126 replies to this topic

[Skötkonung]

One gram of protein per kilogram is restricted compared to the average american diet. The source regarding the ketogenic diet for children ( http://www.imminst.o...t...ost&id=6910 ) states that "The typical ratio of fats to carbohydrates and protein (in terms of grams) is 3:1 or 4:1" so protein and carbohydrates are considered equal as antagonists to ketone production.

4:1 is not a low protein diet. It is average. I looked at some ketogenic diets and I found one that is 4:1:1 for Fat, Protein, and Carbohydrate respectively.

1000 calories from fat would mean 250 calories coming form both carbohydrate and protein each. Scale that by a factor of 1.5 to achieve more realistic numbers for an adult male. 1,500 calories from fat and 375 from protein and carbohydrate each. At 4 calories per 1g of protein, that means an adult consuming a 2,250 calorie diet would be consuming 93.75g protein or over 16.67% dietary protein. Not high, but slightly above average compared to most Americans. Carbohydrates are maintained at the same 93.75g, which is enough to induce some level of ketone production, while also allowing for consumption of fruits and vegetables.

1:3 would yield higher results.

Lots of assumptions and guesses. No need for that. Here is an exact description:

Energy distribution:
Fat

90%

LCT

100%

Carbohydrate

1.60 %

Protein

8.40 %

http://www.shsna.com/pages/ketocal.htm

So certainly a low protein diet.

http://www.epilepsy..../ketogenic.html
"The diet provides approximately 90 per cent of the child’s caloric requirement as fat (cream, butter, mayonnaise), one gram per kilogram of body weight as protein, and minimal carbohydrate intake. The diet must be supplemented with vitamins and calcium."

http://indianpediatrics.net/aug2009/669.pdf
This study on the ketogenic diet and epileptics indicates protein was given at the WHO recommendation.

Which comes out to 1g / kg.
http://www.fao.org/docrep/003/AA040E/AA040E09.htm#ch8

So again, a 180lb man consuming 2000 calories a day needs 82g protein daily. That is 328 calories or 15%.

[Blue]

One gram of protein per kilogram is restricted compared to the average american diet. The source regarding the ketogenic diet for children ( http://www.imminst.o...t...ost&id=6910 ) states that "The typical ratio of fats to carbohydrates and protein (in terms of grams) is 3:1 or 4:1" so protein and carbohydrates are considered equal as antagonists to ketone production.

4:1 is not a low protein diet. It is average. I looked at some ketogenic diets and I found one that is 4:1:1 for Fat, Protein, and Carbohydrate respectively.

1000 calories from fat would mean 250 calories coming form both carbohydrate and protein each. Scale that by a factor of 1.5 to achieve more realistic numbers for an adult male. 1,500 calories from fat and 375 from protein and carbohydrate each. At 4 calories per 1g of protein, that means an adult consuming a 2,250 calorie diet would be consuming 93.75g protein or over 16.67% dietary protein. Not high, but slightly above average compared to most Americans. Carbohydrates are maintained at the same 93.75g, which is enough to induce some level of ketone production, while also allowing for consumption of fruits and vegetables.

1:3 would yield higher results.

Lots of assumptions and guesses. No need for that. Here is an exact description:

Energy distribution:
Fat

90%

LCT

100%

Carbohydrate

1.60 %

Protein

8.40 %

http://www.shsna.com/pages/ketocal.htm

So certainly a low protein diet.

http://www.epilepsy..../ketogenic.html
"The diet provides approximately 90 per cent of the child's caloric requirement as fat (cream, butter, mayonnaise), one gram per kilogram of body weight as protein, and minimal carbohydrate intake. The diet must be supplemented with vitamins and calcium."

http://indianpediatrics.net/aug2009/669.pdf
This study on the ketogenic diet and epileptics indicates protein was given at the WHO recommendation.

Which comes out to 1g / kg.
http://www.fao.org/docrep/003/AA040E/AA040E09.htm#ch8

So again, a 180lb man consuming 2000 calories a day needs 82g protein daily. That is 328 calories or 15%.

Again your own dubious calculations and assumptions. FAO is not the same as WHO. FAO does not state 1 g/kg for adults. They state "For adults the protein requirement per kg body weight is considered to be the same for both sexes at all ages and body weights within the acceptable range. The value accepted for the safe level of intake is 0.75 g per kg per day, in terms of proteins with the digestibility of milk or egg."

But again, no need for these homemade claims. We can see the exact energy percent from protein here:

http://www.shsna.com/pages/ketocal.htm

Energy from protein is 8.4% so again a very low protein intake.

[Blue]

More nasty things from the ketogenic diet for children with epilepsy:

"Cardiac complications of the ketogenic diet, in the absence of selenium deficiency, have not been reported. Twenty patients on the ketogenic diet at one institution were investigated. Prolonged QT interval (QTc) was found in 3 patients (15%). There was a significant correlation between prolonged QTc and both low serum bicarbonate and high beta-hydroxybutyrate. In addition, three patients had evidence of cardiac chamber enlargement. One patient with severe dilated cardiomyopathy and prolonged QTc normalized when the diet was discontinued."
http://www.neurology...ract/54/12/2328

QTc, which relates to timing and beat of the heart, is typically abnormal in seizure patients regardless of diet.

The QT interval in epilepsy patients compared to controls
http://neurologyasia...s/20073_068.pdf


Long QT syndrome presenting as epileptic seizures in an adult
"A 50 year old woman with a previous diagnosis of epilepsy presented to the emergency department with a generalised seizure. Her admission ECG showed QT prolongation secondary to bradycardia and a subsequent seizure in the department demonstrated that these events were secondary to cerebral hypoperfusion during episodes of torsades de pointes. This case illustrates how long QT syndrome can masquerade convincingly as epilepsy, delaying treatment and exposing the patient to a high risk of sudden cardiac death. Careful ECG analysis is recommended for all patients presenting with seizures."

The researchers are ignoring the fact that the Inuit lived free of cardiac problems.
http://www.cbc.ca/he...diet010921.html

The first link does not work, the seoncd is a case report which does not claim that QT prolongation is more common among epileptics, the third is a new story and not a study of CVD disease from the traditional Inuit diet.

"Objective It is a common notion that coronary heart disease (CHD) is rare among the Inuit, possibly due to a high intake of omega-3-fatty acids. The scientific evidence for this is weak and to some extent based on uncertain mortality statistic. The aim of this study was to assess the prevalence of markers of CHD among Greenland Inuit, and to study associations between markers of CHD and behavioral and biological variables.Design We studied prevalence of angina pectoris (AP), self-reported myocardial infarction (MI), and ECG defined MI and ischaemia in a population survey among 1316 Inuit living in Greenland. Blood tests were supplemented by structured interviews, anthropometry,and measurements of blood pressure, and the participants received an oral glucose tolerance test.Results The prevalence of symptomatic CHD (AP, self-reported MI) was 7.3% among men and 6.9%among women, and 12.2% and 13.4% of men and women had ischaemic ECG changes. The overall prevalence of CHD (AP+self-reported MI+ECGdefined MI) was 10.8% in men and 10.2% in women. The highest prevalence was observed in the least westernized areas in Greenland. Physicalin activity, low education, dyslipidemia, hypertension and diabetes were associated with CHD. Conclusion The prevalence of markers of CHD was not different from that in Western populations. The Inuit is a population undergoing rapid social and health transitions, with the emergence of cardiovascular risk factors,and there is a need for critical rethinking of cardiovascularepidemiology in this population."
http://linkinghub.el...021915007000494

Edited by Blue, 26 October 2009 - 07:58 AM.

[Blue]

Here is a study which finds lower ischemic disease among Inuits in 1963 than today based on ECG data.

