75 replies to this topic

[TheFountain]

Rwac, just because you liberate fat from your fat stores doesn't been they are being burned. "My" body uses glucose for fuel much better than fats for fuel. I have a feeling that some people can liberate their fat stores during exercise only to have the fat go back to being fat after exercise <---- this is only a conjecture though.

Then why would it be on a list of things 'we know' to be beneficial?

Edited by TheFountain, 06 October 2009 - 11:21 PM.

[HaloTeK]

Fountain - what are you talking about? I only listed polyunsaturated fats as being detrimental -- we really are uncertain about other ratios of glucose, monos, saturated fats for optimal health. Though, think it might be beneficial to eat fats in the proportion that we have in our tissues- which is usually around 55% mono, 45% sat -- and remember I'm saying nothing of absolute fat intakes-- because we don't know what is optimal yet.

Rwac, just because you liberate fat from your fat stores doesn't been they are being burned. "My" body uses glucose for fuel much better than fats for fuel. I have a feeling that some people can liberate their fat stores during exercise only to have the fat go back to being fat after exercise <---- this is only a conjecture though.

Then why would it be on a list of things 'we know' to be beneficial?

[TheFountain]

Another problem with high fat paleo diets is that generally a good portion of the fat consumed is from animal sources, and animal fat is known to contain high levels of arachidonic acid which has been linked to colorectal disorders and increased cancer potential. I wonder if it is the processing methods that yield more O6 rather than 03? I think if you are going to do a high fat diet, let the sources of fat not be animals, but healthy plant based sources like Olive oil, coconut oul, sunflower oil, etc.

[niner]

I made the list to focus in on what we have good data on, too many people are focusing on absolute carb or fat intake and are being dogmatic about what they consume. Let me phrase this again-- PEOPLE ARE BEING DOGMANTIC ABOUT WHAT THEY CONSUME.

HaloTek, I think you have a great list. I basically agree with the whole thing.

One of the studies that made me think polyunsaturates were really bad for AGEs was this one(as referenced on JLLs blog) http://inhumanexperi...-comparing.html . Even though we do not know the polyunsaturated fat intake (poor study design), the fact that lacto-ovos had higher glycation than the vegans (who had higher fructose intake) - leads me to believe that polyunsaturates are what caused the difference. If you believe I have infered wrong, you can take that opinion. It also leads me to believe that polyunsaturates are possibly a greater danger than fructose.

PUFAs are bad, but this study is kind of indirect evidence. We do know that the glycation potential of fructose is ten times that of glucose, but I don't know how to compare that to the dangers of PUFAs. More double bonds in PUFAs = more possibility of oxidation... In that regard, saturated fats are our friends. I'd rather not have a ton of PUFAs hanging out in my membranes, and look forward to losing them over time. It's really appalling that mainstream nutritional knowledge still considers "High in polyunsaturates!" to be a health claim. There are really some deeply held memes out there that are going to be hard to overturn. Imagine telling people "Oh, by the way, cooking your food is killing you..." That one goes over real well. But see the work of Helen Vlassara. The data is shocking.

[david ellis]

http://www.proteinpo...idative-stress/

Dr Eades covers this topic and he points towards a study done on humans.

Effect of short-term ketogenic diet on redox status of human blood.

Nazarewicz RR, Ziolkowski W, Vaccaro PS, Ghafourifar P.
Division of Vascular Surgery, Department of Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH 43210, USA.
The present study investigated the effect of a ketogenic diet on the blood redox status of healthy female subjects. Twenty healthy females with mean body mass index of 21.45 +/- 2.05 kg/m(2) were provided a low-carbohydrate (55 +/- 6 g; 13% total energy), high-fat (138 +/- 16 g; 74% total energy), calorie-restricted (-465 +/- 115 kcal/d) diet. The followings were tested prior to and after 14 days consumption of the diet: Whole body, body weight and total body fat; blood, complete blood count, red blood cells, white blood cells, hemoglobin, and hematocrit; plasma, 3-beta-hydroxybutyrate, total antioxidative status, and uric acid; red blood cells, total sulfhydryl content, malondialdehyde, superoxide dismutase activity, and catalase activity. After 14 days, weight loss was significant whereas no changes were detected in body fat. No alterations were observed in blood count or morphology. 3-beta-hydroxybutyrate, total antioxidative status, uric acid, and sulfhydryl content were significantly increased. There were no alterations in malondialdehyde, or superoxide dismutase or catalase activity. The present study demonstrates that 14 days of a ketogenic diet elevates blood antioxidative capacity and does not induce oxidative stress in healthy subjects.
PMID: 17663642 [PubMed - indexed for MEDLINE]

Unfortunate that a high-fat ketogenic diet AND strong calorie restriction was introduced as the same time. Calorie restriction and weight loss has strong health promoting effects so very difficult to know what the ketogenic diet contributed.

