Wednesday, June 04, 2008

IHD and ghee

Just while ghee is in focus, there's this abstract from Jaipur. There's a typo three lines from the end where the 1 is missing from the "greater than 1 kg". I've re checked the "greater than" sign in IBIDS and it is correct, the one is still missing.

So the ghee eaters were fatter, ate more calories, more sat fat and more monounsaturated fat. Same total PUFA as the low ghee eaters. Oh, they had less coronary heart disease too. The only serious potential confounder is that the ghee eaters were younger. With multivariate analysis to account for this, p was still less than 0.001. The odds ratio was 0.23. I think this means that they were less than a quarter as likely to have a heart attack. Eat your heart out statinators! Oh!!! That pun was NOT intentional. If only ghee were patentable!

Of course the dietitians probably forgot to ask about sugar consumption. If they did check, they're not saying. Certainly not in the abstract. This gets a bit tedious sometimes!

Fatty acid intake summary from the abstract:

"This group [ghee eaters] consumed significantly more calories, saturated and mono-unsaturated fats while the consumption of polyunsaturated fats was similar in the two groups"

"Fatty acid intake analysis showed that group 1 males consumed more mono-unsaturated (n-9) fatty acids than group 2. Intake of polyunsaturated n-3 and n-6 fatty acids was similar"

I take it from the second quote that the cardiologists are falling back on monounsaturates to save the lipid hypothesis. In their repetition, they forgot to repeat the higher saturated fat intake. Some people are just so forgetful!

But it looks to me to be more likely that you can eat extra calories and be fatter while being less likely to have heart disease, provided your excess calories come from non PUFA fat sources. The sugar intake? If anyone has the full text, and if it was even remotely enquired about, I'll bet it was lower in the healthier, heavier ghee eaters.



frank said...

They didn't state whether the ghee was the real stuff made from butter or the Vanaspati ghee - a vegetarian goop with high levels of trans FAs. I will assume that because Rajasthan is in the North, the ghee was most likely the butter type.

Peter said...

Sounds disgusting. The reduced CVD points that way too!


. said...

You confused me a bit there. Reading the whole post it seems clear that the high-ghee eaters had lower heart disease, but the "they" in the third sentence of the second paragraph seems to refer to "the low ghee eaters" (closest precedent). So my heart sank (no pun intended) for a moment there.

On the issue of "fatter," it rather depends on the baseline, doesn't it? Scarlett Johansson is a lot "fatter" than, say, Nicole Ritchie, but is Scarlett obese?

This observation may seem flippant, but regarding Indians I think it's relevant. Many Indians are very, very thin, but there's a growing middle (pun intended) class that increasingly suffers from obesity. So "fatter" doesn't mean much without context.

Gyan said...

Often I read about oxidized cholesterol (also called oxysterol, I think) in ghee being a problem. Is this something I should worry about?

Gyan said...

Because ghee consumption in rural Rajasthan should be correlated with income (no despising of ghee) and also white sugar consumation is also positively correlated with income, I would expect that people eating ghee>1 kg also had more white sugar consumption (but still small compared with Western levels of consumption).
Fruit consumption in rural Rajsthan is likely to be small
but very highly correlated with income.

Peter said...

Hi Gyan,

I've never worried about oxidation of cholesterol in food. My guess was that cooking started by someone sticking a lump of meat over a fire. Lots of interesting chemicals formed there, but we've been doing it for quite some time (how long depends on which time line you read). I frequently scramble my eggs. Lipid peroxides forming in my blood is another matter, these I'd avoid...

The omega 3-6 ratio in eggs will be dependent on what the chickens ate, but battery hens, yes, lots of omega 6. How much omega 6 is "bad" I don't know, but if the amount is low you will still allow alpha linolenic acid to elongate. The total iv feeding papers basically compared safflower oil based preps with soy oil based preps to get DHA defciency in humans. Safflower oil has an omega 6:3 of 115:1 and causes DHA deficiency with neurological signs. Soy oil is omega 6:3 of 6:1 and doesn't, it even corrects that induced by by safflower oil. Such patients got zero preformed DHA as they were on total iv feeding. So even on a relatively high PUFA intake a ratio of omega 6:3 of 6:1 seems acceptable. Grass fed butter is about 1:1, I've no info on grain fed butter, but it will probably be 4:1 or less, based on carcass fatty acid ratios for grain fed beef. Either will go a long way to balance the eggs if your PUFA intake is high enough that you are worried about the ratios...