Background The prevalence of coronary heart disease among Greenland Inuit today issimilar to that of western populations. The cardiovascular risk profile among Inuit has changed over the past four decades with the introduction of a western life style. An unaltered prevalence of coronary heart disease has been proposed, but no pre-westernisation data exist.Aim To describe pre-westernisation prevalence of coronary heart disease among East Greenland Inuit.Design A population study of 1851 Inuit living in East Greenland was conducted in 1962–1964. It included ECG, cardiac auscultation and recording of symptoms. ECGs were evaluated for ischemic signs, arrhythmia, hypertrophy, and conduction abnormalities.Results The participation rate was 97%. A12-lead ECG was performed in 181 adults,including 65% of men aged 40 years and above. Hypertrophy was seen in 15% and peaked in 30–39 year olds. Pathological conduction disturbances were seen in 4% and 1% had ischemic signs. The age-standardised prevalence of ischemic ECG findings was 5.5%. Abnormal ECG findings did not correlate with pathologic findings on cardiac auscultation or symptoms related to heart disease. Conclusions Hypertrophy peaked among 30 years olds. Ischemic ECG findings were present in East Greenland Inuit before westernisation, the prevalence clearly lower than today.
http://linkinghub.el...021915008005285

This study has some similarities with the one on the epileptic children. Hypertrophy and conduction disturbances in both cases. These would more likely manifest as sudden death due to arrythmias rather than the usual ischemic syndromes and would likely not be attributed to heart disease until very recently. Of course, the hypertrophy for the Inuits might be due heavy aerobic work, if that was common previously.

Edited by Blue, 26 October 2009 - 12:18 PM.

[rabagley]

I want to go back to this reference for a minute:

"Abstract The aim was to study the effect of a standardized oral fat load (OFL) on different inflammatory parameters in a large sample of adult healthy subjects (n = 286) of both sexes. The fat load was given between 08:00 and 09:00 h after a 12-h fast. [...snip...] We observed that the OFL induces a complex and massive systemic inflammatory response that includes IL-6, TNF-α, hsCRP, and cell adhesion molecules, even before Tg significantly rises."[/b]
http://www.springerl...8n32355687p665/

So yes, carbohydrates cause a postprandial inflammation, but so does fat.

I don't think that anyone even moderately informed about fats would say that fat is an anti-inflammatory substance because "fat" is not one substance. Some fatty acids are anti-inflammatory (most omega-3 FA's), some are pro-inflammatory (most omega-6 FA's), while most fatty acids are neutral on inflammation. Can someone with access to the full article post some details about the specific "standardized oral fat load", ideally the fatty acid breakdown, though a simple list of oils/fats used would be a good start?

I found at least two other "standardized oral fat loads" in literature. One "oral fat load", from 1975, was a "full cream concentrated milk". A more recent "oral fat load", from 2000, was a mixture of:

3.5% dried skimmed milk, 19.25% butter, 23.75% peanut oil, 22% chocolate, 30.25% water, 0.75% gelatin, 0.25% sorbic acid and 0.25% potassium sorbide

That's something to go on at least. The chocolate is ~6% w-6 and 0% w-3, the peanut oil is ~32% w-6 and 0% w-3, most butter has almost no PUFA's. That "standardized oral fat load" is ~9% highly inflammatory w-6 fatty acids with almost no compensating w-3 fatty acids. I would predict an inflammatory response from eating that...

[kismet]

Looks like it was the cream-variety which is rather high in saturated fat? I'd prefer to see high MUFA compared to high SFA or PUFA (or even more specific break downs, but one could certainly dig up interesting papers if one was inclined to do so).
I skimmed the study, unfortunately they didn't include a "placebo" group.

The test drink consisted of 350 ml whipping cream (35% fat), two tablespoons of chocolate-fl avored syrup, one tablespoon of granulated sugar, and one tablespoon of instant nonfat dry milk. This volume contained 1147 kcal, of which 12% was from protein, 20% from carbohydrate, and 68% from fat. It had 472 mg cholesterol and a polyunsaturated/saturated ratio of 0.06. A weight-adjusted meal (1 g fat per kg body weight) was served containing approximately 400 ml of the mixture...

Edited by kismet, 27 October 2009 - 02:17 PM.

[Blue]

I want to go back to this reference for a minute:

"Abstract The aim was to study the effect of a standardized oral fat load (OFL) on different inflammatory parameters in a large sample of adult healthy subjects (n = 286) of both sexes. The fat load was given between 08:00 and 09:00 h after a 12-h fast. [...snip...] We observed that the OFL induces a complex and massive systemic inflammatory response that includes IL-6, TNF-α, hsCRP, and cell adhesion molecules, even before Tg significantly rises."[/b]
http://www.springerl...8n32355687p665/

So yes, carbohydrates cause a postprandial inflammation, but so does fat.

I don't think that anyone even moderately informed about fats would say that fat is an anti-inflammatory substance because "fat" is not one substance. Some fatty acids are anti-inflammatory (most omega-3 FA's), some are pro-inflammatory (most omega-6 FA's), while most fatty acids are neutral on inflammation. Can someone with access to the full article post some details about the specific "standardized oral fat load", ideally the fatty acid breakdown, though a simple list of oils/fats used would be a good start?

I found at least two other "standardized oral fat loads" in literature. One "oral fat load", from 1975, was a "full cream concentrated milk". A more recent "oral fat load", from 2000, was a mixture of:

3.5% dried skimmed milk, 19.25% butter, 23.75% peanut oil, 22% chocolate, 30.25% water, 0.75% gelatin, 0.25% sorbic acid and 0.25% potassium sorbide

That's something to go on at least. The chocolate is ~6% w-6 and 0% w-3, the peanut oil is ~32% w-6 and 0% w-3, most butter has almost no PUFA's. That "standardized oral fat load" is ~9% highly inflammatory w-6 fatty acids with almost no compensating w-3 fatty acids. I would predict an inflammatory response from eating that...

Well, in this sense carbohydrates are also neutral regarding inflammation. The studies quoted looked only at postprandial inflammation after a meal. Not more long-term changes caused by consuming a particular diet for weeks or months.

Different researchers seem to use different fat loads.

[Blue]

Looks like it was the cream-variety which is rather high in saturated fat? I'd prefer to see high MUFA compared to high SFA or PUFA (or even more specific break downs, but one could certainly dig up interesting papers if one was inclined to do so).
I skimmed the study, unfortunately they didn't include a "placebo" group.

The test drink consisted of 350 ml whipping cream (35% fat), two tablespoons of chocolate-fl avored syrup, one tablespoon of granulated sugar, and one tablespoon of instant nonfat dry milk. This volume contained 1147 kcal, of which 12% was from protein, 20% from carbohydrate, and 68% from fat. It had 472 mg cholesterol and a polyunsaturated/saturated ratio of 0.06. A weight-adjusted meal (1 g fat per kg body weight) was served containing approximately 400 ml of the mixture...

I had hoped they used a pure fat meal.

[rabagley]

Looks like it was the cream-variety which is rather high in saturated fat? I'd prefer to see high MUFA compared to high SFA or PUFA (or even more specific break downs, but one could certainly dig up interesting papers if one was inclined to do so).
I skimmed the study, unfortunately they didn't include a "placebo" group.

The test drink consisted of 350 ml whipping cream (35% fat), two tablespoons of chocolate-fl avored syrup, one tablespoon of granulated sugar, and one tablespoon of instant nonfat dry milk. This volume contained 1147 kcal, of which 12% was from protein, 20% from carbohydrate, and 68% from fat. It had 472 mg cholesterol and a polyunsaturated/saturated ratio of 0.06. A weight-adjusted meal (1 g fat per kg body weight) was served containing approximately 400 ml of the mixture...

I had hoped they used a pure fat meal.

Exactly. That "standardized oral fat load" is pretty high in fructose and glucose in those highly processed sugars and while glucose is not directly pro-inflammatory, fructose is. The liver will stop all other activity to convert fructose into free triglycerides until complete (fructose is 10x as reactive as glucose in sugar-protein reactions and your liver seems to consider it toxic enough to focus on it to the exclusion of all other risks).

This "detail" should have been in the abstract and people could see what these researchers thought constituted a "fair" fat load. Yikes.

[rabagley]

Looks like it was the cream-variety which is rather high in saturated fat? I'd prefer to see high MUFA compared to high SFA or PUFA (or even more specific break downs, but one could certainly dig up interesting papers if one was inclined to do so).
I skimmed the study, unfortunately they didn't include a "placebo" group.

The test drink consisted of 350 ml whipping cream (35% fat), two tablespoons of chocolate-fl avored syrup, one tablespoon of granulated sugar, and one tablespoon of instant nonfat dry milk. This volume contained 1147 kcal, of which 12% was from protein, 20% from carbohydrate, and 68% from fat. It had 472 mg cholesterol and a polyunsaturated/saturated ratio of 0.06. A weight-adjusted meal (1 g fat per kg body weight) was served containing approximately 400 ml of the mixture...

