The current data clearly extend these findings to Asian populations with substantially lower average levels of cholesterol, and confirm that effects are similar in men and women"


Peter said...

HL posted a Great paper illustrating a 5-step framework to identify denialism:

Denialism: what is it and how should scientists respond?

Charles is a bullet proof denialist or just a regular Joe with sub-optimal IQ:

"The third characteristic is selectivity, drawing on isolated papers that challenge the dominant consensus or highlighting the flaws in the weakest papers among those that support it as a means of discrediting the entire field"

This kind of Galileo - the purveyor of truth complex is very easy to detect in RAZZ as well:

"Denialists are usually not deterred by the extreme isolation of their theories, but rather see it as the indication of their intellectual courage against the dominant orthodoxy and the accompanying political correctness, often comparing themselves to Galileo".

Good luck buddies with your alternative body of science "showing weaknesses in lipid theory":

"An example of the former is the much-cited Lancet paper describing intestinal abnormalities in 12 children with autism, which merely suggested a possible link with immunization against measles, mumps and rubella. This has been used extensively by campaigners against immunization, even though 10 of the paper's 13 authors subsequently retracted the suggestion of an association. Fortunately, the work of the Cochrane Collaboration in promoting systematic reviews has made selective citation easier to detect.

Another is a paper published by the British Medical Journal in 2003,21 later shown to suffer from major flaws, including a failure to report competing interests,22 that concluded that exposure to tobacco smoke does not increase the risk of lung cancer and heart disease. This paper has been cited extensively by those who deny that passive smoking has any health effects, with the company Japan Tobacco International still quoting it as justification for rejecting ‘the claim that ETS is a cause of lung cancer, heart disease and chronic pulmonary diseases in non-smokers’ as late as the end of 2008.23"

George Henderson said...

@ Peter,

what makes you think that one person's LDL means the same thing as another persons?

It's not even a disease, what you call high LDL can be associated with health, so what is the point of cookie cutter diagnosis?

Healthy Longevity said...

Just like elevated LDL, hypertension, hyperglycemia, obesity, and smoking status are not diseases, they are causal risk factors for disease. Not everyone with these risk factors will develop disease but it dangerous advice to suggest that someone with these risk factors should not be concerned that they are at risk for developing disease.

Anonymous said...

You are a fundamentalist, HealthLongevity:

I have news for you. GENES deterime how long you will live. That is where the SCIENCE is headed.

If you do not have the "centenarian gene" you will not live to 100 regardless.

YOU are in denial and 100 % certain.

Richard Feynman was not 100 % sure of ANYTHING.

Nature gives us different answers all the time. Science itself is extremely overrated.

Our BEST scientific theories humanity has should NOT be "taken to the bank." They are ONLY APPROXIMATIONS OF THE TRUTH AT VERY BEST, MANY ARE OUTRIGHT WRONG.

YOU never learned this.

The Humane Hominid said...

@George Henderson: so what is the point of cookie cutter diagnosis?

Risk assessment and diagnosis are different things.

The Humane Hominid said...

No, RAZZ, a theory is not simply an approximation of the truth. It's a robust and well-substantiated explanation of some aspect of the natural world, based on a body of facts that have been repeatedly confirmed through experiment and observation. And importantly, a theory has predictive power. Science doesn't just make guesses, and experiments aren't only attempts to disprove a hypothesis. In fact, experiments don't usually seek to actively disprove anything. We just set them up in a way that's capable of revealing whether a hypothesis is supported or not. We do this by making predictions based on our hypothesis, then checking our experimental results to see if they conform to the prediction or not. We recognize confirmatory evidence when it emerges from experiment, and we treat it as such, adding it to the body of facts that support a given theory.

Jimmy Gee said...


No use trying to reason with Don-followers - they apparently have this whole "nutrition thing" figured out.

Anonymous said...

Wrong HUmaneHominoid

Theories do have a lot of evidence behind them BUT:

Our best scientific theories are ONLY APPROXIMATIONS OF THE TRUTH AT VERY BEST. ALL we can be in science is LESS WRONG.


And some other lesser quality theories are OUTRIGHT WRONG.

Einstein's General Relativity ( very well suported for over 100 years)is NOT "correct", it's ONLY the current very best guess as to how the universe works at large scales.

The NEW breakthrough will be LESS WRONG than Einstein.

it is YOU who does not understand science

ALL scientific theories are TENTAIVE, NO EXCEPTIONS.


Feynman would have told you this himself.

P.S. I AGREE 100 % Jimmy :)

Anonymous said...

The SCIENCE of nutrition is EXTREMELY UNCERTAIN. Too LITTLE is known to SCIENCE- REAL SCIENCE about nutrition.