More care would be needed for pregnancy and lactation, ordinary adults seem pretty robust...

Re the ghee paper, It had occurred to me that income probably never got factored in to the multivariate analysis...

Chainey, yes, there might well be a lot of excessively thin people in the low ghee consumption group. That's one more problem with just having the abstract of the paper.


PS the other big hole in the abstract is how they assessed coronary heart disease!

Anonymous said...

Also, Gyan, oxidized cholesterol is only bad if your LDL is small dense (Pattern B), not large fluffy. Ghee seems to cause the large fluffy LDL molecules, which are protective. So it's not really a problem, I think, unless you eat lots of grain and/or refined sugars. Jan Kwasniewski had something about how the carb intake was inversely correlated to the LDL particle size. But it seems to be a problem with grains (esp wheat) and refined sugars mostly. It takes the combination of several risk factors to cause heart disease. A diet high in PUFAs, wheat, and refined sugars seems like the ideal way to cause a myocardial infarction.

(scroll down to middle, "A case for high-fat nutrition", 3rd graph)

Anonymous said...

"Safflower oil has an omega 6:3 of 115:1 and causes DHA deficiency with neurological signs." (Peter)

I've read that safflower oil has a 255:1 ratio of omega 6:3. Also, it is extremely high in PUFA (80%) in general, which is bad IMO.

"Soy oil is omega 6:3 of 6:1 and doesn't, it even corrects that induced by by safflower oil."

Soybean oil is still high in PUFAs (60%) and will cause free radicals and inflammation. The people would be much healthier on IV feeding of ghee, beef suet, coconut oil, etc. Low-PUFA is better than high-PUFA, even if the ratio is worse.

"So even on a relatively high PUFA intake a ratio of omega 6:3 of 6:1 seems acceptable."

Perhaps in terms of one paramater, neurological problems, but I think people eating low-PUFA would still live longer and healthier. Soybean oil is junk, compared to butter or ghee or beef fat. It's a metabolic poison. I like to consider all the factors. Not just omega 6:3 ratios, but the total amount of PUFAs as a percentage of calories. The ideal, IMO, is a high ratio of MUFA/PUFA, and SFA/PUFA, with low total PUFA.

Gyan said...

The Heretic reference is alarming for me. Turns out I am right in the danger zone with 45% fat (28% SFA, 4% PUFA) and 41% carb.
I guess I need to reduce carb by cutting down wheat and fruits --mango season in India right now!
Do you think 30% carb and 55% fat is fine?

Peter said...


Bruce and I eat very differently on a macronutrient basis. Personally 50g/d of carbs is plenty, 80 is a lot and I never do 100g. I'm a LC eater and do regard fruit and wheat as particularly problematic. To go high carb (say 30% of calories) you are putting enormous trust in PUFA as the sole problem.


Gyan said...

As a desk-bound worker I consume fewer calories say 1600-1800, so a 40% carb translate to 160-180 g only,

Exactly how valid is the Insulin Model that predicts Danger Zone between Low carb diet and Low Fat Diet?.
There are equations but no consideration as to the type of fat, D3 status and physical activity and how the carbs are prepared?
Are these factors trivial relative to the macronutrient ratio?
Although I must say that Indian middle class tend to have macro ratio in this Zone and is falling sick rather more
than low-fat eating rural population.

Anonymous said...

"Do you think 30% carb and 55% fat is fine?" (Gyan)

Well, that's what the data from the one study would suggest. Maybe more like 60% fat and 25% carbs would be best. At that level small dense LDL (Pattern B) should go away. But I'd like to see more data comparing all kinds of carbohydrates, like honey, potatoes, fruit, etc.

"Bruce and I eat very differently on a macronutrient basis." (Peter)

Not necessarily. I eat a little bit more carbs and protein and slightly less fat (esp PUFAs). Probably more raw food, too, including "unheated" honey.

"To go high carb (say 30% of calories) you are putting enormous trust in PUFA as the sole problem."