Thanks for the info. Yeah, cream is quite high in SFA, but those don't bother me. Most SFA's are neutral or beneficial to overall health, and outside of rare circumstances, they don't contribute to inflammatory processes. On the control group, in these short-term effects studies, the subjects generally act as their own controls. They repeat the test two or four times, and for half of the trials don't provide the fat load and then make the same measurements on the same schedule. It's not a real control since it lacks ingestion, but it's accepted practice in these postprandial studies.

Which does lead to another question. Anxiety is pro-inflammatory and in our modern culture, people are terrified of fat. I wonder if the subjects' conversations around eating a heavy, rich drink might have increased their inflammatory markers... I change my mind, I want a placebo drink too!

Edited by rabagley, 27 October 2009 - 05:11 PM.

[Blue]

Most SFA's are neutral or beneficial to overall health

http://www.imminst.o...pid-t33878.html

Edited by Blue, 27 October 2009 - 05:23 PM.

[rabagley]

Most SFA's are neutral or beneficial to overall health

http://www.imminst.o...pid-t33878.html

The human studies you list have the classic problem of grouping trans-fatty acids and saturated fatty acids into one category of fats and presenting the results as if there is some similarity between the two after consumption. Since this was widely believed until only a few years ago, this is a very common mistake in almost all studies of fat until just recently. In fact, you'll still see it in animal studies since the chow recipes have resisted change more than human beings.

Most of the recent data indicates that TFA's are so dangerous that any study that allows them in the same category with any other mix of fats will show substantial negative effects in that category, so the assumptions in the studies you mention are not sound and all results that don't differentiate between TFA intake and SFA intake (butter and margarine added into one result on the questionnaire, for instance) are grossly invalid.

I would be interested in seeing any study which successfully distinguished between TFA's and SFA's and still reached the same conclusions as those. Until then, I do not consider any of the studies you quoted to actually substantiate a claim that SFA's are anything but neutral or rarely beneficial. This is a bit of a trap that I've laid out for you, as you'll find that modern studies which successfully avoid obvious confounders will substantiate my claims. Most of the associations between SFA intake and positive or negative effects are insignificant, though there are a few, like the effects of lauric acid to upregulate large particle HDL and large particle LDL where there is a significant positive effect.

[Blue]

Most SFA's are neutral or beneficial to overall health

http://www.imminst.o...pid-t33878.html

The human studies you list have the classic problem of grouping trans-fatty acids and saturated fatty acids into one category of fats and presenting the results as if there is some similarity between the two after consumption. Since this was widely believed until only a few years ago, this is a very common mistake in almost all studies of fat until just recently. In fact, you'll still see it in animal studies since the chow recipes have resisted change more than human beings.

Most of the recent data indicates that TFA's are so dangerous that any study that allows them in the same category with any other mix of fats will show substantial negative effects in that category, so the assumptions in the studies you mention are not sound and all results that don't differentiate between TFA intake and SFA intake (butter and margarine added into one result on the questionnaire, for instance) are grossly invalid.

I would be interested in seeing any study which successfully distinguished between TFA's and SFA's and still reached the same conclusions as those. Until then, I do not consider any of the studies you quoted to actually substantiate a claim that SFA's are anything but neutral or rarely beneficial. This is a bit of a trap that I've laid out for you, as you'll find that modern studies which successfully avoid obvious confounders will substantiate my claims. Most of the associations between SFA intake and positive or negative effects are insignificant, though there are a few, like the effects of lauric acid to upregulate large particle HDL and large particle LDL where there is a significant positive effect.

They do not group trans fat and saturated into one category. Regarding "modern studies which successfully avoid obvious confounders will substantiate my claims.", sources please. No, I am not going to do your job for you.

Edited by Blue, 27 October 2009 - 08:52 PM.

[rabagley]

Most SFA's are neutral or beneficial to overall health

http://www.imminst.o...pid-t33878.html

The human studies you list have the classic problem of grouping trans-fatty acids and saturated fatty acids into one category of fats and presenting the results as if there is some similarity between the two after consumption. Since this was widely believed until only a few years ago, this is a very common mistake in almost all studies of fat until just recently. In fact, you'll still see it in animal studies since the chow recipes have resisted change more than human beings.

Most of the recent data indicates that TFA's are so dangerous that any study that allows them in the same category with any other mix of fats will show substantial negative effects in that category, so the assumptions in the studies you mention are not sound and all results that don't differentiate between TFA intake and SFA intake (butter and margarine added into one result on the questionnaire, for instance) are grossly invalid.

I would be interested in seeing any study which successfully distinguished between TFA's and SFA's and still reached the same conclusions as those. Until then, I do not consider any of the studies you quoted to actually substantiate a claim that SFA's are anything but neutral or rarely beneficial. This is a bit of a trap that I've laid out for you, as you'll find that modern studies which successfully avoid obvious confounders will substantiate my claims. Most of the associations between SFA intake and positive or negative effects are insignificant, though there are a few, like the effects of lauric acid to upregulate large particle HDL and large particle LDL where there is a significant positive effect.

They do not group trans fat and saturated into one category. Regarding "modern studies which successfully avoid obvious confounders will substantiate my claims.", sources please. No, I am not going to do your job for you.

All epidemiological studies of that age mixed together TFA's and SFA's because it has been impossible to separate them for most processed foods until the labelling requirements changed and the basic mechanism of food questionnaires doesn't allow enough specificity or accuracy to look for high or low TFA variants. Further, that mixing is one of the classic problems with food questionnaires where people were not trained to be careful about distinguishing between butter and margarine, even if there were separate spaces on the form.

As for SFA's and health recast into modern studies, I know of a few offhand.

http://www.ncbi.nlm....ogdbfrom=pubmed

Additional analysis of the seven countries study:

http://thepaleodiet......gust 2009.pdf

Well referenced short article on low-carb, diabetes, etc.

http://www.diabetesh...st/?section=301

For a laundry list of studies showing beneficial or neutral effects of SFA's, I'm going to punt you over to a somewhat hyperbolic (but very broadly informed) blogging doctor:

http://drbganimalpha...crpola-out.html

Observed regression of arterial plaque on a high-fat diet:

http://drbganimalpha...framingham.html

Butter (butyric acid) moderates Lp(a) levels (significant correlate with CHD), better than other oils.

http://drbganimalpha...ngerous-at.html

[Blue]

Most SFA's are neutral or beneficial to overall health

http://www.imminst.o...pid-t33878.html

The human studies you list have the classic problem of grouping trans-fatty acids and saturated fatty acids into one category of fats and presenting the results as if there is some similarity between the two after consumption. Since this was widely believed until only a few years ago, this is a very common mistake in almost all studies of fat until just recently. In fact, you'll still see it in animal studies since the chow recipes have resisted change more than human beings.

Most of the recent data indicates that TFA's are so dangerous that any study that allows them in the same category with any other mix of fats will show substantial negative effects in that category, so the assumptions in the studies you mention are not sound and all results that don't differentiate between TFA intake and SFA intake (butter and margarine added into one result on the questionnaire, for instance) are grossly invalid.

I would be interested in seeing any study which successfully distinguished between TFA's and SFA's and still reached the same conclusions as those. Until then, I do not consider any of the studies you quoted to actually substantiate a claim that SFA's are anything but neutral or rarely beneficial. This is a bit of a trap that I've laid out for you, as you'll find that modern studies which successfully avoid obvious confounders will substantiate my claims. Most of the associations between SFA intake and positive or negative effects are insignificant, though there are a few, like the effects of lauric acid to upregulate large particle HDL and large particle LDL where there is a significant positive effect.

They do not group trans fat and saturated into one category. Regarding "modern studies which successfully avoid obvious confounders will substantiate my claims.", sources please. No, I am not going to do your job for you.

All epidemiological studies of that age mixed together TFA's and SFA's because it has been impossible to separate them for most processed foods until the labelling requirements changed and the basic mechanism of food questionnaires doesn't allow enough specificity or accuracy to look for high or low TFA variants. Further, that mixing is one of the classic problems with food questionnaires where people were not trained to be careful about distinguishing between butter and margarine, even if there were separate spaces on the form.