Plant based diets are NOT a panacea. ALL food carries RISK. ALL DIETARY DECISIONS ARE A MINEFILED THROUGH WHICH WE CAREFULLY TREAD. ANYBODY who does not ACKNOWLEDGE this is lying.

There are ALSO agents in PLANT foods that likely help INTITIATE atherosclerosis AND CONTRIBUTE TO CANCER.

The Humane Hominid said...


Typing in all caps does not strengthen your point.

"It's all tentative" is the fallback position of fundamentalists, quacks, New Agers and all others with a pet claim with no science on its side. What you call "less wrong" is also accurately described as "more precise." Semantic games do not strengthen your point, either.

At the end of the day, you are arguing by mere assertion, which don't cut the mustard with us science types who've actually designed and run experiments.

Anonymous said...

You have no understanding of how science works. I am trying to EDUCATE you.

Most people on the Internet do not. That is WHY they fall for these blogs which almost NEVER admit UNCERTAINTY AND UNKNOWNS- SOMETHING ALL GENUINE SCIENCE DOES.

Look into my buddy URGELT of YouTube.

Peter said...


please, ban this Razz fella. Even cholesterol denialists with their blogs have done so.

He is a troll who cannot engage in a meaningfull debate.

The Humane Hominid said...


I'm currently a scientist-in-training who helps teach evolutionary biology at the university level. Your antics towards me are amateurish, at best. You remind me of the creationist students who sometimes turn up in our classes looking to be disruptive and preachy, making it difficult for the other students to actually learn anything.

I assure you, you are the one who doesn't understand how science works. Your type never does, and the worst part is you think you do. You perfectly embody both Pauli's "not even wrong" principle, and Hawking's warning that the enemy of knowledge isn't ignorance, but the illusion of knowledge.

You could easily prove me wrong by proposing an experiment design to test an alternative to the lipid hypothesis. Be sure to include an affirmative hypothesis of your own that is quantifiable, makes a prediction, clearly identifies dependent and independent variables, and includes a clear explanation of what constitutes a supportive outcome.

But I won't be holding my breath.

Jimmy Gee said...


Interesting comment:

"I assure you, you are the one who doesn't understand how science works. Your type never does, and the worst part is you think you do. You perfectly embody both Pauli's "not even wrong" principle, and Hawking's warning that the enemy of knowledge isn't ignorance, but the illusion of knowledge."

The reason I find it interesting is the part about "illusion". I think most people who comment here in a manner that does not support this blog's tenents are in fact pointing out the "illusion" that many cited so called "experiments" involving nutrition espouse.

I think RAZZ has a point. There is much uncertainty, and simply re-examining and citing observational studies (epidemiology, meta-analyses, mendelian trials....) can only point in a direction, but are by no means proof.

Healthy Longevity said...


RAZZ like many other people who comment here are either inferring that the evidence linking smoking and passive smoking to chronic diseases is very weak (lack of evidence from large clinical trials), or that they have a completely different set of expectations for what dietary and cholesterol research needs to deliver.

Diethelm et al. published an excellent review addressing the five characteristics of denialism, the forth being the creation of impossible expectations of what research can deliver.

In the early 1990s, Philip Morris tried to promote a new standard, entitled Good Epidemiological Practice (GEP) for the conduct of epidemiological studies. Under the GEP guidelines, odds ratios of 2 or less would not be considered strong enough evidence of causation, invalidating in one sweep a large body of research on the health effects of many exposures. Although Philip Morris eventually scaled back its GEP programme, as no epidemiological body would agree to such a standard, British American Tobacco still uses this criterion to refute the risk associated with passive smoking.

The likes of Colpo and other cholesterol denialists actually make the tobacco industry’s expectations seem permissive, as they typically demand for odd ratios of >3 and even refuse to consider evidence from meta-analyses of over 100 randomized controlled trials. History has shown us that the consequences of such denialism results in the unnecessary loss of millions of lives.

Jimmy Gee said...

@ HL,

Why are you bringing up smoking in regards to RAZZ's posts???

I don't see where RAZZ is talking about this at all.

RAZZ is talking about uncertainty, which is rife in nutritional research and "science" in general.

When evidence builds up on both sides of the argument then the weigh of the evidence (for either side) needs to be questioned.

What courses through our arteries and veins is vastly complex in content and in its interaction with our cells. Reducing something like CAD / CVD to singular components is ludicrous.

Anonymous said...


YOU are the one who does not understand science. CRANKS are the ONLY peole who are certain.

Did YOU know Einstein DOUBTED his OWN theories? Einstein ADMITTED UNKNOWNS DAILY. And how LITTLE we actually know about Nature.

YOU are the crank, Hominoid. Up yours, Peter. Keep quiet, you laughable Internet loser.