It's not the sole problem, but it's clearly a part of the problem. More PUFAs in the diet cause more damage to the arteries from oxysterols and other organs via lipid peroxides. I think the Kitavans are protected by their intake of coconut fat. There are also other groups, like Tokelau and Puka Puka, that eat similar to the Kitavans. I bet their arteries are clean, because their diet's low in PUFAs and thus the cholesterol's full of oleic acid rather than n-6. It's possible that certain types of carbs produce small dense LDL. Most of the studies implicate wheat and refined sugar, but I've pointed out studies showing that honey has the opposite effect as sugar. Here are more studies about this.

Anonymous said...

"Exactly how valid is the Insulin Model that predicts Danger Zone between Low carb diet and Low Fat Diet?" (Gyan)

I think the study from Stan/Heretic was epidemiological, so I would say the carbs were probably white sugar and flour and HFCS. I found studies showing that those carbs cause very different effects to honey, tubers, roots, and fruit. They really don't have much in common at all.

"Are these factors trivial relative to the macronutrient ratio?"

I'd say everything matters and you have to look at the whole diet and lifestyle to make a judgement. The folks in Kitava, Tokelau, and Puka Puka suggest that some carbs, like potatoes and tubers, are fine. The modern (sedentary) lifestyle needs to be factored into claims against carbs. Today's problems are due in large degree to grains and refined sugar and processed milk and toxic vegetable oils, IMO. Beyond that I think a lot of arguments should be qualified by saing they only apply to sedentary people and not to the people who engage in hard exercise or labor on a daily basis.

I agree with Peter that an average person should cut carbs to nothing, because they don't do enough labor or exercise to use them. They will gain weight over time, if not soon after they finish growing. That is a no-brainer. However, I think the problem is the sedentary lifestyle and the type of carbs. The obesity epidemic didn't really begin until very recently. But there are other health problems caused by the lack of vigorous exercise. The body has not evolved for sitting at a desk, sitting on a couch, etc.

Cristian said...

An interisting research:

1: J Am Coll Nutr. 2008 Feb;27(1):109-16.

Lipid metabolism and antioxidant status in sucrose vs. potato-fed rats.

Robert L, Narcy A, Rayssiguier Y, Mazur A, Rémésy C.

INRA, Unité de Nutrition Humaine, Equipe Stress Métabolique et Micronutriments,
Centre de Clermont-Ferrand/Theix, 63122 Saint-Genès Champanelle, France.

OBJECTIVE: Consumption of high levels of simple carbohydrates is associated with
several metabolic disorders in humans and in laboratory animals, including
symptoms of an early stage of metabolic syndrome (syndrome X). This disorder has
several cardiovascular risk factors, such as hypertriglyceridemia, and is
associated with an increase in oxidative stress. In contrast to sucrose, potato,
a source of complex carbohydrates and antioxidant micronutrients, was thought to
improve lipid metabolism and antioxidant protection. METHODS: We investigated the
effects of diets containing i) complex dietary carbohydrates and antioxidant
micronutrients (potato Solanum tuberosum L.), ii) complex carbohydrates (starch)
and iii) a simple carbohydrate (sucrose) on lipid metabolism and antioxidant
status in rats. RESULTS: An increase in short chain fatty acid (SCFA) pools was
observed in the cecum of rats fed a potato-based diet, resulting from an increase
in all SCFAs, especially propionate (+360%, P < 0.0001). Feeding rats a
potato-based diet for 3 weeks led to a decrease in cholesterol (-37%, potato vs.
control and -32%, potato vs. sucrose) and triglycerides (-31%, potato vs. control
and -43%, potato vs. sucrose) concentrations in triglyceride-rich lipoproteins
(TGRLP) fractions. The antioxidant status was decreased by sucrose consumption
and improved by potato consumption. CONCLUSIONS: Our present results suggest that
consumption of complex carbohydrates (provided as cooked potatoes), in
combination with different antioxidant micronutrients, may enhance the
antioxidant defences and improve lipid metabolism, when compared with starch
(complex carbohydrates) and to sucrose consumption (source of simple sugar).
These effects limit oxidative stress and reduce the risk of developing the
associated degenerative diseases, including cardiovascular disease, and could
have potential in cardiovascular disease prevention.