As for SFA's and health recast into modern studies, I know of a few offhand.

http://www.ncbi.nlm....ogdbfrom=pubmed

Additional analysis of the seven countries study:

http://thepaleodiet......gust 2009.pdf

Well referenced short article on low-carb, diabetes, etc.

http://www.diabetesh...st/?section=301

For a laundry list of studies showing beneficial or neutral effects of SFA's, I'm going to punt you over to a somewhat hyperbolic (but very broadly informed) blogging doctor:

http://drbganimalpha...crpola-out.html

Observed regression of arterial plaque on a high-fat diet:

http://drbganimalpha...framingham.html

Butter (butyric acid) moderates Lp(a) levels (significant correlate with CHD), better than other oils.

http://drbganimalpha...ngerous-at.html

You are actually arguing that they could not separate trans fats and saturated fats in 2003? Only one of the studies is older than than. Epidemiological studies do not base their claims on food lablels. Instead they use food testing databases which certainly included trans fats in 2002. One example:
http://www.agingeye....en/transfat.php

Regarding you opinion that these peer-reviewed studies used poor food questionaires, do you have an actual good source substantiating that?

You cited a study arguing that dairy food consumption may not be associated with CVD. What has that do with saturated fats in general and cognitive decline?

Then there is a study regarding a "unified theory" for fat quality and coronary heart disease prevention. One of its conclusions statea: "High consumption of palmitate may increase CHD risk. The relationship of stearate, laurate, and myristate to CHD is less clear. Partial substitution of MUFAs for palmitate, and perhaps other SFAs, may reduce CHD risk and is unlikely to cause harm."!!! Regardless, again a study on CVD, not cognitive decline.

Then there is a lecture about low-carbohydrate diets. What has that to do with saturated fats and cognitive decline? Neither is mentioned.

Then there is a link to blog discussing various studies. Most looks to be looking at lab tests or short-term outcomes such as weight loss. Not what is really important, mortality and morbidity. Cannot see that any of them discuss cognitive decline.

Then another blog and a case report about a patient taking niacin and statins and maybe having a diet change which caused some plaque regression. Certainly not evidence for anything regarding diet.

Then yet another blog now about Lp(a). Lp(a) is dangerous to those with high ldl which likely includes those on a high fat diet. The treatment for high lp(a) is lowering ldl. There are no studies showing that lowering lp(a) itself is good.
http://www.mayoclini...8/june-06b.html

Edited by Blue, 27 October 2009 - 10:20 PM.

[rabagley]

...snip...

Thanks for taking the time to read that, though you clearly skimmed the blog entries. All I was substantiating was the assertion that SFA's are either neutral or occasionally beneficial. Wasn't necessarily trying to contradict some of the specifics you mentioned.

As for lowering LDL as a means of reducing CVD risk, I'm not convinced there is any significant benefit (http://content.onlin.../full/44/5/1009), though raising HDL does seem to be significant (to raise HDL consume lauric acid, niacin). Increasing the average size of LDL particles also seems to have a benefit (http://www.cli-onlin...dex.php?id=2120) (to increase LDL particle size: consume palmitic acid, niacin, eliminate fructose). The mention of Lp(a) was part of a description of athersclerosis reversal. Perhaps the Lp(a) lowering was incidental to the process, but the fact that it was lowest during the reversal process in all known cases of reversal makes me perk up. Also, Lp(a) does seem to have it's own distinct correlation with CVD risk (http://www.mayoclini...8/june-06b.html) even if it is smaller than the correlation for LDL (to lower Lp(a), consume butyric acid, niacin).

As for the blog, that one doctor is one of a small group of doctors (Track Your Plaque) getting athersclerotic reversal through diet (wheat free, low carb, high fat, whole foods), niacin, Vitamin D3, and fish oil. Blood lipid targets: free TriG 60 mg/dl, LDL-C 60 mg/dl large particles, HDL 60 mg/dl large particles, D3 60ng/ml, Lp(a) 0. Though not everyone gets reversal, just about everyone stops further atheroma growth. And many individuals are observing reductions in the measured size of atheromas, without statins or any other prescription drugs, and perhaps most surprising to those who believe in the lipid hypothesis, it happens only on a high-fat, high-saturated-fat, high-dietary-cholesterol diet. Other cardiologists don't believe that reversal is possible or that it is a spontaneous process that defies explanation. I'm going with the group actually getting reversal.

[Blue]

Thanks for taking the time to read that, though you clearly skimmed the blog entries. All I was substantiating was the assertion that SFA's are either neutral or occasionally beneficial. Wasn't necessarily trying to contradict some of the specifics you mentioned.

Claims certainly not substantiated. You may be under the impression that the paleo blogs reflect the current scientific consensus. They do no. Their usual tactic is to rely on short-term changes in variables such as dubious lab markerrs (lp(a)) is one example as noted above) or short-term weight loss. They usually ignore studies regarding what is important, morbidity and mortality studies, such as these collected from some of my previous discussions:

"The quality of dietary fat in relation to cardiovascular disease forms the basis of the diet-heart hypothesis. Current recommendations on dietary fat now emphasise quality rather than quantity. The focus of this review is to summarise the results from prospective cohort studies on dietary fat and cardiovascular disease outcomes. Relatively few prospective cohort studies have found an association between dietary fat quality and cardiovascular disease, partly because of limitations in estimating dietary intake. Saturated and trans fatty acids have increased cardiovascular risk in several studies. Both n-6 and n-3 polyunsaturated fatty acids have been associated with lower cardiovascular risk. Within the n-6 series, linoleic acid seems to decrease cardiovascular risk. Within the n-3 series the long-chain fatty acids (eicosapentaenoic and docosahexaenoic acids) are associated with decreased risk for especially fatal coronary outcomes, whereas the role of alpha-linolenic acid is less clear. Dietary fat quality also influences the activity of enzymes involved in the desaturation of fatty acids in the body. Serum desaturase indices have been consistently associated with adverse cardiovascular outcomes. Data from metabolic and clinical studies reinforce findings from observational studies supporting recommendations to replace saturated and trans fat with unsaturated fat in the prevention of cardiovascular disease."
http://www.ncbi.nlm....pubmed/18328267

"OBJECTIVES: To determine by how much statins reduce serum concentrations of low density lipoprotein (LDL) cholesterol and incidence of ischaemic heart disease (IHD) events and stroke, according to drug, dose, and duration of treatment. DESIGN: Three meta-analyses: 164 short term randomised placebo controlled trials of six statins and LDL cholesterol reduction; 58 randomised trials of cholesterol lowering by any means and IHD events; and nine cohort studies and the same 58 trials on stoke. MAIN OUTCOME MEASURES: Reductions in LDL cholesterol according to statin and dose; reduction in IHD events and stroke for a specified reduction in LDL cholesterol. RESULTS: Reductions in LDL cholesterol (in the 164 trials) were 2.8 mmol/l (60%) with rosuvastatin 80 mg/day, 2.6 mmol/l (55%) with atorvastatin 80 mg/day, 1.8 mmol/l (40%) with atorvastatin 10 mg/day, lovastatin 40 mg/day, simvastatin 40 mg/day, or rosuvastatin 5 mg/day, all from pretreatment concentrations of 4.8 mmol/l. Pravastatin and fluvastatin achieved smaller reductions. In the 58 trials, for an LDL cholesterol reduction of 1.0 mmol/l the risk of IHD events was reduced by 11% in the first year of treatment, 24% in the second year, 33% in years three to five, and by 36% thereafter (P < 0.001 for trend). IHD events were reduced by 20%, 31%, and 51% in trials grouped by LDL cholesterol reduction (means 0.5 mmol/l, 1.0 mmol/l, and 1.6 mmol/l) after results from first two years of treatment were excluded (P < 0.001 for trend). After several years a reduction of 1.8 mmol/l would reduce IHD events by an estimated 61%. Results from the same 58 trials, corroborated by results from the nine cohort studies, show that lowering LDL cholesterol decreases all stroke by 10% for a 1 mmol/l reduction and 17% for a 1.8 mmol/l reduction. Estimates allow for the fact that trials tended to recruit people with vascular disease, among whom the effect of LDL cholesterol reduction on stroke is greater because of their higher risk of thromboembolic stroke (rather than haemorrhagic stroke) compared with people in the general population. CONCLUSIONS: Statins can lower LDL cholesterol concentration by an average of 1.8 mmol/l which reduces the risk of IHD events by about 60% and stroke by 17%."
http://www.ncbi.nlm....pubmed/12829554