The Humane Hominid said...

When evidence builds up on both sides of the argument then the weigh of the evidence (for either side) needs to be questioned.

Nope. A build-up of evidence is considered confirmation of a hypothesis. If there are competing hypotheses, experiments are conducted. The hypothesis with the most evidence is advanced, the one with the least is discarded. Most hypotheses are wrong.

Preponderance of the evidence is how hypotheses become theories. It's not a popularity contest, and scientists do not spend all our time perpetually questioning every single statement someone makes. If the critical mass of evidence supports a statement, we consider it settled and move on.

The thing denialists never get about the scientific method is that it's about reducing uncertainty, not enshrining it.

Jimmy Gee said...


You are a confused individual: You attempt to refute what I am trying to say by using points that actually agree with what I am saying.

Very odd indeed.

Jimmy Gee said...

Again to HH,

The issue at hand is uncertainty. And yes, preponderance of evidence is the path taken to move forward in development and understanding. However, when it comes to nutrition, many open-minded individuals would say that a critical mass of evidence has yet to amass for either side (vegan vs omnivore).

Also, I do not know how long you have been in "research", but I can tell you first-hand that "popularity" can have more to do with establishing a theory than you think.

Anonymous said...

Humane Hominoid does not at all understand the ESSENCE science. EVERYTHING is TENTATIVE. EVERYTHING.

NOBODY who calls himself a scientist should EVER declare that ANY theory is beyond future revision, EVEN DRASTIC REVISION, no matter how solid the support for that theory may seem to him.

I will leave you with quotes from Albert Einstein, a man on another plane intellectually:

"A scientific person will never understand why he should believe opinions only because they are written in a certain book.

Furthermore, he will NEVER believe that the results of his own attempts are final."

- Albert Einstein

"I consider it quite possible that physics cannot be based on the field concept, i.e. on continuous structures.

In that case nothing remains of my entire castle in the air, gravitation theory included, and of the rest of modern physics."

- Albert Einstein

READ AND LEARN THAT Humane Hominoid. Veganism is an unscientific dogmatic CULT- nothing more.

People like Dr. Fuhrman are SCAMMERS. So is Mark Sisson. NONE admit to uncertainty and VAST unknowns about nutrition.

The Humane Hominid said...

@Jimmy Gee:

The hypothesis in question isn't "vegan vs. omnivore." Either one can be healthy. I was referring to "lipid hypothesis vs. (insert alternate claim here)."

I contend that the lipid hypothesis has the preponderance of evidence on its side. Those who wish to overturn it will need much stronger evidence, beginning with dietary factors that correlate better to the diseases in question than saturated fat and cholesterol do. Explaining away the data from animal models will also be a huge hurdle.

@RAZZ -- No one here has declared any theory beyond revision. However, you need to recognize that in the real world, revision of a theory is almost always a simple refinement of its explanatory and predictive power, rather than a complete overhaul.

Established theories are not subjected to major revision without good reason. Einstein, for instance, wasn't some Newton denier who happened to get lucky. He was investigating an actual mystery that Newtonian mechanics (+ Galileo) didn't explain very well. And his discovery did not overturn Newtonian physics, but rather complemented it.

Rejection of an established theory or well-supported hypothesis without stronger evidence on your side is denialism, not skepticism.

Jimmy Gee said...


Yet another interesting statement:
"Rejection of an established theory or well-supported hypothesis without stronger evidence on your side is denialism, not skepticism."

You seem to assume that anyone who is skeptical is automatically rejecting. You also assume that your contention is supported by the most powerful evidence.

You may contend that the lipid hypothesis has the prepondernace of evidence, but simply because I question the interpretation of "preponderance", that I am practicing "denialism".

There are many unanswered observations that cast doubt, leading to skepticism. That doesn't automatically imply denial.

Peter said...

Pathologic denialists are all the same whether the issue at hand is creationism or cholesterol theory.

Evolution denialists maintain that the theoy of evolution is just another faith-based theory with no scientific support. Razz aims to iniate a meta-discourse about science and use it against cholesterol theory. I think it's fair to say that neither Razz nor Jimmy plays the game with a full deck.

Jimmy Ghee,

do you feel like you are in a position where your personal opinions about an universally accepted theory counts? Do you think you have something meaningfull to say about a theory that is advocated by all respected health institutions around the world?

Just like creationists, the cholesterol denialists do not have nothing but infantile speculations to provide as alternative explanation or model. When faced with a meta-analysis regression curve of 108 randomized controlled trials showing that lowering LDL cholesterol significantly reduces coronary events and all cause mortality independent of changes in triglycerides, HDL or the non-lipid lowering effects of various drug classes, the denialists insisist a world wide conspiracy initiated by the "multi-billion dollar" statin industry (who lost all of their exclusive patents already some time ago and has no financial incentive to expand the market anymore than aspirin merchants have).