But reducing calories doesn't always improve lipid oxidation, so I wonder if this study can be tossed aside. The group with low fat and the strongest caloric restriction has the opposite effect.

[Gern]

Correct me if I'm wrong, but 60% to 65% of calories from fat still leaves some 35% to 40% possibly from carbs and that is nowhere near a ketogenic diet. It seems to me, like most studies of "low carb" diets, they are nowhere near the carb levels Atkins used in his diet/

[timar]

Seeing that topic coming up, I can't help to feel sad about the state of this forum, the nutritional blogosphere and science journalism at large.

 

Yes, high saturated-fat/animal-protein diets do indeed cause insulin resistance. The evidence is strong and conclusive, encompassing all levels of research from epidemiology to RTCs to animal and in vitro studies on the cellular pathways. It should be considered an indisputable scientific fact but alas it is not - well in nutritional science it is, but certainly not in the media and on the blogosphere, where self-proclaimed nutritonal gurus and sensationalist writers without scientific training prevail over reason and evidence, often even promoting diets diametrically opposed to it, gratefully supported by powerful food lobby interests. It is a shame really, but it only exemplifies a dangerous disconnect that is a symptom of questionable socio-cultural developments most pronounced in the US (where they are breeding creatures like Trump) but also increaslingly apparent throughout the world.

 

Oh, and by the way, I'm not promoting a vegan diet. I'm not even a vegetarian. I just know how to discern facts from fantasy and science from wishful thinking when it comes to nutrition.

Edited by timar, 10 September 2016 - 01:30 PM.

[sthira]

Seeing that topic coming up, I can't help to feel sad about the state of this forum, the nutritional blogosphere and science journalism at large.

Yes, me too. Generalized nutrition is mostly solved: eat a whole foods plant based diet (fruits, vegetables, legumes, nuts, olive oil, hit RDAs, target-supplement dietary shortfalls) avoid junk food, SAD, sugary drinks, animal protein high in sat-fat( maybe eat the shit occasionally and in small amounts) blah bleh blih... Over and over and over we recirculate the same tired questions to generalized nutrition issues that have been solved already.

MOVE ON.

Individualized nutrition --eating what's "best" for us, each individual snowflakey human, personally, individually at the particular stage of life we're in now -- this is a more interesting topic. But individualized nutrition is a technical problem, and we've no wholesale devices yet to measure within each body what we need precisely now to eat, and again later what to eat...

But even with an absolutely "perfect" diet from sunup to sundown, from birth to death, year in and year out, day after day after fucking day...we eat perfectly, never faltering for what's nutritionally best for us at the moving target of individual biology -- perfect nutrition may only grant a few extra years of healthy living. Healthy living is nothing to scoff, though, obviously, but the problems of aging are elsewhere.

To slow aging is a political issue, it's not nutrition: less than 3 percent of the budget of the National Institute on Aging, the key source of major funding in the US for research on aging, is spent on studying the fundamental biology of aging -- less than 3%!!! -- and that’s a liberal estimate. More than 50 percent of NIA's budget is devoted to Alzheimer’s-disease research. No one is arguing that we stop research on Alzheimer’s. Point to the fact that there is an enormous difference between research on aging and age-related diseases. If you cured Alzheimer’s or nutritional problems tomorrow, these solutions would add only a small amount of time to the average life expectancy in this country.

Our priorities are fucked. Until public policy straightens these, people will continue to obsess about the things we think can control: what we eat, how we excersize, bla blah bla...

[aza]

hey timar, could you post a few examples of rcts showing this using whole foods? If saturated fat increases insulin resistance but the food matrix reduces it or has no effect, then there is still no point to avoiding it. Unless someone is putting a tablespoon of butter in their coffee or trying to eat as much saturated fat as possible because it is "health promoting". In which case, stop doing that. As for animal protien i agree many people overdo it and there is no need to eat more then your activity requires. From what i've been able to find, the maximum amount of protien people can utilise is most likely between 100g and 130g.

[aza]

i had a quick look and found this study, although their definition of high sat fat was only 15%. It also used whey powder instead of a whole food based protein source, still interesting though. http://www.ncbi.nlm....pubmed/25332473

These findings suggest that short-term intake of BCAAs can influence insulin dynamics. However, in this group of overweight and obese individuals, neither high protein nor SF intake affected insulin sensitivity or plasma concentrations of lipids and lipoproteins.

Edited by aza, 11 September 2016 - 05:36 AM.

[Wagner83]

Seeing that topic coming up, I can't help to feel sad about the state of this forum, the nutritional blogosphere and science journalism at large.