"Objective: To assess the effect of reduction or modification of dietary fat intake on total and cardiovascular mortality and cardiovascular morbidity.
Design: Systematic review.
Data sources: Cochrane Library, Medline, Embase, CAB abstracts, SIGLE, CVRCT registry, and biographies were searched; trials known to experts were included.
Included studies: Randomised controlled trials stating intention to reduce or modify fat or cholesterol intake in healthy adult participants over at least six months. Inclusion decisions, validity, and data extraction were duplicated. Meta-analysis (random effects methodology), meta-regression, and funnel plots were performed.
Results: 27 studies (30 902 person years of observation) were included. Alteration of dietary fat intake had small effects on total mortality (rate ratio 0.98; 95% confidence interval 0.86 to 1.12). Cardiovascular mortality was reduced by 9% (0.91; 0.77 to 1.07) and cardiovascular events by 16% (0.84; 0.72 to 0.99), which was attenuated (0.86; 0.72 to 1.03) in a sensitivity analysis that excluded a trial using oily fish. Trials with at least two years' follow up provided stronger evidence of protection from cardiovascular events (0.76; 0.65 to 0.90).
Conclusions: There is a small but potentially important reduction in cardiovascular risk with reduction or modification of dietary fat intake, seen particularly in trials of longer duration."
http://www.bmj.com/c...ct/322/7289/757

"BACKGROUND: Results of previous randomised trials have shown that interventions that lower LDL cholesterol concentrations can significantly reduce the incidence of coronary heart disease (CHD) and other major vascular events in a wide range of individuals. But each separate trial has limited power to assess particular outcomes or particular categories of participant. METHODS: A prospective meta-analysis of data from 90,056 individuals in 14 randomised trials of statins was done. Weighted estimates were obtained of effects on different clinical outcomes per 1.0 mmol/L reduction in LDL cholesterol. FINDINGS: During a mean of 5 years, there were 8186 deaths, 14,348 individuals had major vascular events, and 5103 developed cancer. Mean LDL cholesterol differences at 1 year ranged from 0.35 mmol/L to 1.77 mmol/L (mean 1.09) in these trials. There was a 12% proportional reduction in all-cause mortality per mmol/L reduction in LDL cholesterol (rate ratio [RR] 0.88, 95% CI 0.84-0.91; p<0.0001). This reflected a 19% reduction in coronary mortality (0.81, 0.76-0.85; p<0.0001), and non-significant reductions in non-coronary vascular mortality (0.93, 0.83-1.03; p=0.2) and non-vascular mortality (0.95, 0.90-1.01; p=0.1). There were corresponding reductions in myocardial infarction or coronary death (0.77, 0.74-0.80; p<0.0001), in the need for coronary revascularisation (0.76, 0.73-0.80; p<0.0001), in fatal or non-fatal stroke (0.83, 0.78-0.88; p<0.0001), and, combining these, of 21% in any such major vascular event (0.79, 0.77-0.81; p<0.0001). The proportional reduction in major vascular events differed significantly (p<0.0001) according to the absolute reduction in LDL cholesterol achieved, but not otherwise. These benefits were significant within the first year, but were greater in subsequent years. Taking all years together, the overall reduction of about one fifth per mmol/L LDL cholesterol reduction translated into 48 (95% CI 39-57) fewer participants having major vascular events per 1000 among those with pre-existing CHD at baseline, compared with 25 (19-31) per 1000 among participants with no such history. There was no evidence that statins increased the incidence of cancer overall (1.00, 0.95-1.06; p=0.9) or at any particular site. INTERPRETATION: Statin therapy can safely reduce the 5-year incidence of major coronary events, coronary revascularisation, and stroke by about one fifth per mmol/L reduction in LDL cholesterol, largely irrespective of the initial lipid profile or other presenting characteristics. The absolute benefit relates chiefly to an individual's absolute risk of such events and to the absolute reduction in LDL cholesterol achieved. These findings reinforce the need to consider prolonged statin treatment with substantial LDL cholesterol reductions in all patients at high risk of any type of major vascular event."
http://www.ncbi.nlm....pubmed/16214597

"Aims/hypothesis The aim of this study was to investigate the association of dietary macronutrient composition and energy density with the change in body weight and waist circumference and diabetes incidence in the Finnish Diabetes Prevention Study.Subjects and methods Overweight, middle-aged men (n=172) and women (n=350) with impaired glucose tolerance were randomised to receive either 'standard care' (control) or intensive dietary and exercise counselling. Baseline and annual examinations included assessment of dietary intake with 3-day food records and diabetes status by repeated 75-g OGTTs. For these analyses the treatment groups were combined and only subjects with follow-up data (n=500) were included.<a name="ASec3">Results Individuals with low fat (<median) and high fibre (>median) intakes lost more weight compared with those consuming a high-fat (>median), low-fibre (<median) diet (3.1 vs 0.7 kg after 3 years). In separate models, hazard ratios for diabetes incidence during a mean follow-up of 4.1 years were (highest compared with lowest quartile) 0.38 (95% CI 0.19–0.77) for fibre intake, 2.14 (95% CI 1.16–3.92) for fat intake, and 1.73 (95% CI 0.89–3.38) for saturated-fat intake, after adjustment for sex, intervention assignment, weight and weight change, physical activity, baseline 2-h plasma glucose and intake of the nutrient being investigated. Compared with the low-fat/high-fibre category, hazard ratios were 1.98 (95% CI 0.98–4.02), 2.68 (95% CI 1.40–5.10), and 1.89 (95% CI 1.09–3.30) for low-fat/low-fibre, high-fat/high-fibre, and high-fat/low-fibre, respectively.Conclusions/interpretation Dietary fat and fibre intake are significant predictors of sustained weight reduction and progression to type 2 diabetes in high-risk subjects, even after adjustment for other risk factors."
http://www.springerl...670082865607x6/

"BACKGROUND: Some previous prospective studies showed that dietary intake of omega3 polyunsaturated fatty acids was associated with lower risk of heart failure (HF), but no study has examined the association between plasma fatty acids and HF. METHODS: We included 3,592 white participants from the Minneapolis field center of the Atherosclerosis Risk in Communities (ARIC) Study, aged 45 to 64 at baseline (1987-1989), initially free of coronary heart disease, stroke, and HF and who had cholesterol ester and phospholipid plasma fatty acids measured. Participants were followed through 2003, and incident HF was defined by a hospital discharge or death including a HF International Classification of Diseases code. RESULTS: During the 14.3-year follow-up, we identified 197 cases of HF (110 for men and 87 for women). After adjustment for age and other confounders, higher saturated fatty acids, especially myristic (14:0) acid, were associated positively with incident HF in both men and women. Higher arachidonic (20:3,omega6) and long-chain omega3 polyunsaturated fatty acids, especially docosahexaenoic (22:6,omega3) acid, were associated inversely with HF in women but not in men. Neither plasma alpha-linolenic nor eicosapentaenoic acid was associated with incident HF. CONCLUSIONS: In both men and women, greater levels of saturated fatty acids may increase risk of HF. In women, arachidonic acid and long-chain omega3 polyunsaturated fatty acids may decrease risk of HF."
http://www.ncbi.nlm....pubmed/19061714

As for lowering LDL as a means of reducing CVD risk, I'm not convinced there is any significant benefit (http://content.onlin.../full/44/5/1009), though raising HDL does seem to be significant (to raise HDL consume lauric acid, niacin). Increasing the average size of LDL particles also seems to have a benefit (http://www.cli-onlin...dex.php?id=2120) (to increase LDL particle size: consume palmitic acid, niacin, eliminate fructose). The mention of Lp(a) was part of a description of athersclerosis reversal. Perhaps the Lp(a) lowering was incidental to the process, but the fact that it was lowest during the reversal process in all known cases of reversal makes me perk up. Also, Lp(a) does seem to have it's own distinct correlation with CVD risk (http://www.mayoclini...8/june-06b.html) even if it is smaller than the correlation for LDL (to lower Lp(a), consume butyric acid, niacin).