Luckily for public health major organizations such as Harvard School of Public Health are not hijacked by mentally unstable cranks who refer to Einstein when faced a a meta-analysis regression curve of 108 randomized controlled trials showing that lowering LDL cholesterol significantly reduces coronary events and all cause mortality independent of changes in triglycerides, HDL or the non-lipid lowering effects of various drugs:

"Choose foods with healthy fats, limit foods high in saturated fat, and avoid foods with trans fat""

"Cut back on red meat, cheese, milk, and ice cream. Red meat (beef, pork, lamb) and dairy products are high in saturated fat.


Jimmy Gee said...

@ Ah Peter,

You managed to fulfill my expectations of you; name-calling, the "creationist deflection" and "my study's bigger than your study".

It's not about all the studies you can cite, but the uncertainty brought to the table and ignored by many on this blog.

Go on believing - you must be right - it's all as simple as LDL. Now it (CVD, CHD....) can all be fixed.

I guess time will tell...

Jimmy Gee said...

Oh and Peter,

Linked within the same site you linked to the following can be found.

Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease.

Siri-Tarino PW, Sun Q, Hu FB, Krauss RM.


During 5-23 y of follow-up of 347,747 subjects, 11,006 developed CHD or stroke. Intake of saturated fat was not associated with an increased risk of CHD, stroke, or CVD. The pooled relative risk estimates that compared extreme quantiles of saturated fat intake were 1.07 (95% CI: 0.96, 1.19; P = 0.22) for CHD, 0.81 (95% CI: 0.62, 1.05; P = 0.11) for stroke, and 1.00 (95% CI: 0.89, 1.11; P = 0.95) for CVD. Consideration of age, sex, and study quality did not change the results.

Of course I'm sure you'll comment that the study is irrelevant for some reason.

Healthy Longevity said...


The meta-analysis Peter cites is of such a great size and methodological quality that it would need very powerful evidence to overturn. Simply criticizing him by saying “my study’s bigger than your study” does little. You can raise uncertainty about virtually any established health claim, but doing so as history has shown us typically results in a lost opportunity to save lives.

Perhaps LDL does not explain 100% of CHD cases, but you are trying to downplay the importance of lowering LDL by suggesting that it is not a major CHD risk factor when in fact it is. It has been demonstrated that an 80% reduction in CHD risk could occur by lowering LDL by 2 mmol/L (77.34 mg/dl) early in life. These findings should not be overlooked considering how many lives this could potentially save merely because one enjoys consuming an LDL raising diet.

Large expert panels from prominent health authorities such as WHO-FAO and WCRF-AICR have come to the conclusion that diets should be predominantly plant based. They have not reached such conclusions by engaging in some secretive conspiracy, but by carefully reviewing the evidence.

The Humane Hominid said...


OK, I'll bite: a genuine skeptic can clearly explain what evidence would convince him. So, what realistically-obtainable evidence would convince you of the validity of the lipid hypothesis? Please be as specific as possible.

If you can't do this, you are indeed a denier rather than a skeptic.

Peter said...

"Of course I'm sure you'll comment that the study is irrelevant for some reason".

Well, don't you think that the meta-analysis you cited that was largely based on cross-sectional epidemiology utilizing low-quality questionares with dubious calculation patterns that were revealed by a prominent scientist such as Jeremiah Stamler, was irrelevant given the discussion at hand?

I Actually did the mistake of quating Harvard whose staff is known for harbouring half cranks whose idea of carbohydrate induced dyslipidemia puts them somewhat on a contration position in the biomedical community. Professor Mozzafarian wants us to believe that WHI -trial is higly important evidence showing that overall fat intake does not influence coronary heart disease risk while leaving it for others to pinpoint that the intervention group of WHI tinkered fat from 40% to 30% of calories without showing any difference in the intake of fruits, whole-grains, legumes and vegetables. So far, the biomedical community have not embraced their theory with open arms as Jeremiah Stamler nicely illustrates (see also the response by katan el al:)