 

Yes, high saturated-fat/animal-protein diets do indeed cause insulin resistance. The evidence is strong and conclusive, encompassing all levels of research from epidemiology to RTCs to animal and in vitro studies on the cellular pathways. It should be considered an indisputable scientific fact but alas it is not - well in nutritional science it is, but certainly not in the media and on the blogosphere, where self-proclaimed nutritonal gurus and sensationalist writers without scientific training prevail over reason and evidence, often even promoting diets diametrically opposed to it, gratefully supported by powerful food lobby interests. It is a shame really, but it only exemplifies a dangerous disconnect that is a symptom of questionable socio-cultural developments most pronounced in the US (where they are breeding creatures like Trump) but also increaslingly apparent throughout the world.

 

Oh, and by the way, I'm not promoting a vegan diet. I'm not even a vegetarian. I just know how to discern facts from fantasy and science from wishful thinking when it comes to nutrition.

 

¨So would you say using decent amounts of butter and eggs is unhealthy? As far as I know eating a good number of eggs daily has not been connected with any particular risks.

[Darryl]

As we're discussing insulin resistance, egg consumption is associated with diabetes risk:

 

Shin et al, 2013. Egg consumption in relation to risk of cardiovascular disease and diabetes: a systematic review and meta-analysis. The American journal of clinical nutrition, pp.ajcn-051318.

Comparison of the highest category (>1 egg/d) of egg consumption with the lowest (<1 egg/wk or never) resulted in a pooled HR (95% CI) of ... 1.42 (1.09, 1.86) for type 2 diabetes.

 

Egg consumption doesn't markedly change saturated fat intake, certainly not enough to account for a 42% increased diabetes risk, but it has a more marked effect on other dietary intakes like choline, methionine, and arachidonic acid. Plasma choline is associated with metabolic syndrome, and egg consumption is the best predictor of plasma choline.

 

Konstantinova et al, 2008. Divergent associations of plasma choline and betaine with components of metabolic syndrome in middle age and elderly men and women. The Journal of nutrition, 138(5), pp.914-920.

Konstantinova et al, 2008. Dietary patterns, food groups, and nutrients as predictors of plasma choline and betaine in middle-aged and elderly men and women.The American journal of clinical nutrition, 88(6), pp.1663-1669.

 

In excess, methionine is certainly the most toxic amino acid, causing liver oxidative stress and damage, and conversely, methionine restriction increases insulin sensitivity and fat oxidation in animal studies, and fat oxidation in humans. Egg albumen may the highest methionine protein commonly consumed by humans, and a single egg contains half of the daily methionine + cysteine requirement. At least 6 studies have found plasma methionine levels elevated in metabolic disease, but whether that's due to higher intake or intrinsic defects in metabolism isn't known. Reviewed here:

 

Adams, 2011. Emerging perspectives on essential amino acid metabolism in obesity and the insulin-resistant state. Advances in Nutrition: An International Review Journal, 2(6), pp.445-456.

 

Arachidonic acid is the precursor of a number of proinflammatory signaling molecules, and eggs from grain-fed hens are fairly high in it (156 mg/100 g), responsible for 18% of average dietary intake. Higher adipose tissue arachidonic acid content is associated with a six-fold increase in metabolic syndrome, but this is likely more due to differences in fatty acid metabolism than differences in dietary intake.

 

Williams et al, 2007. Adipose tissue arachidonic acid and the metabolic syndrome in Costa Rican adults. Clinical nutrition, 26(4), pp.474-482.

 

On high fat diets, I agree with Timar above, the causal role of high long-chain saturated fat intake in insulin resistance and diabetes is a solved issue in nutrition science. There's remaining dispute over which mechanisms that mediate this (accumulation of diacylglycerols in muscle and liver cells, ceramide biosynthesis, lipid rafting/ER stress, metabolic endotoxemia, etc.) are the most attractive drug targets. Long-chain saturated fats are certainly not the only dietary factor that plays a role, as high fructose consumption is similarly effective at inducing experimental metabolic syndrome.