PMID: 18460489 [PubMed - in process]

Peter said...

Hi cristian,

Interesting, the main fascinating aspect to me is why starch should be worse than potatoes, which would appear to bring us back to gluten derived insulin like peptides and insulin mimesis of WGA. Any idea of whether it was a wheat derived starch source and if it came with the associated protein?

Also worth considering that humans don't have a ceacum and have very very different lipoprotein patterns to rats... Still interesting.

I see this group has quite a lot of publications along these lines.


Stan Bleszynski said...

Hi Peter,
Interesting discussion, you are doing tremendous job! Different topic, I found a fascinating discussion at this forum:

JeffN Re: McDougall Diet and Glycation End Products

That post is quoting some dodgy papers on AGE (Advanced Glycation End products) illustrating that the animal food is supposed to contain hundreds times more of the AGE than the plant produce.

Clin J Am Soc Nephrol 1: 1293-1299, 2006. Advanced Glycation End Products and Nephrotoxicity of High-Protein Diets


Journal of the American Dietetic Association
April 2005 (Vol. 105, Issue 4, Page 647)

Interestingly the forum participants and Jeff N (moderator) seem unable to explain why do omnivores have lover AGE level in blood than vegans and vegetarians! I am not sure how to explain these "AGE in food" papers. AGE's must be coming from the interaction with carbs - no carbohydrates no AGE, otherwise where would the "glycation" part came from if all there was were protein and fat?


Stan Bleszynski said...

Gyan wrote:

"Do you think 30% carb and 55% fat is fine?"

In my very limited experience, that seems to be fine for children but not for adults. Such a diet would result in weight gain unless you learn to control calories very rigidly. Once you up fat (animal fat) to above 50% it is so much easier just to push it to 60-70% and forget about all those carbohydrates (except green veg).

"Exactly how valid is the Insulin Model that predicts Danger Zone between Low carb diet and Low Fat Diet?."

Are you talking about this?

I don't really know how valid it is, it is just a heurestical model. Do not use it as a medical reference baceuse it may be way off! I wish somebody tested it, shouldn't be too difficult.


frank said...

There may be more AGEs in cooked meat but the meat also contains carnosine, which prevents absorption of AGEs. Vegetarians have far higher AGE serum levels despite generally using gentler cooking methods because they consume a great deal of fructose. Fructose is 7-10 times more reactive than glucose.

Peter said...

Hi Stan,

Nice to see you about! Just finishing a weekend working so minimal net time available. Hee hee, but you do visit some seedy places on the net... BTW I've been trying to get a handle on the numbers for AGEs and ALEs in the blood stream and whether dietary AGEs actually matter. The two things which do seems top matter to me are hyperglycaemia for AGES (does the McDougall think that diabetics suddenly start eating lots of grilled beef to raise their AGEs?????) and PUFA. Try making a lipid peroxide from palmitic acid!

When flicking around the McDougall site I found this whinning pdf about the WHEL study (For anyone who missed it this was the WHEL study). Apparently the participants lied about their food in take!!!!! McDougall knows.... Just read the calories in vs calories out bits, a cracker! Oh those naughty women, giving fruit and vegetables a bad name by bingeing on donuts and heavily grilled steak then claiming to have had just a small fruit juice that day. Does he think that breast cancer produces no drive to conform? These people were trying to save their life with the gifts from plants!!!!!! Misguided yes, but liars? Only if the results are appalling for McDougall.

Reminds me of Gibney. Hard to say who has done most damage.


Peter said...

Hi Frank,

Mmmm fructose, yummieee.


Cristian said...

Markedly Blunted Metabolic Effects of Fructose in Healthy Young Female Subjects Compared With Male Subjects
Caroline Couchepin, MD, Kim-Anne Lê, MSC, Murielle Bortolotti, MSC, Joana Amarante da Encarnaçao, BSC, Jean-Baptiste Oboni, BSC, Christel Tran, MD, Philippe Schneiter, PHD and Luc Tappy, MD

From the Department of Physiology, Lausanne University School of Biology and Medicine, Lausanne, Switzerland

Corresponding author: Luc Tappy, MD, Department of Physiology, 7 Rue du Bugnon, CH-1005 Lausanne, Switzerland. E-mail:

OBJECTIVE—To compare the metabolic effects of fructose in healthy male and female subjects.