Regarding item 8 on macronutrient alternatives to SFA, the current articles (1, 2) express concern about possible unfavorable metabolic influences of carbohydrate—eg, on triglycerides, HDL cholesterol, and small LDL particles. No mention is made of the fact that international epidemiologic data cast doubt as to the generalizability of “carbohydrate-induced dyslipidemia”: eg, Seven Countries Study baseline data (1960s) on Italy and Japan, the latter with dietary total fat of ≈10% of kcal (≈3% SFA, 3% MUFA, 3% PUFA); high, mostly complex, total carbohydrate; favorable serum lipid concentrations; and low CHD rates. Similarly, in the late 1990s (4), macronutrient intakes in Japan and China compared with the United States were higher in total available carbohydrate (54%, 65%, and 49% of kcal, respectively), starch, vegetable protein, alcohol (men); lower (Japan, China compared with the United States) in total fat and SFA (6% and 5% of kcal, respectively), trans fatty acids, cholesterol (China), Keys dietary lipid score, sugars; also lower in BMI (4). Note the amount of SFA (5–6% of kcal), which was an observed finding for the Chinese/Japanese population samples (4); the authors (1) are incorrect in describing recommendations for this amount of SFA as an “extrapolation” without a database. Serum total cholesterol, LDL cholesterol, triglycerides, glycated hemoglobin, uric acid, and fibrinogen were lower in Japanese in Japan than in Japanese Americans in Hawaii, and HDL cholesterol was higher (in men) or as high (in women)—ie, with no evidence of carbohydrate-induced dyslipidemia/metabolic syndrome. Other studies have reported corresponding data from China (7) and from Italy. The current articles (1, 2) also neglect the 3 DASH (Dietary Approaches to Stop Hypertension)/OmniHeart feeding trials (8, 9) in regard to the likely benefit of replacing SFA with complex carbohydrate. The authors are inaccurate in concluding (Abstract; 1) that “there are few epidemiologic or clinical trial data to support a benefit of replacing saturated fat with carbohydrate.”


Anyways, the half-cranks in Harvard are not really challenging the lipid theory, they just try to compliment it, as you can see health authorities such as Harvard with their half-cranks have no problem warning you about the dangers of saturated fat (together with refined carbohydrates).

Frank Hu, the co-author of the meta-analysis you quated, february 2012:

Why is red meat harmful? “Saturated fat, which can lead to cardiovascular disease, is really just the beginning of the story,” explains Hu”


Peter said...

American Heart Association provides great information to us vegetarians

...vegetarian diet can be unhealthy if it contains too many calories and/or saturated fat and not enough important nutrients.

•Protein: You don't need to eat foods from animals to have enough protein in your diet. Plant proteins alone can provide enough of the essential and non-essential amino acids, as long as sources of dietary protein are varied and caloric intake is high enough to meet energy needs.

•Whole grains, legumes, vegetables, seeds and nuts all contain both essential and non-essential amino acids. You don't need to consciously combine these foods ("complementary proteins") within a given meal.


Razz and Ghee aim to sabotage and confuse information that is based on the predespondence of scientific evidence. Denialists such as Jimmy Ghee aim to confuse us and mislead our attention from a meta-analysis regression curve of 108 randomized controlled trials showing that lowering LDL cholesterol significantly reduces coronary events and all cause mortality independent of changes in triglycerides, HDL or the non-lipid lowering effects of various drugs to a meta-analysis (Siri-Tarino et al., 2010) that harbours a major weakness in the form of imprecise dietary assessment methods without even mentation the limitations and shortcomings of the study; about half of the studies used utilized 1-d dietary assessments or some other unvalidated method. As Katan et al. (2010) highlight, food intake varies from day to day, and there is a substantial literature showing that a single 24-h recall provides a poor estimation of the usual dietary intake of an individual.

"Such methods cannot reliably rank individuals by their long-term intake, especially within populations with a uniformly high saturated fat intake. Such imprecision in the assessment of disease determinants systematically reduces the strength of association of determinants with the disease. This is referred to as attenuation or regression dilution bias. Observational studies that used such dietary assessment methods failed to show an association between diet and serum cholesterol concentrations. This shows the shortcomings of such dietary methods, because the effect of diet on serum cholesterol concentrations has been well established in randomized controlled trials. Thus, the lack of a significant association between saturated fat intake and CHD may well reflect the consequences of regression dilution bias"

"We believe that the conclusions of Siri-Tarino et al are invalid and are likely to mislead the general population"

Peter said...

Preponderance of evidence, that is. English not a first language.

Jimmy Gee said...

@ HL, HH and Peter,

You still don't get it:

HH - look up the definition of skepticism instead of imposing your definition.

HL and Peter:

As expected back-pedaling when confronted with the potential that there is more than one possible explanation.

I've said it before:

Readers of this blog beware, and think for yourself.

Anonymous said...

There is NO proponderance of evidence with the cholesterol HYPOTHESIS.

That is the problem

WEIGHT of the evidence is what matters in SCIENCE. Isaac Newton said it himself. WEIGHT of the evidence

The tiniest of veins never become atherosclerotic and they have JUST AS MUCH CHOLESTEROL FLOWING THROUGH THEM as do arteries.