As for the blog, that one doctor is one of a small group of doctors (Track Your Plaque) getting athersclerotic reversal through diet (wheat free, low carb, high fat, whole foods), niacin, Vitamin D3, and fish oil. Blood lipid targets: free TriG 60 mg/dl, LDL-C 60 mg/dl large particles, HDL 60 mg/dl large particles, D3 60ng/ml, Lp(a) 0. Though not everyone gets reversal, just about everyone stops further atheroma growth. And many individuals are observing reductions in the measured size of atheromas, without statins or any other prescription drugs, and perhaps most surprising to those who believe in the lipid hypothesis, it happens only on a high-fat, high-saturated-fat, high-dietary-cholesterol diet. Other cardiologists don't believe that reversal is possible or that it is a spontaneous process that defies explanation. I'm going with the group actually getting reversal.

Regarding the blog doctor, with multiple supplement and diet changes it is impossible to tell what is the effect of the diet. For example, there are many case reports that high-dose D3 by itself will greatly increase HDL, far greater increases than the small change on HDL seen from lowering carbohydrates seen in studies.

Regarding what lab markers are important for CVD, see this 2008 consensus statement by the American Diabetes Association and the American College of Cardiology Foundation
http://content.onlin...acc.2008.02.034

Some extracts:
"A large body of research, ranging from molecular to population studies, indicates that elevated LDL cholesterol is a major predictor of CVD, including in populations with CMR or diabetes. ^"

"The size of LDL particles can also be measured. As small dense LDL particles seem to be particularly atherogenic (30), assessment of particle size has intuitive appeal. Both LDL particle concentration and LDL size are important predictors of CVD (31). However, the Multi-Ethnic Study of Atherosclerosis suggested that on multivariate analyses, both small and large LDL were strongly associated with carotid intima-media thickness (24), while the Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial (VA-HIT) showed that both were significantly related to coronary heart disease (CHD) events (28). The association of small LDL and CVD may simply reflect the increased number of LDL particles in patients with small LDL. Hence, it is unclear whether LDL particle size measurements add value to measurement of LDL particle concentration."

" Lipoprotein(a) [Lp(a)], an apoB-containing LDL-like particle with enhanced binding to intimal proteoglycans and prothrombotic effect, also predicts CVD. There is little evidence that insulin resistance or diabetes influences Lp(a) concentrations. The clinical utility of routine measurement of Lp(a) is unclear, although more aggressive control of other lipoprotein parameters may be warranted in those with high concentrations of Lp(a)."

"Measurements of HDL subfractions or apoA1 appear to provide little clinical value beyond measurements of HDL cholesterol (49)."

"In the fasting state, plasma triglycerides are primarily found in VLDL, so plasma triglyceride measurements are used as a surrogate measure of VLDL. Triglycerides are a univariate predictor of CVD in many studies but often not an independent predictor in multivariate analyses. This may be because triglycerides are highly linked to abnormalities in HDL and LDL and because of high biological and laboratory variability. Similarly, there are no clinical trial data establishing that lowering triglycerides in individuals with or without diabetes independently leads to lower CVD event rates when one adjusts for changes in HDL cholesterol. Chylomicron remnants may be atherogenic in a manner similar to VLDL remnants. There is little population-based evidence that chylomicron remnants are linked to CVD, but several studies show consistent elevations of chylomicron remnants in individuals with familial combined hyperlipidemia and diabetes, conditions associated with atherosclerosis. Measures of chylomicron remnants are not readily available."

In short, the favorite lab tests the paleo blogs like to cite (except HDL) as support are of little value.

Edited by Blue, 28 October 2009 - 04:28 PM.

[oehaut]

I'd just like to point a few facts that makes it no so easy to blame SFA.

There's a bunch of population consuming high-animal-fat diet that don't have much CVD

1. The Masai http://www.ncbi.nlm....p;ordinalpos=7
2. The Polynesian http://www.ncbi.nlm....mp;ordinalpos=4
3. The samburu http://www.ncbi.nlm.nih.gov/pubmed/1391127...$=activity
4. The French http://www.ncbi.nlm....mp;ordinalpos=4
5. The Spanish http://www.ncbi.nlm.nih.gov/pubmed/7754987...$=activity
6. Sweden http://www.ncbi.nlm.nih.gov/pubmed/490089?log$=activity

There's also population consuming low amount of animal fat diet and still have high CVD

1. The Jews in Israel http://www.ncbi.nlm....mp;ordinalpos=8

2. Indian http://www.ncbi.nlm.nih.gov/pubmed/5651243?log$=activity ://http://www.ncbi.nlm.nih.gov/pubmed/...#036;=activity ://http://www.ncbi.nlm.nih.gov/pubmed/...#036;=activity

Anybody reviewing most of the primary study on the subject will realise that it is far from being sure that saturated fatty acid cause CVD.

Just see, for example

http://www.ncbi.nlm....mp;ordinalpos=1

http://www.ncbi.nlm....=pmtitlesearch4

http://www.ncbi.nlm....=citationsensor

http://www.ncbi.nlm....=pmtitlesearch4

http://www.ncbi.nlm.nih.gov/pubmed/2643423...$=activity


Now, as for insulin resistance, in human study, it's far from being proven that SFA cause insulin resistance http://www.ncbi.nlm....pubmed/18394213

As for inflammation, at least short chain fatty acid seems to be anti-inflammatory http://www.ncbi.nlm.nih.gov/pubmed/1752173...$=activity

The mechanism by which SFA could have promoted Inflammation was said to be by stimulating Toll-like receptors but it's doesnt seems to be the case
http://www.ncbi.nlm....=citationsensor

I'm sure you are all aware of these recent studies which found no association between SFA and CVD or mortality

http://www.ncbi.nlm....=citationsensor

http://www.ncbi.nlm....=citationsensor

You probably know that study, which found that in post-menauposal women, the more carbs and the less SFA, the more atherosclerosis women got.

http://www.ncbi.nlm....=citationsensor

As for that study that you cited, Blue, http://www.bmj.com/c...ct/322/7289/757 I don't know if you read the whole paper but in the end the authors clearly state that if you take out omega-3 interventions, the association between the other type of fat and CHD is non-signifiant.

Finally, it's the first time i'm seeing something about cognitive decline and SFA so i'll read those study and see what this is about.

I just think MANY things contradict the theory that SFA are bad for us. Too many actually to make me beleive this. Especially considering that this whole hypothesis is out from the seven country study which is probably the most flawed study of science history.

Always open to be proven wrong tho.

So far tho i'll keep eating my grass-fed steak as we evolved on and will embrace butter much more than vegetable oil.

Edited by oehaut, 23 November 2009 - 11:08 PM.

[oehaut]

I forgot to add that

Saturated fat raise LDL yes but it's mainly large and buoyant LDL particle which doesnt appear to be atherogenic.

http://www.ncbi.nlm....=citationsensor

Also Saturated fat raise both HDL and LDL and it's mostly the ratio of HDL to LDL that matter, and it seems like TG to HDL is even better for predicting CVD (because high TG and low HDL is pattern B, which actually has small dense LDL)

I've also seen in another post someone asking Why, if saturated fat are that bad, is most of the mother milk composed of it?

I'm asking the same.

We know that it's only polyunsaturated fatty acid that are found in the atherosclerotic plaque http://www.ncbi.nlm..../pubmed/7934543

It's quite easy to understand since they are so easily prone to oxidation. Oxidative stress seems to play a role in many pathologies. Saturated are stable and don't oxydize.

Why do we have such a bias againsnt saturated fat? Is it just plain dogma?

[kismet]

Why do we have such a bias againsnt saturated fat? Is it just plain dogma?

May I ask a counter-question? I hate to spoil the fun, but...

There's a bunch of population consuming high-animal-fat diet that don't have much CVD

Why do people so often support this hypothesis with the weakest form of evidence? Uncontrolled, cross-sectional, ecologic observations amount to nothing. Different peoples, a gazillon of different variables which bias the results. Among observational studies the only ones that really matter are prospective, well-controlled studies (and some of those you do in fact cite).