RESEARCH DESIGN AND METHODS—Fasting metabolic profile and hepatic insulin sensitivity were assessed by means of a hyperglycemic clamp in 16 healthy young male and female subjects after a 6-day fructose overfeeding.

RESULTS—Fructose overfeeding increased fasting triglyceride concentrations by 71 vs. 16% in male vs. female subjects, respectively (P < 0.05). Endogenous glucose production was increased by 12%, alanine aminotransferase concentration was increased by 38%, and fasting insulin concentrations were increased by 14% after fructose overfeeding in male subjects (all P < 0.05) but were not significantly altered in female subjects. Fasting plasma free fatty acids and lipid oxidation were inhibited by fructose in male but not in female subjects.

CONCLUSIONS—Short-term fructose overfeeding produces hypertriglyceridemia and hepatic insulin resistance in men, but these effects are markedly blunted in healthy young women.

A causal role for uric acid in fructose-induced metabolic syndrome
Takahiko Nakagawa,1 Hanbo Hu,1 Sergey Zharikov,1 Katherine R. Tuttle,2 Robert A. Short,2,3 Olena Glushakova,1 Xiaosen Ouyang,1 Daniel I. Feig,4 Edward R. Block,1 Jaime Herrera-Acosta,5,{dagger} Jawaharlal M. Patel,1 and Richard J. Johnson1

1Division of Nephrology, Hypertension, and Transplantation, University of Florida, Gainesville, Florida; 2Department of Research, The Heart Institute of Spokane, and 3Biostatistics, Washington State University, Spokane, Washington; 4Division of Nephrology-Medicine, Baylor College of Medicine, Houston, Texas; and 5Departamento de Nefrologia, Instituto Nacional de Cardiologia Ignacio Chavez, Tlalpan, Mexico

Submitted 6 April 2005 ; accepted in final form 26 September 2005

The worldwide epidemic of metabolic syndrome correlates with an elevation in serum uric acid as well as a marked increase in total fructose intake (in the form of table sugar and high-fructose corn syrup). Fructose raises uric acid, and the latter inhibits nitric oxide bioavailability. Because insulin requires nitric oxide to stimulate glucose uptake, we hypothesized that fructose-induced hyperuricemia may have a pathogenic role in metabolic syndrome. Four sets of experiments were performed. First, pair-feeding studies showed that fructose, and not dextrose, induced features (hyperinsulinemia, hypertriglyceridemia, and hyperuricemia) of metabolic syndrome. Second, in rats receiving a high-fructose diet, the lowering of uric acid with either allopurinol (a xanthine oxidase inhibitor) or benzbromarone (a uricosuric agent) was able to prevent or reverse features of metabolic syndrome. In particular, the administration of allopurinol prophylactically prevented fructose-induced hyperinsulinemia (272.3 vs.160.8 pmol/l, P < 0.05), systolic hypertension (142 vs. 133 mmHg, P < 0.05), hypertriglyceridemia (233.7 vs. 65.4 mg/dl, P < 0.01), and weight gain (455 vs. 425 g, P < 0.05) at 8 wk. Neither allopurinol nor benzbromarone affected dietary intake of control diet in rats. Finally, uric acid dose dependently inhibited endothelial function as manifested by a reduced vasodilatory response of aortic artery rings to acetylcholine. These data provide the first evidence that uric acid may be a cause of metabolic syndrome, possibly due to its ability to inhibit endothelial function. Fructose may have a major role in the epidemic of metabolic syndrome and obesity due to its ability to raise uric acid.

My hyphotesis to explain why men are more prone to develop a big belly:


P.S. I beg your pardon for my poor english, I'm italian.

Cristian said...