There are major problems with the cholesterol hypothesis and A LOT of WEIGHT behind the CONTRADICTORY evidence.

Science is moving AWAY from the traditional cholesterol hypothesis.

People on here have an EMOTIONAL ATTACHMENT to a DEAD THEORY.

Anonymous said...

Dr. Darisuh Mozaffarian is at least BEING HONEST that there is NO EVIDENCE saturated fat causes CAD.

ONLY PROCESSED meats are linked to CAD.

Healthy Longevity said...


Mozaffarian et al. actually published an updated review very recently based on more recent research regarding the relationship between unprocessed red and processed meats and the risk of CHD and T2D, concluding:
"The overall findings suggest that neither unprocessed red nor processed meat consumption is beneficial for cardiometabolic health, and that clinical and public health guidance should especially prioritize reducing processed meat consumption."

They suggest that heme iron and dietary cholesterol may partly explain why unprocessed red meat is associated with an increased risk of CHD and T2D.

Healthy Longevity said...
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Healthy Longevity said...


Katan et. al asserted in regards to this meta-analysis:
“First, the notion that there exists such a thing as “the effect of saturated fat” is flawed. A lower intake of saturated fat implies an increased intake of some other source of calories to maintain caloric balance. Different substitutions for saturated fat have different effects on risk of coronary heart disease (CHD) and need to be discussed separately.”

Regarding this limitation of the meta-analysis, Hu FB and Sun Q, the two authors of this meta-analysis who do not receive grants from the National Dairy Council that funded this meta-analysis reported elsewhere in a paper they co-authored that:
“however, in this meta-analysis saturated fat was compared with other calorie sources, primarily refined carbohydrates, and high intake of refined carbohydrates has been associated with a high risk of CHD.”

In regards to this meta-analysis Stamler J asserted:

“Of 15 studies that unequivocally concern the SFA-CHD relation, 4 did not include other dietary lipids or serum lipids among covariates. Their CHD relative risks (RRs) ranged from 1.22 to 2.77—ie, >1.07, which was the estimated CHD RR in the meta-analysis (2). Do these larger RRs reflect freedom from confounding and overadjustment?”

“the meta-analysis (2) reported its findings as independent of a quality score including diet assessment. Of the 16 CHD studies, 4 relied on one 24-h dietary recall; the SFA-CHD RR was >1.00 for only one of these studies. Seven used a food-frequency questionnaire (FFQ); the RR was >1.00 in 3 of these studies. Five used dietary history or multiday food record; the RR was >1.00 in all 5 studies, even though 3 were adjusted for serum or dietary lipids (2). These facts, which were unnoted in the meta-analysis (2), prompt the question: Did low-level reliability (reproducibility) of dietary SFA data drive RR values toward 1.00 (the regression-dilution bias problem)? No data on SFA reliability are given.”

“The ability to evaluate the validity of dietary data on free-living people is limited (4); validity was not assessed in the meta-analysis. Also, the meta-analysis says nothing about the problem for the 16 studies of possible bias in SFA-CHD findings due to dietary change (eg, reduced SFA intake) in people with higher serum total cholesterol seeking to lower total cholesterol/CHD risk (as occurred for the earliest of the 16 studies).”


Furthermore Stamler used the same studies and same methodology used in this meta-analysis to show that saturated fat was associated with a 32% increased risk of fatal coronary heart disease, despite the above mentioned limitations which would have likely biased these findings towards null. I see little plausible reason why anyone truly interested in saving lives would omit such a critical detail, and certainly question the motivations of such people.

Perhaps you are able to provide a plausible reason as to why you failed to mention to the readers of this blog of this association between saturated fat and an increased risk of fatal coronary heart disease without trying to change the topic? Do you believe that the reader need not be made aware of such details when trying to make informed dietary decisions? How are they to think for themselves without being provided with these details?

Peter said...

In Razz's crank psyche everything in the surrounding world is uncertain except that butter and saturated fatty acids are safe and have no role in coronary heart disease.

Saturated fats and Inuits.

Consumption of omega-3 fatty acids is not associated with a reduction in carotid atherosclerosis: the Genetics of Coronary Artery Disease in Alaska Natives study

“Dietary intake of omega-3 FAs in a moderate-to-high range does not appear to be associated with reduced plaque, but is negatively associated with IMT.The presence and extent of carotid atherosclerosis among Eskimos is higher with increasing consumption of saturated FAs”.


Jimmy Gee said...

To HL, HH and Peter,

You still just don't get it. My point is "The literature is rife with uncertainty".

The never-ending argument of "THIS study reported failings with THAT study" and the opposing rebuttals only lends support to the issue of uncertainty.