We know that it's only polyunsaturated fatty acid that are found in the atherosclerotic plaque http://www.ncbi.nlm..../pubmed/7934543

It's quite easy to understand since they are so easily prone to oxidation. Oxidative stress seems to play a role in many pathologies. Saturated are stable and don't oxydize.

Another point is taking such cross-sectional observations ("PUFA is found in plaques") and mechanistically, retrospectively fitting them to the desired hypothesis ("PUFA is bad"). The same could be done to condem all types of fats ("plaques are composed of fat" -> a low fat diet will be protective) but it's flawed reasoning as you must know. The reverse and the current working hypothesis seems to be that some PUFAs may be protective and therefore localise to plaques.
The question is why do the fatty acids localise to those tissues, what do they do there and do they predict CVD; in essence, the question is about the clinical impact of your mechanistic speculation, which in and of itself counts for almost nothing (as does my speculation, btw).

Good reasoning is very important.

Edited by kismet, 24 November 2009 - 11:53 PM.

[oehaut]

Why do we have such a bias againsnt saturated fat? Is it just plain dogma?

May I ask a counter-question? I hate to spoil the fun, but...

There's a bunch of population consuming high-animal-fat diet that don't have much CVD

Why do people so often support this hypothesis with the weakest form of evidence? Uncontrolled, cross-sectional, ecologic observations amount to nothing. Different peoples, a gazillon of different variables which bias the results. Among observational studies the only ones that really matter are prospective, well-controlled studies (and some of those you do in fact cite).

We know that it's only polyunsaturated fatty acid that are found in the atherosclerotic plaque http://www.ncbi.nlm..../pubmed/7934543

It's quite easy to understand since they are so easily prone to oxidation. Oxidative stress seems to play a role in many pathologies. Saturated are stable and don't oxydize.

Another point is taking such cross-sectional observations ("PUFA is found in plaques") and mechanistically, retrospectively fitting them to the desired hypothesis ("PUFA is bad"). The same could be done to condem all types of fats ("plaques are composed of fat" -> a low fat diet will be protective) but it's flawed reasoning as you must know. The reverse and the current working hypothesis seems to be that some PUFAs may be protective and therefore localise to plaques.
The question is why do the fatty acids localise to those tissues, what do they do there and do they predict CVD; in essence, the question is about the clinical impact of your mechanistic speculation, which in and of itself counts for almost nothing (as does my speculation, btw).

Good reasoning is very important.

Ok. But isn't the hypothesis born from an observationnal study? (Seven country) which was totaly flawed. That's actually what all started this bias agasint SFA. So pardon me if I chose a bunch of observational studies to show that the relation found in Key's study is far from being seen everywhere (and that's exactly why he cherry picked his data)

Also, you probably have read the whole message, i'm also talking about controlled trial which are very contradictory to say the least.


The obversionnal study i'm pointing to only put more weight on the fact that SFA per se might not be bad at all since we know population eating a lot of it and not having any problems. So yeah, it's obivous, in every case there's other factors involved.

And the other things we blame them doing, (inflammation, insulin resistance, thrombotic) have no solid human evidence to them.

Have you ever review the whole primary controlled study on diet with low SFA and high PUFA to prevent CVD? As I said, it is very controversial, and actually most of the studies don't find any benefits in decreasing SFA or increasing PUFA.

I'm not sure i'm following you here.

The fact that PUFA are found within the atherosclerotic plaque is not my "desired" hypothesis but mainly the most current one which state that PUFA uptake behind the endothelium wall by macrophage to eventualy become smooth cell cannot happen without some sort of modification of the LDL, oxydation being the most frequent one, because receptors have a loop-system regulating clean LDL particule. It juste makes sens to find some ox-ldl particule rich in w-6 and w-3 inside the plaque since only these one can ox.

http://www.ncbi.nlm.nih.gov/pubmed/3579725...$=activity
http://www.ncbi.nlm....mp;ordinalpos=1

Edited by oehaut, 25 November 2009 - 12:53 AM.

[kismet]

There's no other way of saying it, but the first 8 links, starting with Masai, are trash (they're not epidemiology, they're a particularly worthless type of epidemiology; no one said you can't use epidemiology). Everyone involved would greatly benefit if people concentrated on high(er) quality evidence, as you did later in your post.
Whatever the current hypothesis of atherogenesis is, it's of very, very low importance compared to clinical data. That is my whole point, guys, only provide evidence that matters.

Edited by kismet, 25 November 2009 - 07:30 PM.

[oehaut]

There's no other way of saying it, but the first 8 links, starting with Masai, are trash (they're not epidemiology, they're a particularly worthless type of epidemiology; no one said you can't use epidemiology). Everyone involved would greatly benefit if people concentrated on high(er) quality evidence, as you did later in your post.
Whatever the current hypothesis of atherogenesis is, it's of very, very low importance compared to clinical data. That is my whole point, guys, only provide evidence that matters.

Right I totaly agree with you.

Then just looking at the controlled trial of low-saturated fat should close this discussion about wheter saturated fat are good or not since most study did not find any advandtage to lowering SFA.

I guess this is what you mean by clinical data that matter?

[warner]

Lp(a) is dangerous to those with high ldl which likely includes those on a high fat diet. The treatment for high lp(a) is lowering ldl. There are no studies showing that lowering lp(a) itself is good.
http://www.mayoclini...8/june-06b.html

This conflicts with my personal experience (and is not supported by the references you've been citing).
A higher fat diet lowered my LDL, greatly lowered triglycerides, raised HDL, and reduced weight by about 30 pounds.
My blood sugar rarely exceeds 130 mg/dl after meals, on a diet with about 100g carbs per day.
My calorie intake is normal (i.e., I'm not restricting calories relative to my size).
A recent battery of tests shows that I am about as healthy as I can expect to be for my age.
So what benefit would I gain on a higher-carb diet?
What exactly are you suggesting/promoting?

(btw, in my case, calorie restriction increases my glaucoma risk, so that is not an option)

[JLL]

There's no other way of saying it, but the first 8 links, starting with Masai, are trash (they're not epidemiology, they're a particularly worthless type of epidemiology; no one said you can't use epidemiology). Everyone involved would greatly benefit if people concentrated on high(er) quality evidence, as you did later in your post.
Whatever the current hypothesis of atherogenesis is, it's of very, very low importance compared to clinical data. That is my whole point, guys, only provide evidence that matters.

Do you have evidence that matters (using your own criteria) showing that high-fat consumption leads to CVD? I don't think so.

[Blue]

Lp(a) is dangerous to those with high ldl which likely includes those on a high fat diet. The treatment for high lp(a) is lowering ldl. There are no studies showing that lowering lp(a) itself is good.
http://www.mayoclini...8/june-06b.html

This conflicts with my personal experience (and is not supported by the references you've been citing).
A higher fat diet lowered my LDL, greatly lowered triglycerides, raised HDL, and reduced weight by about 30 pounds.
My blood sugar rarely exceeds 130 mg/dl after meals, on a diet with about 100g carbs per day.
My calorie intake is normal (i.e., I'm not restricting calories relative to my size).
A recent battery of tests shows that I am about as healthy as I can expect to be for my age.
So what benefit would I gain on a higher-carb diet?
What exactly are you suggesting/promoting?

(btw, in my case, calorie restriction increases my glaucoma risk, so that is not an option)

The quote, supported by a source, talks about lp(a). None of the personal experiences you state refer to lp(a).

A high fat diet may, at least short-term, lead to a greater weight loss than a high carbohydrate diet. If the weight loss remains long-term, then that is a strong argument for a high-fat diet, at least for the overweight. But if there is no long-term difference in weight loss, then the argument for a high-fat diet become much less convincing. Long-term isocaloric diets, say a year or so, shows little difference on most variables between high-fat and high-carbohydrate diets.

Regarding what fats are best, that is yet another subject.

[Blue]

There's no other way of saying it, but the first 8 links, starting with Masai, are trash (they're not epidemiology, they're a particularly worthless type of epidemiology; no one said you can't use epidemiology). Everyone involved would greatly benefit if people concentrated on high(er) quality evidence, as you did later in your post.
Whatever the current hypothesis of atherogenesis is, it's of very, very low importance compared to clinical data. That is my whole point, guys, only provide evidence that matters.