 

In clinical nutrition, we've known for a very long time that low-fat, high starch diets are an effective approach to improve insulin sensitivity, and in those with diabetes, reduce and often eliminate the requirement for insulin. Some of the trials:

 

1935 Effects of the high carbohydrate-low calorie diet upon carbohydrate tolerance in diabetes mellitus
1955 Low-fat diet and therapeutic doses of insulin in diabetes mellitus
1958 Effect of rice diet on diabetes mellitus associated with vascular disease
1976 Beneficial effects of a high carbohydrate, high fiber diet on hyperglycemic diabetic men
1977 Effect of carbohydrate restriction and high carbohydrates diets on men with chemical diabetes
1979 High-carbohydrate, high-fiber diets for insulin-treated men with diabetes mellitus
1981 High carbohydrate high in fibre diet in diabetes
1982 Response of non-insulin-dependent diabetic patients to an intensive program of diet and exercise
1983 Long-term use of a high-complex-carbohydrate, high-fiber, low-fat diet and exercise in the treatment of NIDDM patients
1994 Diet and exercise in the treatment of NIDDM: the need for early emphasis
1999 Toward improved management of NIDDM: A randomized, controlled, pilot intervention using a lowfat, vegetarian diet
2005 The effects of a low-fat, plant-based dietary intervention on body weight, metabolism, and insulin sensitivity
2006 A low-fat vegan diet improves glycemic control and cardiovascular risk factors in a randomized clinical trial in individuals with type 2 diabetes
2006 Effect of short‐term Pritikin diet therapy on the metabolic syndrome
2009 A low-fat vegan diet and a conventional diabetes diet in the treatment of type 2 diabetes: a randomized, controlled, 74-wk clinical trial

 

 

 

Edited by Darryl, 17 October 2016 - 09:11 AM.

[aza]

What do you think about this study darryl? https://www.ncbi.nlm...pubmed/26993632.

 

[pamojja]

Seeing that topic coming up, I can't help to feel sad about the state of this forum, the nutritional blogosphere and science journalism at large.

 

Yes, high saturated-fat/animal-protein diets do indeed cause insulin resistance. The evidence is strong and conclusive, encompassing all levels of research from epidemiology to RTCs to animal and in vitro studies on the cellular pathways. It should be considered an indisputable scientific fact but alas it is not - well in nutritional science it is, but certainly not in the media and on the blogosphere, where self-proclaimed nutritonal gurus and sensationalist writers without scientific training prevail over reason and evidence, often even promoting diets diametrically opposed to it, gratefully supported by powerful food lobby interests. It is a shame really, but it only exemplifies a dangerous disconnect that is a symptom of questionable socio-cultural developments most pronounced in the US (where they are breeding creatures like Trump) but also increaslingly apparent throughout the world.

 

Oh, and by the way, I'm not promoting a vegan diet. I'm not even a vegetarian. I just know how to discern facts from fantasy and science from wishful thinking when it comes to nutrition.

 

I was vegetarian for 30 years with no saturated fat or animal-protein intake for 30 years, and developed pre-diabetes. With a blood-glucose meter I singled out those foods which caused the biggest blood-glucose spikes, and therefore avoided to turn the predicament of full blown diabetes around. Guess what? It wasn't fat at all, which I therefore even increased against my life-long dislike. To follow facts of science, but ignore the facts of one's own bio-individuality, wouldn't only be 'wishful thinking', but insanity.
 

[Darryl]

aza, its a newer meta-analysis that includes several new studies, which contradict the prior result. In particular a new study from Finland, which is the only study to find a significant reduction in T2D risk. It also attempts to do a dose-response meta (the prior analysis just compared highest and lowest intakes), which reduces effect size.

 

Why did the outlier (Virtanen 2015) find a negative association? It states:

Most studies have assessed egg intake by using food-frequency questionnaires, which do not usually contain detailed information about egg consumption, such as eggs in mixed dishes or eggs used in baking. However, this would add random error to the estimates of egg intake, which would attenuate the true associations. One potential explanation for the opposite findings is that eggs are seldom consumed in isolation but are usually eaten as part of a mixed dish. For example, in many countries, eggs are commonly consumed with processed red meat, such as bacon, sausages, or burgers, and processed red meat has been associated with a higher risk of T2D. Also, in many studies that found a positive association between higher egg intake and risk of T2D or cardiovascular disease, those who consumed more eggs were also more likely to smoke and have lower leisure-time physical activity. This was not observed in our study cohort 

 

It's not the first Finnish study which contradicted the studies from America, there was a prior one from 2005 that found non-significantly inverse associations.

 

So, either there's unadjusted confounding by overall dietary pattern in the American studies, or there's something unique to Finnish egg consumption, that results in outcomes different from American (or even Swedish) egg consumption.

 

The largest Finnish egg producer uses an oat+flaxseed feed for its hens, which would be expected to markedly shift the n6/n3 ratio. This suggests to me that it isn't the choline or protein content of eggs that matters, but its ratio of arachidonic acid to eicosapentanoic acid (EPA). Perhaps if flaxseed fed hen's eggs can be found at your grocer they'd have benefits in T2D progression. 

Edited by Darryl, 21 October 2016 - 05:35 AM.

[aza]

Thanks for the input darryl I do think confounding factors are far more likely though.

I dont see how the small amount of omega 3's from the switch would have that much of an effect, although i do think it would contribute .