The lipid hypothesis supporters and skeptics are all the same as far as I am concerned because the epidemiological evidence is not cause and effect and cannot possibly account for confounding no matter how much anyone tortures the data. The nutritional epidemiology game is one played out too much on paper with little support in the real world. Confounding will always lead to uncertainty and any statistician worth their weight will tell you that. Even if you artificially inflate the "n" with meta-analyses, you still have that much more potential confounding - even if the inflated "n" yields a "significant" p-value - and I don't care what selection criteria the paper-jockeys use to select studies - they can't possibly know the true effects of confounding.

Epidemiological data-mining can only ever generate ideas/questions to investigate.

Can anyone on this site actually prove that a RR of say, 2, from an epidemiological review (because that's what they really are - just reviews and not true studies) was used to design a truly controlled RCT, in humans, that supported the RR of 2?

Peter said...


being fully aware about the hostility the cholesterol denialist and tobabbo advocates show towards epidemiology, eg. several high-quality prospective cohort studies consisting millions of people and adjusted for regression diluation bias showing the positive, independent and log-linear nature of the association of total serum cholesterol and coronary heart disease and ischemic stroke even within populations that have very low cholesterol levels as the baseline compared to people living in Western societies, I actually cited a meta-analysis regression curve consisting 108 hard clinical randomized controlled trials showing that lowering LDL cholesterol significantly reduces coronary events and all cause mortality independent of changes in triglycerides, HDL or the non-lipid lowering effects of various drug classes.

Jimmy Gee said...


Now you are calling people hostile as well as denialists - amazing.

So to get back on track - Uncertainty is the issue.

BTW - I can't get you link to work.

Jimmy Gee said...


Got the link to work. Looks like another "review" type article - pick some studies, mix together and try to mathematically prove a point.

Even the authors indicate:

"Nevertheless, the relation described by a meta-regression is observational—that is, although the original studies may be randomised trials, a meta-regression across trials does not have the benefit of randomisation to support a causal interpretation and thus risks bias by confounding. Moreover, regression analysis typically ignores the effect of measurement errors in the independent variables."

They attempt to recover with:

"Although this may be problematic to the extent that older studies used less precise methods to determine lipid subfractions, our meta-regression involves mean values of the independent variables. The standard errors of these means are substantially smaller than the standard deviations of individual participants’ values, which should mitigate the problem."

However, I don't see much that would call them certain in their conclusions.

Healthy Longevity said...
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Healthy Longevity said...


What do studies require to show an RR of 2 in order to be informative, are you Philip Morris in disguise?

In the early 1990s, Philip Morris tried to promote a new standard, entitled Good Epidemiological Practice (GEP) for the conduct of epidemiological studies. Under the GEP guidelines, odds ratios of 2 or less would not be considered strong enough evidence of causation, invalidating in one sweep a large body of research on the health effects of many exposures. Although Philip Morris eventually scaled back its GEP programme, as no epidemiological body would agree to such a standard, British American Tobacco still uses this criterion to refute the risk associated with passive smoking.

All large meta-analyses of randomized trials essentially show the same thing, that lowering LDL reduces the risk of CHD and all-cause mortality. As a denialist you would have others believe that scientists have somehow forged the results of dozens of trials as well as the meta-analyses, and that there is some mass conspiracy amongst the scientists and health authorities who have come to the conclusion that there is a causal association between LDL and CHD, in order in to what seems to be to promote an LDL raising diet. This reminds me of how the Flat Earth Society claims also of some mass conspiracy amongst scientists and that the satellite photo’s showing earth as a sphere is “a fraud, a fake, a piece of trickery or deceit,"

All you do is just copy-and-paste limitations of studies that you do not like and then try and have other people believe that they are meaningless so they do not refrain from consuming LDL raising foods. You also ignore very critical details when citing studies you like, such as evidence that SFA increases the risk of fatal CHD (compared to other lower quality sources of energy), but then refuse to respond as to why you omit such critical details.

The Humane Hominid said...


HH - look up the definition of skepticism instead of imposing your definition.


I'm referring to skepticism as a method of inquiry, as defined by the Skeptic's Society.

Like I said, a good skeptic considers evidence as a whole, and knows what evidence would convince him. If you can't pass this simple test, you are a cynic and a denier, not a skeptic.

Also, I think you and RAZZ both missed my point about correlations: if you reject the correlation between LDL and CVD, you have to produce something that correlates more strongly. The mere fact that something is a correlation does not render it useless. Correlations are not frivolous. They are evidence.

Peter said...
This comment has been removed by the author.
Peter said...


the idea of the meta-regression curve is to provide an estimation, not all the dots fall perfectly on the curve in real life, but in this case they fall very closely to the curve meaning that the curve has a high predictive power.