Right I totaly agree with you.

Then just looking at the controlled trial of low-saturated fat should close this discussion about wheter saturated fat are good or not since most study did not find any advandtage to lowering SFA.

I guess this is what you mean by clinical data that matter?

Have a look at this thread:
http://www.imminst.o...pid-t33878.html

[kismet]

Do you have evidence that matters (using your own criteria) showing that high-fat consumption leads to CVD? I don't think so.

Well, I also don't think so. It's hard to come up with evidence that does not exist and possibly never will, because high(er) fat (>40%) and low(er) carb diets (<<50%) often turn out to be superior, but that's not the point of contention. Saturated fat is. Admittedly I am not sure why we're talking total fat intakes now?
While oehaut did in fact post several links on total fat consumption, I think they're meant to justify saturated fat intakes (which they clearly can't do). There are definitely both prospective, epidemiology and surrogate trials showing that, for instance, replacing saturated with monounsaturated fat is beneficial, but I can't comment on the totality of evidence.
While replacing some carbohydrates with any fat may be healthy, replacing them with mono could be superior still. I think that is the major points that needs refuting. Blue may have posted something on the topic of CHO vs mono, but I am too lazy to look it up right now.

Some comments I can think of regarding the posted studies:

Arteriosclerosis. 1989 Jan-Feb;9(1):129-35.
Test of effect of lipid lowering by diet on cardiovascular risk. The Minnesota Coronary Survey.
Frantz ID Jr, Dawson EA, Ashman PL, Gatewood LC, Bartsch GE, Kuba K, Brewer ER.
Without reading the study, I think it is obvious why it may not strongly support or support SaFa intakes at all. A. the treatment group consumed less SaFa, but considerably more PUFA and slightly less MUFA (both may be detrimental in and of itself, attenuating any relation ship) and B. a trend was seen in sub-group analysis.
Pretty interesting paper, though!

Am J Clin Nutr. 2004 Nov;80(5):1175-84.
Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women.
Mozaffarian D, Rimm EB, Herrington DM.
Interesting finding but may be confounded by low total fat and MUFA intake?

Edited by kismet, 28 November 2009 - 07:09 PM.

[warner]

The quote, supported by a source, talks about lp(a). None of the personal experiences you state refer to lp(a).

A high fat diet may, at least short-term, lead to a greater weight loss than a high carbohydrate diet. If the weight loss remains long-term, then that is a strong argument for a high-fat diet, at least for the overweight. But if there is no long-term difference in weight loss, then the argument for a high-fat diet become much less convincing. Long-term isocaloric diets, say a year or so, shows little difference on most variables between high-fat and high-carbohydrate diets.

Regarding what fats are best, that is yet another subject.

Good luck trying to convince us that lp(a) makes no difference, or that my lp(a) has not been lowered as LDL and TG dropped on a high-fat diet.

As for "long-term isocaloric diet" studies, the key is whether they take into consideration the insulin resistance of the subjects. For overweight subjects with significant insulin resistance (including most prediabetics and T2 diabetics), a lower-carb, higher-fat diet often results in rapid weight loss, as well as improvement in lipid profiles (as in my own case). This occurs even without a change in calorie intake, since the lower insulin levels will reset the body's steady-state weight as more fat is burned and less is stored (which is exactly what occurs in reverse if you give T2 subjects insulin injections to control their blood sugar - most gain weight w/o a change in calorie intake). Moreover, this is the only diet-based way (other than starvation) for people with significant insulin resistance (high blood sugar) to control their blood sugar without the use of drugs. If you doubt this, simply visit some real people with diabetes who are controlling their blood sugar (and weight) via carb restriction, and ask them what happens when consuming even minor amounts of carbohydrate, including "low-glycemic" forms.

OTOH, if one does not have significant insulin resistance (as is the case with most young people), then it doesn't matter much (with respect to weight) whether you're consuming carbs or fat, as shown by many studies, and as you can see in many young people.

With respect to personal weight control, my wife and I have been on a relatively high fat, low carb diet for 7 years. We dropped a lot of weight at the start, and have kept it off without a significant change in calorie intake for all those years. We are also aware (via BG and TG meters) of how our blood glucose and triglycerides behave between and after meals, and of what the risks would be of consuming more carbohydrate (most diabetes-related disease risk increases by 20-40% for each 30 mg/dl rise in BG). Are you suggesting that there is some hidden process going on that will result in our "exploding" at some point in the future? Would you really be willing to risk treating us with a high-carb diet to prevent this imagined blow-up?

I appreciate your efforts, and have learned a lot from this thread (and others where you've posted), but the discussion ends up being a bit surreal when it ignores that big block of insulin-resistant folks out there who have essentially "cured" themselves of diabetic effects with modest carb restriction. I recommend that you visit the Bernstein Forum (free membership) and communicate with some really serious and well-informed diabetic low-carbers before making generalizations about any of this diet stuff.

Edited by warner, 28 November 2009 - 07:58 PM.

[Blue]

The quote, supported by a source, talks about lp(a). None of the personal experiences you state refer to lp(a).

A high fat diet may, at least short-term, lead to a greater weight loss than a high carbohydrate diet. If the weight loss remains long-term, then that is a strong argument for a high-fat diet, at least for the overweight. But if there is no long-term difference in weight loss, then the argument for a high-fat diet become much less convincing. Long-term isocaloric diets, say a year or so, shows little difference on most variables between high-fat and high-carbohydrate diets.

Regarding what fats are best, that is yet another subject.

Good luck trying to convince us that lp(a) makes no difference, or that my lp(a) has not been lowered as LDL and TG dropped on a high-fat diet.

As for "long-term isocaloric diet" studies, the key is whether they take into consideration the insulin resistance of the subjects. For overweight subjects with significant insulin resistance (including most prediabetics and T2 diabetics), a lower-carb, higher-fat diet often results in rapid weight loss, as well as improvement in lipid profiles (as in my own case). This occurs even without a change in calorie intake, since the lower insulin levels will reset the body's steady-state weight as more fat is burned and less is stored (which is exactly what occurs in reverse if you give T2 subjects insulin injections to control their blood sugar - most gain weight w/o a change in calorie intake). Moreover, this is the only diet-based way (other than starvation) for people with significant insulin resistance (high blood sugar) to control their blood sugar without the use of drugs. If you doubt this, simply visit some real people with diabetes who are controlling their blood sugar (and weight) via carb restriction, and ask them what happens when consuming even minor amounts of carbohydrate, including "low-glycemic" forms.

OTOH, if one does not have significant insulin resistance (as is the case with most young people), then it doesn't matter much (with respect to weight) whether you're consuming carbs or fat, as shown by many studies, and as you can see in many young people.

With respect to personal weight control, my wife and I have been on a relatively high fat, low carb diet for 7 years. We dropped a lot of weight at the start, and have kept it off without a significant change in calorie intake for all those years. We are also aware (via BG and TG meters) of how our blood glucose and triglycerides behave between and after meals, and of what the risks would be of consuming more carbohydrate (most diabetes-related disease risk increases by 20-40% for each 30 mg/dl rise in BG). Are you suggesting that there is some hidden process going on that will result in our "exploding" at some point in the future? Would you really be willing to risk treating us with a high-carb diet to prevent this imagined blow-up?

I appreciate your efforts, and have learned a lot from this thread (and others where you've posted), but the discussion ends up being a bit surreal when it ignores that big block of insulin-resistant folks out there who have essentially "cured" themselves of diabetic effects with modest carb restriction. I recommend that you visit the Bernstein Forum (free membership) and communicate with some really serious and well-informed diabetic low-carbers before making generalizations about any of this diet stuff.

I am not saying that lp(a) is unimportant. Or that it has not likely improved for you if your ldl improved. But in almost all studies ldl worsens or improves less on a high-fat diet than on a high-carbohydrate diet. The opposite for hdl and triglycerides. Of course, if you have a large weight loss, that is likely far more important than your particular diet. Short term a high-fat or high-protein diet may produce a better weight loss than a high-carbohydrate. Studies (and, yes, anecdotal evidence) suggests this. The question is the long-term effects on weight. I will shortly return to this in a separate thread regarding what the literature says.

Edited by Blue, 28 November 2009 - 08:23 PM.