Still on the topic of male/female differences:

Metabolic Syndrome in the Rat: Females Are Protected Against the Pro-Oxidant Effect of a High Sucrose Diet
Jérôme Busserolles1, Andrzej Mazur, Elyett Gueux, Edmond Rock and Yves Rayssiguier2

Centre de Recherche en Nutrition Humaine d’Auvergne, Unité des Maladies Métaboliques et Micronutriments, INRA, Theix, 63122 Saint-Genés-Champanelle, France

Metabolic syndrome is more prevalent in men than in women. In an experimental dietary model of metabolic syndrome, the high-fructose–fed rat, oxidative stress has been observed in males. Given that estradiol has been documented to exert an antioxidant effect, we investigated whether female rats were better protected than males against the adverse effects of a high-sucrose diet, and we studied the influence of hormonal status in female rats. Males and females were first fed a sucrose-based or starch-based diet for 2 weeks. In the males, the plasma triglyceride (TG)-raising effect of sucrose was accompanied by significantly lowered plasma {alpha}-tocopherol and a significantly lowered {alpha}-tocopherol/TG ratio (30%), suggesting that vitamin E depletion may predispose lipoproteins to subsequent oxidative stress. In males, after exposure of heart tissue homogenate to iron-induced lipid peroxidation, thiobarbituric reactive substances were significantly higher in the sucrose-fed than in the starch-fed rats. In contrast, in sucrose-fed females, neither a decrease in vitamin E/TG ratio nor an increased susceptibility of heart tissue to peroxidation was observed, despite both a significantly decreased heart superoxide dismutase activity (14%) and a significant 3-fold increase in plasma nitric oxide concentration compared with starch-fed females. The influence of hormonal status in female rats was then assessed using intact, ovariectomized, or estradiol-supplemented ovariectomized female rats fed the sucrose or starch diet for 2 weeks. After exposure of heart tissue to iron-induced lipid peroxidation, higher susceptibility to peroxidation was found only in ovariectomized females fed the sucrose diet compared with the starch group and not in intact females or ovariectomized females supplemented with estradiol. Thus, estrogens, by their effects on antioxidant capacity, might explain the sexual difference in the pro-oxidant effect of sucrose diet resulting in metabolic syndrome in rats.

Stan Bleszynski said...

Re: ...the gifts from plants!

I made that mistake last year advising my mom (age 79) to consume her portion of carbohydrates (50g) in form of something else than bread (which she never tolerated)

Result: she started eating two apples a day and got painful gout disease in her finger joints a couple of months later. It took us a few months to figure it out and remedy it (due to your posts on the subject of fructose and gout - thanks!)

"Gift From Plants" - lovely title!


Peter said...

Hi Cristian,

Nice papers, interesting that females are moderately protetced from fructose, at least until menopause. It does seem to be males who go around with that "11 months pregnant (with twins)" look, rather more than females. The bit about decreasing lipid oxidation fits in neatly with the idea that fructose essentially never reaches the systemic circulation and is rapidly converted to palmitic acid which should be highly oxidation resistant. Of course the uric acid will help too! But yes, fructose=hepatic insulin resistance, certainly in men. Elevated ALT rears its head again too!


Yes, there's all sorts of individual tweaks. OD is a great base, but there's still scope for individualisation. Glad your mum is better. Our strawberries are cropping now, have to watch out as they will probably be a major carb source for a few weeks...

All the best


Anonymous said...
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Anonymous said...

Stan, you said that 55% fat and 30% carbs would be OK for children, but bad for most adults. What about 60% fat and 25% carbs? That is what the graph from your article "A Case for high fat nutrition" suggested would drop small dense LDL to zero.

There are clear differences between carbs. Like say wheat vs. potatoes, sucrose vs. honey. Heated honey vs. unheated (or comb) honey. All these foods have different potentials for causing obesity and disease. I lost from 175 to 165 lbs (79.5 to 75 kg) by switching to raw food, including raw meats, raw eggs, raw milk, raw cream, raw fish, and raw oils. From my experience, I feel that unheated honey is healthier than fruits. Raw juices are better than whole fruit.

When you are talking about raw food I don't think there is any way most people could get fat on it, and I'm dubious that diseases like gout are possible on a largely raw diet. The fact that someone developed gout on fruit does not prove that fruit was the cause, if they were also eating other food (esp processed). Maybe a raw diet will prevent gout. I don't know for sure, but I have seen this argument being made before.

Walter Voegtlin said in his book we should cook fruit and remove all of the peels and seeds. That's another theory to consider. I'm not arguing that raw food is the cure for every disease, but I think that when some disease occurs we should definitely consider cooked food as a potential suspect. Only humans cook.