Moreover, you missed the opportunity to place this meta-analysis regression curve consisting of 108 randomized controlled trials showing that lowering LDL cholesterol significantly reduces coronary events and all cause mortality independent of changes in triglycerides, HDL or the non-lipid lowering effects of various drugs, in a meaningfull context, such as the high quality prospective cohort studies including millions of participants and adjusted for regression dilution bias, that I referred to, showing a positive, independent and log-linear association of TC cholesterol and coronary heart disease and ischemic stroke even within population with very low serum cholesterol levels as the baseline and lastly, the mendelian randomized controllod trials consisting over million people showing that prolonged exposure to low LDL since birth dramatically reduces cardiovaslcular mortality consistently and independently of the mechanism used.

Effect of Long-Term Exposure to Lower Low-Density Lipoprotein Cholesterol Beginning Early in Life on the Risk of Coronary Heart Disease:

When we look at the preponderance of evidence, we can clearly estimate that the uncertainty in regards to lipid theory does not really exist, either in real life nor in theory. The uncertainty is only there only in the form denialists with their crank psyche.

Jimmy Gee said...

To HL HH and Peter,

Your posts are so tiring to read, which I'm sure is intentional. You go on and on and on with such misplaced rebuttals to anyone who disagrees. Then you continue to use a less than mature method for communicating.

This will be my last post here as there are many better blogs to contribute to. I'm sure that pleases most on this blog. However, I will state my original intent in responding to the original series.

Uncertainty exists regarding the nutritional epidemiological review of the lipid hypothesis. Does that mean that people should disregard exploration of the concept - not at all. It does mean that those who choose to interpret their meaning as a cause and effect while ignoring the fat that the reviews are observational, are misguided. The best that these reviews can offer is that at times specific combinations of reviews (meta-analyses) reveal an association.

Best of luck to those who believe the problem has been solved and can now rest knowing the absolute path to no heart disease and the like are in their past. Who knows, maybe you are right - of course I'm not certain you really believe it.

The Humane Hominid said...

Uncertainty exists regarding the nutritional epidemiological review of the lipid hypothesis.

You overstate the level uncertainty, and make more of it than it warrants.

Our point is that the lipid hypothesis is NOT BASED SOLELY ON EPIDEMIOLOGY. Or even primarily on it. There is a huge amount of physical and biochemical evidence for it, as well... including all those mechanistic animal studies your kind are so fond of completely ignoring, often despite claiming the mantle of an "evolutionary" perspective on diet and health.

Also, another key point on epidemiology that you guys always ignore: correlations are not created equal. Cholesterol skeptics have a burden of proof to identify factors that correlate better and more consistently than LDL and SF. If they can't do this, they're not skeptics and they're not practicing science. And if they can't do this, the current correlations stand as valid evidence bolstering the physical and biochemical data.

Best of luck to you, too.

Anonymous said...

Dr. Mozaffarian said in his lecture that it is processed meats that are the problem. He never mentioned unprocessed red.

I can put up the link to the lecture.

Healthy Longevity said...

When was this Mozaffarian lecture? I am guessing it is likely based off of the 2010 meta-analysis which only included limited data about fresh red meat. The brand new review covers a lot more recent data including that from the Harvard studies and concluded that both red and processed meats are unfavourable for heart health.

Nevertheless one of the main flaws in Mozaffarian’s arguments is that he typically compares foods such as fresh red meat to all other sources of energy combined, which is typically processed junk food. Such analyses fail to be very informative especially when he fails to mention this limitation. Even if the majority of studies show no association with a certain food compared to all other sources of energy combined, it still likely means that this food is probably unhealthy. This is why every time someone like you on this blog says “there is no relationship between x food and CVD etc.”, it makes it obvious that this person either does not know what they are talking about or are intentionally trying to confuse people.

Anonymous said...

No genuine scientist will point to a hunk of unprocessed meat and say :

"This is he cause of heart disease."

Only 100 % cocksure dogmatic vegans do that. People like Fuhrman, Campbell, etc. These people do NOT represent science- neither does Anthony Colpo

They ALL have an agenda.

I know the essence of science. Too little is known about nutrition for your certitude.

Albert Einstein and Richard Feynman knew science. You would do well to adopt their attitude.

Diana said...


Slaughtering animals is not kind. It is extremely cruel. In fact I've come to think that the whole process of creating livestock is inherently cruel.

What do you think of killing wildlife with one clean shot?

Diana said...

Don, I have another question for you, which I'm sure you'll ignore, as you ignored my first one.

Traditional Chinese medicine, of which you are an adherent, is responsible for most of the rare animal poaching that goes on in the world. (One example: rhino horn.)

How can you can be a vegan and support a system that is based on the slaughter of rare animals?